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Prof. Huizhen Zhang
College of Public Health, Zhengzhou University, Zhengzhou, Henan, 450001, P.R. China

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0 Environmental Toxicology
0 Mechanism
0 Toxicity
0 environmental & health
0 microcystins

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Research article
Published: 28 June 2021 in International Journal of Environmental Health Research
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Microcystin-leucine arginine (MC-LR), an important hepatoxin, has the effect of promoting hepatocarcinogenesis. MicroRNA-122 (miR-122), an important tumor suppressor in liver, plays an important role in promoting cell apoptosis. Previous studies found that the expression of miR-122 was reduced after MC-LR exposure in liver. In this study, C57BL/6 mice were exposed to saline, negative control agomir, and MC-LR with or without miR-122 agomir transfection. The results indicated that MC-LR promoted the expressions of tumor suppressor genes and decreased the expressions of anti-apoptotic proteins B cell lymphoma-2 (Bcl-2) and Bcl-2-like 2 (Bcl-w), causing hepatocyte apoptosis. Under MC-LR exposure, miR-122 agomir transfection could further increase the expressions of tumor suppressor genes and the release of cytochrome-c (Cyt-c) and decrease the expressions of Bcl-2 and Bcl-w. In conclusion, miR-122 reduction can mitigate MC-LR-induced apoptosis to a certain extent, which in turn, it is likely to have contributed to MC-LR-induced hepatocarcinogenesis.

ACS Style

Rui Wang; Haohao Liu; Xingde Du; Ya Ma; Zhihui Tian; Shiyu Zhang; Linjia Shi; Hongxiang Guo; Huizhen Zhang. MicroRNA-122 overexpression promotes apoptosis and tumor suppressor gene expression induced by microcystin-leucine arginine in mouse liver. International Journal of Environmental Health Research 2021, 1 -12.

AMA Style

Rui Wang, Haohao Liu, Xingde Du, Ya Ma, Zhihui Tian, Shiyu Zhang, Linjia Shi, Hongxiang Guo, Huizhen Zhang. MicroRNA-122 overexpression promotes apoptosis and tumor suppressor gene expression induced by microcystin-leucine arginine in mouse liver. International Journal of Environmental Health Research. 2021; ():1-12.

Chicago/Turabian Style

Rui Wang; Haohao Liu; Xingde Du; Ya Ma; Zhihui Tian; Shiyu Zhang; Linjia Shi; Hongxiang Guo; Huizhen Zhang. 2021. "MicroRNA-122 overexpression promotes apoptosis and tumor suppressor gene expression induced by microcystin-leucine arginine in mouse liver." International Journal of Environmental Health Research , no. : 1-12.

Review article
Published: 30 May 2021 in Environment International
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Microcystins (MCs) are the most widely distributed cyanotoxins, which can be ingested by animals and human body in multiple ways, resulting in a threat to human health and the biodiversity of wildlife. Therefore, the study on toxic effects and mechanisms of MCs is one of the focuses of attention. Recently, the Omics techniques, i.e. genomics, transcriptomics, proteomics and metabolomics, have significantly contributed to the comprehensive understanding and revealing of the molecular mechanisms about the toxicity of MCs. This paper mainly reviews current literature using the Omics approaches to explore the toxicity mechanism of MCs in liver, gonad, spleen, brain, intestine and lung of multiple species. It was found that MCs can exert strong toxic effects on various metabolic activities and cell signal transduction in cell cycle, apoptosis, destruction of cell cytoskeleton and redox disorder, at protein, transcription and metabolism level. Meanwhile, it was also revealed that the alteration of non-coding RNAs (miRNA, circRNA and lncRNA, etc.) and gut microbiota plays an essential regulatory role in the toxic effects of MCs, especially in hepatotoxicity and reproductive toxicity. In addition, we summarized current research gaps and pointed out the future directions for research. The detailed information in this paper shows that the application and development of Omics techniques have significantly promoted the research on MCs toxicity, and it is also a valuable resource for exploring the toxic mechanism of MCs.

ACS Style

Ya Ma; Haohao Liu; Xingde Du; Ziang Shi; Xiaohui Liu; Rui Wang; Shiyu Zhang; Zhihui Tian; Linjia Shi; Hongxiang Guo; Huizhen Zhang. Advances in the toxicology research of microcystins based on Omics approaches. Environment International 2021, 154, 106661 .

AMA Style

Ya Ma, Haohao Liu, Xingde Du, Ziang Shi, Xiaohui Liu, Rui Wang, Shiyu Zhang, Zhihui Tian, Linjia Shi, Hongxiang Guo, Huizhen Zhang. Advances in the toxicology research of microcystins based on Omics approaches. Environment International. 2021; 154 ():106661.

Chicago/Turabian Style

Ya Ma; Haohao Liu; Xingde Du; Ziang Shi; Xiaohui Liu; Rui Wang; Shiyu Zhang; Zhihui Tian; Linjia Shi; Hongxiang Guo; Huizhen Zhang. 2021. "Advances in the toxicology research of microcystins based on Omics approaches." Environment International 154, no. : 106661.

Review article
Published: 19 February 2021 in Environmental Research
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Microcystins (MCs) are the most common cyanobacteria toxins in eutrophic water, which have strong hepatotoxicity. In the past decade, epidemiological and toxicological studies on liver damage caused by MCs have proliferated, and new mechanisms of hepatotoxicity induced by MCs have also been discovered and confirmed. However, there has not been a comprehensive and systematic review of these new findings. Therefore, this paper summarizes the latest advances in studies on the hepatotoxicity of MCs to reveal the effects and mechanisms of hepatotoxicity induced by MCs. Current epidemiological studies have confirmed that symptoms or signs of liver damage appear after human exposure to MCs, and a long time of exposure can even lead to liver cancer. Toxicological studies have shown that MCs can affect the expression of oncogenes by activating cell proliferation pathways such as MAPK and Akt, thereby promoting the occurrence and development of cancer. The latest evidence shows that epigenetic modifications may play an important role in MCs-induced liver cancer. MCs can cause damage to the liver by inducing hepatocyte death, mainly manifested as apoptosis and necrosis. The imbalance of liver metabolic homeostasis may be involved in hepatotoxicity induced by MCs. In addition, the combined toxicity of MCs and other toxins are also discussed in this article. This detailed information will be a valuable reference for further exploring of MCs-induced hepatotoxicity.

ACS Style

Linjia Shi; Xingde Du; Haohao Liu; Xinghai Chen; Ya Ma; Rui Wang; Zhihui Tian; Shiyu Zhang; Hongxiang Guo; Huizhen Zhang. Update on the adverse effects of microcystins on the liver. Environmental Research 2021, 195, 110890 .

AMA Style

Linjia Shi, Xingde Du, Haohao Liu, Xinghai Chen, Ya Ma, Rui Wang, Zhihui Tian, Shiyu Zhang, Hongxiang Guo, Huizhen Zhang. Update on the adverse effects of microcystins on the liver. Environmental Research. 2021; 195 ():110890.

Chicago/Turabian Style

Linjia Shi; Xingde Du; Haohao Liu; Xinghai Chen; Ya Ma; Rui Wang; Zhihui Tian; Shiyu Zhang; Hongxiang Guo; Huizhen Zhang. 2021. "Update on the adverse effects of microcystins on the liver." Environmental Research 195, no. : 110890.

Journal article
Published: 18 February 2021 in Ecotoxicology and Environmental Safety
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As an emerging pollutant in the aquatic environment, microcystin-LR (MC-LR) can enter the body through multiple pathways, and then induce apoptosis and gonadal damage, affecting reproductive function. Previous studies focused on male reproductive toxicity induced by MC-LR neglecting its effects on females. The apoptotic signal-regulated kinase 1 (ASK1) is an upstream protein of P38/JNK pathway, closely associated with apoptosis and organ damage. However, the role of ASK1 in MC-LR-induced reproductive toxicity is unclear. Therefore, this study investigated the role of ASK1 in mouse ovarian injury and apoptosis induced by MC-LR. After MC-LR exposure, ASK1 expression in mouse ovarian granulosa cells was increased at the protein and mRNA levels, and decreased following pretreatment by antioxidant N-acetylcysteine, suggesting that MC-LR-induced oxidative stress has a regulatory role in ASK1 expression. Inhibition of ASK1 expression with siASK1 and NQDI-1 could effectively alleviate MC-LR-induced mitochondrial membrane potential damage and apoptosis in ovarian granulosa cells, as well as pathological damage, apoptosis and the decreased gonadal index in ovaries of C57BL/6 mice. Moreover, the P38/JNK pathway and downstream apoptosis-related proteins (P-P38, P-JNK, P-P53, Fas) and genes (MKK4, MKK3, Ddit3, Mef2c) were activated in vivo and vitro, but their activation was restrained after ASK1 inhibition. Data presented herein suggest that the ASK1-mediated P38/JNK pathway is involved in ovarian injury and apoptosis induced by MC-LR in mice. It is confirmed that ASK1 has an important role in MC-LR-induced ovarian injury, which provides new insights for preventing MCs-induced reproductive toxicity in females.

ACS Style

Xingde Du; Haohao Liu; Xiaohui Liu; Xinghai Chen; Le Yuan; Ya Ma; Hui Huang; Yueqin Wang; Rui Wang; Shiyu Zhang; Zhihui Tian; Linjia Shi; Huizhen Zhang. Microcystin-LR induces ovarian injury and apoptosis in mice via activating apoptosis signal-regulating kinase 1-mediated P38/JNK pathway. Ecotoxicology and Environmental Safety 2021, 213, 112066 .

AMA Style

Xingde Du, Haohao Liu, Xiaohui Liu, Xinghai Chen, Le Yuan, Ya Ma, Hui Huang, Yueqin Wang, Rui Wang, Shiyu Zhang, Zhihui Tian, Linjia Shi, Huizhen Zhang. Microcystin-LR induces ovarian injury and apoptosis in mice via activating apoptosis signal-regulating kinase 1-mediated P38/JNK pathway. Ecotoxicology and Environmental Safety. 2021; 213 ():112066.

Chicago/Turabian Style

Xingde Du; Haohao Liu; Xiaohui Liu; Xinghai Chen; Le Yuan; Ya Ma; Hui Huang; Yueqin Wang; Rui Wang; Shiyu Zhang; Zhihui Tian; Linjia Shi; Huizhen Zhang. 2021. "Microcystin-LR induces ovarian injury and apoptosis in mice via activating apoptosis signal-regulating kinase 1-mediated P38/JNK pathway." Ecotoxicology and Environmental Safety 213, no. : 112066.

Journal article
Published: 05 December 2020 in Food and Chemical Toxicology
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Microcystin-LR (MC-LR) is an emerging water pollutant produced by eutrophication of water. It could be absorbed into human body via contaminated food and drinking water causing severe reproductive toxicity. Previous studies showed that MC-LR could regulate autophagy by inducing endoplasmic reticulum (ER) stress thereby causing female reproductive toxicity. However, the molecular mechanisms of MC-LR-induced autophagy remain to be elucidated. It is known that IRE1 and CaMKKβ pathways are two important pathways involved in autophagy induced by ER stress. Hence, this paper investigated the roles of both pathways in MC-LR-induced autophagy in mouse ovarian cells. The results showed that MC-LR significantly up-regulated the expression of autophagy marker proteins LC3Ⅱ and BECLIN1 and down-regulated the expression of P62 in vivo and in vitro. MC-LR-caused increase of autophagosomes could be observed in KK-1 cells by MDC staining. MC-LR induced the formation of autolysosomes as indicated by the overlap of LAMP1 and LC3. Meanwhile, MC-LR significantly activated the proteins in IRE1 pathway (IRE1, XBP1 and JNK) and in CaMKKβ pathway (CaMKKβ, AMPK, mTOR). Furthermore, MC-LR caused weight loss and ovarian histopathological damage in mice. In contrast, after the expression and function of IRE1 and CaMKKβ with siRNA in vitro and by inhibitors (4μ8C and STO-609, respectively) in vivo, the up-regulation of LC3Ⅱ and BECLIN1 and the degradation of P62 induced by MC-LR were significantly suppressed. MC-LR-induced autophagosomes in KK-1 cells and autolysosomes in mouse ovarian cells were also decreased. Moreover, the knockdown of IRE1 and CaMKKβ relieved MC-LR-induced histopathological injury to mouse ovaries. These results indicated that MC-LR induced ovarian cell autophagy and ovarian injury via IRE1 and CaMKKβ pathways. This study is the first study revealing the molecular mechanisms of MC-LR-induced autophagy of ovarian cells and providing new insights into the female reproductive toxicity of MC-LR.

ACS Style

Ya Ma; Haohao Liu; Xingde Du; Pavankumar Petlulu; Xinghai Chen; Rui Wang; Shiyu Zhang; Zhihui Tian; Linjia Shi; Hongxiang Guo; Huizhen Zhang. IRE1 and CaMKKβ pathways to reveal the mechanism involved in microcystin-LR-induced autophagy in mouse ovarian cells. Food and Chemical Toxicology 2020, 147, 111911 .

AMA Style

Ya Ma, Haohao Liu, Xingde Du, Pavankumar Petlulu, Xinghai Chen, Rui Wang, Shiyu Zhang, Zhihui Tian, Linjia Shi, Hongxiang Guo, Huizhen Zhang. IRE1 and CaMKKβ pathways to reveal the mechanism involved in microcystin-LR-induced autophagy in mouse ovarian cells. Food and Chemical Toxicology. 2020; 147 ():111911.

Chicago/Turabian Style

Ya Ma; Haohao Liu; Xingde Du; Pavankumar Petlulu; Xinghai Chen; Rui Wang; Shiyu Zhang; Zhihui Tian; Linjia Shi; Hongxiang Guo; Huizhen Zhang. 2020. "IRE1 and CaMKKβ pathways to reveal the mechanism involved in microcystin-LR-induced autophagy in mouse ovarian cells." Food and Chemical Toxicology 147, no. : 111911.

Journal article
Published: 26 November 2020 in Science of The Total Environment
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Microcystin-leucine arginine (MC-LR), an intracellular toxin to cause reproduction toxicity, is produced by blooming cyanobacteria and widely distributed in eutrophic waters. It is revealed that MC-LR-induced female reproductive toxicity is more severe than male reproductive toxicity. Previous studies mainly focused on male reproductive toxicity, and the molecular mechanisms of MC-LR-induced apoptosis, follicular atresia and infertility in female remain largely unclear. Here, it was found that MC-LR treatment could induce apoptosis, inflammation, follicular atresia, and decrease of gonadal index in mice ovaries. RNA-Seq data showed that the up-regulation of DNA-damage inducible transcript 3 (Ddit3) under endoplasmic reticulum (ER) stress had predominantly regulatory role in MC-LR-induced apoptotic pathway. Furthermore, MC-LR exposure promoted cleavage of activating transcription factor 6 (ATF6, 50kd), inositol-requiring enzyme 1 (Ire1) expression, phosphorylation of IRE1, mitogen-activated protein kinase 5 (Map3k5) and Ddit3 expression, which was accompanied by the upregulation of death receptor 5 (Dr5) and active-caspase-3, and a decrease in Bcl-2 expression. ER stress inhibitor 4-Phenyl butyric acid (4-PBA) ameliorated these MC-LR-induced changes in protein or mRNA level. More importantly, knockdown of Ddit3 suppressed MC-LR-induced cell apoptosis and follicular atresia by directly regulating Dr5 and Bcl-2. Additionally, it was also found that MC-LR increased Map3k5 phosphorylation by inhibiting protein phosphatase 2A (PP2A) activity, and then promoted Ddit3 expression. In short, our data suggests that Ddit3 promotes MC-LR-induced mice ovarian cells apoptosis and follicular atresia via ER stress activation, which provides a new insight into the relation between infertility in females and the emerging water pollutant MC-LR.

ACS Style

Haohao Liu; Zhihui Tian; Yaxin Guo; Xiaohui Liu; Ya Ma; Xingde Du; Rui Wang; Shiyu Zhang; Linjia Shi; Hongxiang Guo; Huizhen Zhang. Microcystin-leucine arginine exposure contributes to apoptosis and follicular atresia in mice ovaries by endoplasmic reticulum stress-upregulated Ddit3. Science of The Total Environment 2020, 756, 144070 .

AMA Style

Haohao Liu, Zhihui Tian, Yaxin Guo, Xiaohui Liu, Ya Ma, Xingde Du, Rui Wang, Shiyu Zhang, Linjia Shi, Hongxiang Guo, Huizhen Zhang. Microcystin-leucine arginine exposure contributes to apoptosis and follicular atresia in mice ovaries by endoplasmic reticulum stress-upregulated Ddit3. Science of The Total Environment. 2020; 756 ():144070.

Chicago/Turabian Style

Haohao Liu; Zhihui Tian; Yaxin Guo; Xiaohui Liu; Ya Ma; Xingde Du; Rui Wang; Shiyu Zhang; Linjia Shi; Hongxiang Guo; Huizhen Zhang. 2020. "Microcystin-leucine arginine exposure contributes to apoptosis and follicular atresia in mice ovaries by endoplasmic reticulum stress-upregulated Ddit3." Science of The Total Environment 756, no. : 144070.

Review article
Published: 28 September 2020 in Environmental Research
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Microcystin-leucine-arginine (MC-LR) is an emerging environmental pollutant produced by cyanobacteria that poses a threat to wild life and human health. In recent years, the reproductive toxicity of MC-LR has gained widespread attention, a large number of toxicological studies have filled the gaps in past research and more molecular mechanisms have been elucidated. Hence, this paper reviews the latest research advances on MC-LR-induced reproductive toxicity. MC-LR can damage the structure and function of the testis, ovary, prostate, placenta and other organs of animals and then reduce their fertility. Meanwhile, MC-LR can also be transmitted through the placenta to the offspring causing trans-generational and developmental toxicity including death, malformation, growth retardation, and organ dysfunction in embryos and juveniles. The mechanisms of MC-LR-induced reproductive toxicity mainly include the inhibition of protein phosphatase 1/2A (PP1/2A) activity and the induction of oxidative stress. On the one hand, MC-LR triggers the hyperphosphorylation of certain proteins by inhibiting intracellular PP1/2A activity, thereby activating multiple signaling pathways that cause inflammation and blood-testis barrier destruction, etc. On the other hand, MC-LR-induced oxidative stress can result in cell programmed death via the mitochondrial and endoplasmic reticulum pathways. It is worth noting that epigenetic modifications are also involved in reproductive cell apoptosis, which may be an important direction for future research. Furthermore, this paper proposes for the first time that MC-LR can produce estrogenic effects in animals as an environmental estrogen. New findings and suggestions in this review could be areas of interest for future research.

ACS Style

Shiyu Zhang; Xingde Du; Haohao Liu; Michael D. Losiewic; Xinghai Chen; Ya Ma; Rui Wang; Zhihui Tian; Linjia Shi; Hongxiang Guo; Huizhen Zhang. The latest advances in the reproductive toxicity of microcystin-LR. Environmental Research 2020, 192, 110254 .

AMA Style

Shiyu Zhang, Xingde Du, Haohao Liu, Michael D. Losiewic, Xinghai Chen, Ya Ma, Rui Wang, Zhihui Tian, Linjia Shi, Hongxiang Guo, Huizhen Zhang. The latest advances in the reproductive toxicity of microcystin-LR. Environmental Research. 2020; 192 ():110254.

Chicago/Turabian Style

Shiyu Zhang; Xingde Du; Haohao Liu; Michael D. Losiewic; Xinghai Chen; Ya Ma; Rui Wang; Zhihui Tian; Linjia Shi; Hongxiang Guo; Huizhen Zhang. 2020. "The latest advances in the reproductive toxicity of microcystin-LR." Environmental Research 192, no. : 110254.

Research article
Published: 14 March 2020 in Environmental Toxicology
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Microcystin‐leucine arginine (MC‐LR) is a cyclic heptapeptide hepatotoxin produced by cyanobacteria. MicroRNA‐122 (miR‐122) is specifically expressed in the liver. This study focuses on the role of miR‐122 in MC‐LR‐induced dysregulation of hepatic iron homeostasis in C57BL/6 mice. The thirty mice were randomly divided into five groups (Control, 12.5 μg/kg·BW MC‐LR, 25 μg/kg·BW MC‐LR, Negative control agomir and 25 μg/kg·BW MC‐LR + miR‐122 agomir). The results show that MC‐LR decreases the expressions of miR‐122, Hamp, and its related regulators, while increasing the content of hepatic iron and the expressions of FPN1 and Tmprss6. Furthermore, miR‐122 agomir pretreatment improves MC‐LR induced dysregulation of hepatic iron homeostasis by arousing the related regulators and reducing the expression of Tmprss6. These results suggest that miR‐122 agomir can prevent the accumulation of hepatic iron induced by MC‐LR, which may be related to the regulation of hepcidin by BMP/SMAD and IL‐6/STAT signaling pathways.

ACS Style

Rui Wang; Xiaohui Liu; Jinxia Wu; Haohao Liu; Wenjun Wang; Xinghai Chen; Le Yuan; Yueqin Wang; Xingde Du; Ya Ma; Michael D. Losiewicz; Xiaofeng Zhang; Huizhen Zhang. Role of microRNA‐122 in microcystin‐leucine arginine‐induced dysregulation of hepatic iron homeostasis in mice. Environmental Toxicology 2020, 35, 822 -830.

AMA Style

Rui Wang, Xiaohui Liu, Jinxia Wu, Haohao Liu, Wenjun Wang, Xinghai Chen, Le Yuan, Yueqin Wang, Xingde Du, Ya Ma, Michael D. Losiewicz, Xiaofeng Zhang, Huizhen Zhang. Role of microRNA‐122 in microcystin‐leucine arginine‐induced dysregulation of hepatic iron homeostasis in mice. Environmental Toxicology. 2020; 35 (8):822-830.

Chicago/Turabian Style

Rui Wang; Xiaohui Liu; Jinxia Wu; Haohao Liu; Wenjun Wang; Xinghai Chen; Le Yuan; Yueqin Wang; Xingde Du; Ya Ma; Michael D. Losiewicz; Xiaofeng Zhang; Huizhen Zhang. 2020. "Role of microRNA‐122 in microcystin‐leucine arginine‐induced dysregulation of hepatic iron homeostasis in mice." Environmental Toxicology 35, no. 8: 822-830.

Journal article
Published: 01 February 2020 in Chemosphere
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Microcystin-leucine arginine (MC-LR) is a variant of microcystins (MCs), which poses a serious threat to the reproductive system. Histone acetylation modification can regulate the expressions of apoptosis-related genes. However the mechanisms of histone acetylation involving MC-LR-induced apoptosis were not understood. This study investigated the change of histone acetylation and its role in apoptosis and cell cycle arrest induced by MC-LR. MC-LR enhanced the activity of histone deacetylase (HDAC), decreased the activity of histone acetylase (HAT), up-regulated the expression of HDAC1, and down-regulated the expressions of Ac-H3 and Ac-H4 in vitro and vivo. Meanwhile, MC-LR induced testicular tissue injury and increased the expressions of apoptosis-related genes, such as Bax, Caspase3 and Caspase8, ultimately causing cells apoptosis in testicular tissues. Furthermore, MC-LR also induced cell cycle arrest in S phase, increased the expression of P21Wif1/Cip1, and inhibited the expressions of cyclinD1, cyclinE1, CDK2 and E2F1. Importantly, HDAC inhibitor Trichostatin A (TSA) could ameliorate MC-LR-induced apoptosis and cell cycle arrest by reverse-regulating the expressions of these proteins. These results indicated that MC-LR could activate the mitochondrial apoptotic pathway and disorder the cell cycle pathway to induce the cell apoptosis by enhancing HDAC activity and reducing histone acetylation of normal testicular cells in SD rats. Hence, histone acetylation has a vital function in MC-LR-induced apoptosis in SD rat testicular cells, which provides a new insight on the reproductive toxicity of male induced by MC-LR.

ACS Style

Yueqin Wang; Haohao Liu; Xiaohui Liu; Xiaofeng Zhang; Jinxia Wu; Le Yuan; Xingde Du; Rui Wang; Ya Ma; Xinghai Chen; Xuemin Cheng; Donggang Zhuang; Huizhen Zhang. Histone acetylation plays an important role in MC-LR-induced apoptosis and cycle disorder in SD rat testicular cells. Chemosphere 2020, 241, 125073 .

AMA Style

Yueqin Wang, Haohao Liu, Xiaohui Liu, Xiaofeng Zhang, Jinxia Wu, Le Yuan, Xingde Du, Rui Wang, Ya Ma, Xinghai Chen, Xuemin Cheng, Donggang Zhuang, Huizhen Zhang. Histone acetylation plays an important role in MC-LR-induced apoptosis and cycle disorder in SD rat testicular cells. Chemosphere. 2020; 241 ():125073.

Chicago/Turabian Style

Yueqin Wang; Haohao Liu; Xiaohui Liu; Xiaofeng Zhang; Jinxia Wu; Le Yuan; Xingde Du; Rui Wang; Ya Ma; Xinghai Chen; Xuemin Cheng; Donggang Zhuang; Huizhen Zhang. 2020. "Histone acetylation plays an important role in MC-LR-induced apoptosis and cycle disorder in SD rat testicular cells." Chemosphere 241, no. : 125073.

Review
Published: 12 September 2019 in Toxins
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The widespread distribution of cyanobacteria in the aquatic environment is increasing the risk of water pollution caused by cyanotoxins, which poses a serious threat to human health. However, the structural characterization, distribution and identification techniques of cyanotoxins have not been comprehensively reviewed in previous studies. This paper aims to elaborate the existing information systematically on the diversity of cyanotoxins to identify valuable research avenues. According to the chemical structure, cyanotoxins are mainly classified into cyclic peptides, alkaloids, lipopeptides, nonprotein amino acids and lipoglycans. In terms of global distribution, the amount of cyanotoxins are unbalanced in different areas. The diversity of cyanotoxins is more obviously found in many developed countries than that in undeveloped countries. Moreover, the threat of cyanotoxins has promoted the development of identification and detection technology. Many emerging methods have been developed to detect cyanotoxins in the environment. This communication provides a comprehensive review of the diversity of cyanotoxins, and the detection and identification technology was discussed. This detailed information will be a valuable resource for identifying the various types of cyanotoxins which threaten the environment of different areas. The ability to accurately identify specific cyanotoxins is an obvious and essential aspect of cyanobacterial research.

ACS Style

Xingde Du; Haohao Liu; Le Yuan; Yueqin Wang; Ya Ma; Rui Wang; Xinghai Chen; Michael D. Losiewicz; Hongxiang Guo; Huizhen Zhang. The Diversity of Cyanobacterial Toxins on Structural Characterization, Distribution and Identification: A Systematic Review. Toxins 2019, 11, 530 .

AMA Style

Xingde Du, Haohao Liu, Le Yuan, Yueqin Wang, Ya Ma, Rui Wang, Xinghai Chen, Michael D. Losiewicz, Hongxiang Guo, Huizhen Zhang. The Diversity of Cyanobacterial Toxins on Structural Characterization, Distribution and Identification: A Systematic Review. Toxins. 2019; 11 (9):530.

Chicago/Turabian Style

Xingde Du; Haohao Liu; Le Yuan; Yueqin Wang; Ya Ma; Rui Wang; Xinghai Chen; Michael D. Losiewicz; Hongxiang Guo; Huizhen Zhang. 2019. "The Diversity of Cyanobacterial Toxins on Structural Characterization, Distribution and Identification: A Systematic Review." Toxins 11, no. 9: 530.

Review article
Published: 03 July 2019 in Environmental Research
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Bisphenol A (BPA) is an industrial component commonly used in synthesis of polycarbonate plastics, epoxy resin and other polymer materials. Due to its mass productions and widespread applications, the presence of BPA is ubiquitous in the environment. BPA can enter the body via different ways such as digestive tract, respiratory tract and dermal tract. As an endocrine disruptor, BPA has estrogen-like and anti-androgen effects causing damages to different tissues and organs, including reproductive system, immune system and neuroendocrine system, etc. Recently, it has been shown that BPA could induce carcinogenesis and mutagenesis in animal models. Here, the underlying mechanisms of BPA-induced multi-organ toxicity were well summarized, involving the receptor pathways, disruption of neuroendocrine system, inhibition of enzymes, modulation of immune and inflammatory responses, as well as genotoxic and epigenetic mechanisms. The aim of this review is to compile the available current research data regarding BPA and provide an overview of the current status of BPA exposure and relevant health effects covering reproductive, developmental, metabolic, immuno, respiratory, hepatic and renal toxicity and carcinogenesis of BPA. This review provides comprehensive data of BPA toxicity on human health and related mechanisms. We also identify any missing data which should be addressed by further studies.

ACS Style

Ya Ma; Haohao Liu; Jinxia Wu; Le Yuan; Yueqin Wang; Xingde Du; Rui Wang; Phelisters Wegesa Marwa; Pavankumar Petlulu; Xinghai Chen; Huizhen Zhang. The adverse health effects of bisphenol A and related toxicity mechanisms. Environmental Research 2019, 176, 108575 .

AMA Style

Ya Ma, Haohao Liu, Jinxia Wu, Le Yuan, Yueqin Wang, Xingde Du, Rui Wang, Phelisters Wegesa Marwa, Pavankumar Petlulu, Xinghai Chen, Huizhen Zhang. The adverse health effects of bisphenol A and related toxicity mechanisms. Environmental Research. 2019; 176 ():108575.

Chicago/Turabian Style

Ya Ma; Haohao Liu; Jinxia Wu; Le Yuan; Yueqin Wang; Xingde Du; Rui Wang; Phelisters Wegesa Marwa; Pavankumar Petlulu; Xinghai Chen; Huizhen Zhang. 2019. "The adverse health effects of bisphenol A and related toxicity mechanisms." Environmental Research 176, no. : 108575.

Research article
Published: 03 June 2019 in Environmental Toxicology
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Microcystin‐LR (MC‐LR), a potent endotoxin, can induce reproductive toxicity. In order to investigate the role and mechanisms of apoptosis (p53‐dependent and mitochondrial pathways) of germ cells induced by MC‐LR, the co‐cultured primary Sertoli‐germ cells from Sprague‐Dawley rats were used for the experiments. Expression levels of proteins, genes, and mitochondrial membrane potential (MMP) were obtained after exposing co‐cultured Sertoli‐germ cells to MC‐LR with or without the addition of the p53 inhibitor, pifithrin‐α (PFT‐α), and MMP inhibitor, cyclosporin A (CsA). Results indicated that MC‐LR could activate p53‐dependent pathway‐associated proteins in Sertoli‐germ cells, leading to a decrease in MMP (indicating the opening of mitochondrial permeability transition pore [mPTP] and the release of Cytochrome‐c [Cyt‐c]) from the mitochondria into the cytoplasm and eventually the induction of apoptosis. PFT‐α inhibited the expression ofp53, ameliorated the MMP of the co‐cultured Sertoli‐germ cells, and prevented the release of Cyt‐c from the mitochondria into the cytoplasm, which reduces the occurrence of apoptosis. Similarly, the decreased release of Cyt‐c from the mitochondria into the cytoplasm and the declined level of apoptosis in Sertoli‐germ cells induced by MC‐LR were observed after the addition of CsA. These results indicated that the apoptosis of the co‐cultured Sertoli‐germ cells induced by MC‐LR was mediated by the p53‐dependent pathway, with the involvement of the opening of mPTP.

ACS Style

Jinxia Wu; Haohao Liu; Hui Huang; Le Yuan; Chuanrui Liu; Yueqin Wang; Xuemin Cheng; Donggang Zhuang; Min Xu; Xinghai Chen; Michael D. Losiewicz; Huizhen Zhang. p53 ‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR. Environmental Toxicology 2019, 34, 1074 -1084.

AMA Style

Jinxia Wu, Haohao Liu, Hui Huang, Le Yuan, Chuanrui Liu, Yueqin Wang, Xuemin Cheng, Donggang Zhuang, Min Xu, Xinghai Chen, Michael D. Losiewicz, Huizhen Zhang. p53 ‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR. Environmental Toxicology. 2019; 34 (10):1074-1084.

Chicago/Turabian Style

Jinxia Wu; Haohao Liu; Hui Huang; Le Yuan; Chuanrui Liu; Yueqin Wang; Xuemin Cheng; Donggang Zhuang; Min Xu; Xinghai Chen; Michael D. Losiewicz; Huizhen Zhang. 2019. "p53 ‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR." Environmental Toxicology 34, no. 10: 1074-1084.

Review
Published: 22 March 2019 in Nutritional Neuroscience
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Objective: The association between vitamin E supplementation and Alzheimer's disease (AD) was controversial because of conflicting data in the literature. This study was designed to systematically evaluate evidence about the efficacy of vitamin E supplementation not only on the risk but also on the progression of AD. Design: Five electronic databases were searched for studies published up to June 2017. Articles reporting vitamin E supplementation and AD were included, and the random-effect model was performed for the meta-analysis about the relationship between vitamin E supplementation and AD. Results: Five cohort studies and three randomized controlled trial (RCT) studies (total n = 14,262) involving 1313 cases about vitamin E effects on the risk of AD and 244 cases about effects on progression of AD. The pooled RR for vitamin E supplemental and risk of AD was 0.81 [95% CI: 0.50–1.33, I2 = 69.2%]. Suitable data could not be extracted to do meta-analysis as there was no unified standard of outcome measure for studies on AD progression. We carefully analyzed and evaluated the authenticity and accuracy of every single trial, while reliable evidence could not be obtained. Conclusions: From what we do, neither the synthetic data on risk of AD nor the critical review on progression of AD could provide enough evidence on our research. Thus, we cannot draw a specific conclusion on the association or correlation between Vitamin E and AD.

ACS Style

Wanyu Wang; Jiao Li; Huizhen Zhang; Xiaokai Wang; Xiaofeng Zhang. Effects of vitamin E supplementation on the risk and progression of AD: a systematic review and meta-analysis. Nutritional Neuroscience 2019, 24, 13 -22.

AMA Style

Wanyu Wang, Jiao Li, Huizhen Zhang, Xiaokai Wang, Xiaofeng Zhang. Effects of vitamin E supplementation on the risk and progression of AD: a systematic review and meta-analysis. Nutritional Neuroscience. 2019; 24 (1):13-22.

Chicago/Turabian Style

Wanyu Wang; Jiao Li; Huizhen Zhang; Xiaokai Wang; Xiaofeng Zhang. 2019. "Effects of vitamin E supplementation on the risk and progression of AD: a systematic review and meta-analysis." Nutritional Neuroscience 24, no. 1: 13-22.

Review
Published: 26 September 2018 in World Journal of Clinical Cases
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Microcystins (MCs) are produced by certain bloom-forming cyanobacteria that can induce toxicity in various organs, including renal toxicity, reproductive toxicity, cardiotoxicity, and immunosuppressive effects. It has been a significant global environmental issue due to its harm to the aquatic environment and human health. Numerous investigators have demonstrated that MC exposure can induce a widespread epidemic of enterogastritis with symptoms similar to food poisoning in areas close to lakes. Both in vivo and in vitro studies have provided evidence of positive associations between MC exposure and gastrointestinal toxicity. The toxicity of MCs on the gastrointestinal tract is multidimensional. MCs can affect gastrointestinal barrier function and shift the structure of gut microbiota in different gut regions. Furthermore, MCs can inhibit the secretion of gastrointestinal digestive enzymes and the release of inflammatory cytokines, which affects the expression of immune-related genes in the intestine. The damage of the intestine is closely correlated to MC exposure because the intestine is the main site for the digestion and absorption of nutrients. The damage to the gastrointestinal tract due to MCs was summarized from different aspects, which can be used as a foundation for further exploration of molecular damage mechanisms.

ACS Style

Jin-Xia Wu; Hui Huang; Lei Yang; Xiao-Feng Zhang; Shen-Shen Zhang; Hao-Hao Liu; Yue-Qin Wang; Le Yuan; Xue-Min Cheng; Dong-Gang Zhuang; Hui-Zhen Zhang. Gastrointestinal toxicity induced by microcystins. World Journal of Clinical Cases 2018, 6, 344 -354.

AMA Style

Jin-Xia Wu, Hui Huang, Lei Yang, Xiao-Feng Zhang, Shen-Shen Zhang, Hao-Hao Liu, Yue-Qin Wang, Le Yuan, Xue-Min Cheng, Dong-Gang Zhuang, Hui-Zhen Zhang. Gastrointestinal toxicity induced by microcystins. World Journal of Clinical Cases. 2018; 6 (10):344-354.

Chicago/Turabian Style

Jin-Xia Wu; Hui Huang; Lei Yang; Xiao-Feng Zhang; Shen-Shen Zhang; Hao-Hao Liu; Yue-Qin Wang; Le Yuan; Xue-Min Cheng; Dong-Gang Zhuang; Hui-Zhen Zhang. 2018. "Gastrointestinal toxicity induced by microcystins." World Journal of Clinical Cases 6, no. 10: 344-354.

Journal article
Published: 27 August 2018 in Chemosphere
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The liver is an important iron storage site and a primary MC-LR target. C57BL/6 and Hfe−/− mice were used to investigate effects and mechanisms of MC-LR on systematic iron homeostasis. Body weight, tissue iron content, hematological and serological indexes, and histopathological were evaluated. Ultrastructure and iron metabolism-related genes and proteins were analyzed. MC-LR induced dose-dependent increases in red blood cells, hemoglobin, and hematocrit. In contrast MC-LR-induced dose-dependent decreases in mean corpuscular volume, hemoglobin, and hemoglobin concentration were observed both C57BL/6 and Hfe−/− mice. In both mouse species, serological indexes increased. Aggravated liver and spleen iron were observed in C57BL/6 mice, consistent with Perls’ Prussian blue staining. However, an opposite trend was observed in Hfe−/− mice. C57BL/6 mice had lower Hamp1 (Hepcidn), Bmp6, Il-6, and Tmprss6. Significant increased Hjv, Hif-1α and Hif-2α were observed in both C57BL/6 and Hfe−/− mice. MC-LR-induced pathological lesions were dose-dependent increase in C57BL/6 mice. More severe pathological injuries in MC-LR groups (25 μg/kg) were observed in Hfe−/− mice than in C57BL/6 mice. In Hfe−/− mice, upon exposure to 25 μg/kg MC-LR, mitochondrial membranes were damaged and mitochondrial counts increased with significant swelling. These results indicated that MC-LR can induce the accumulation of iron in C57BL/6 mice with the occurrence of anemia, similar to thalassemia. Moreover, dysregulation of iron homeostasis may be due to MC-LR-induced Hamp1 downregulation, possibly mediated by hypoxia or the IL6–STAT3 and BMP–SMAD signaling pathways.

ACS Style

Jinxia Wu; Lei Yang; Xiaofeng Zhang; Yang Li; Jianyao Wang; Shenshen Zhang; Haohao Liu; Hui Huang; Yueqin Wang; Le Yuan; Xuemin Cheng; Donggang Zhuang; Huizhen Zhang; Xinghai Chen. MC-LR induces dysregulation of iron homeostasis by inhibiting hepcidin expression: A preliminary study. Chemosphere 2018, 212, 572 -584.

AMA Style

Jinxia Wu, Lei Yang, Xiaofeng Zhang, Yang Li, Jianyao Wang, Shenshen Zhang, Haohao Liu, Hui Huang, Yueqin Wang, Le Yuan, Xuemin Cheng, Donggang Zhuang, Huizhen Zhang, Xinghai Chen. MC-LR induces dysregulation of iron homeostasis by inhibiting hepcidin expression: A preliminary study. Chemosphere. 2018; 212 ():572-584.

Chicago/Turabian Style

Jinxia Wu; Lei Yang; Xiaofeng Zhang; Yang Li; Jianyao Wang; Shenshen Zhang; Haohao Liu; Hui Huang; Yueqin Wang; Le Yuan; Xuemin Cheng; Donggang Zhuang; Huizhen Zhang; Xinghai Chen. 2018. "MC-LR induces dysregulation of iron homeostasis by inhibiting hepcidin expression: A preliminary study." Chemosphere 212, no. : 572-584.

Original research article
Published: 06 August 2018 in Frontiers in Physiology
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Microcystin-leucine arginine (MC-LR) is a cyclic heptapeptide intracellular toxin released by cyanobacteria that exhibits strong reproductive toxicity. However, little is known about its biotoxicity to the female reproductive system. The present study investigates unexplored molecular pathways by which oxidative stress acts on MC-LR-induced endoplasmic reticulum stress (ERs) and autophagy. In the present study, immortalized murine ovarian granular cells (KK-1 cells) were exposed to 8.5, 17, and 34 μg/mL (IC50) of MC-LR with or without N-acetyl-l-cysteine (NAC, 10 mM) for 24 h, and C57BL/6 mice were treated with 12.5, 25.0, and 40.0 μg/kg⋅bw of MC-LR with or without NAC (200 mg/kg⋅bw) for 14 days. The results revealed that MC-LR could induce cells apoptosis and morphologic changes in ovarian tissues, induce oxidative stress by stimulating the generation of reactive oxygen species (ROS), destroying antioxidant capacity, and subsequently trigger ERs and autophagy by inducing the hyper-expression of ATG12, ATG5, ATG16, EIF2α (phosphorylated at S51), CHOP, XBP1, GRP78, Beclin1, and PERK (Thr980). Furthermore, NAC pretreatment partly inhibited MC-LR-induced ERs and autophagy via the PERK/ATG12 and XBP1/Beclin1 pathways. These results suggest that oxidative stress mediated MC-LR-induced ERs and autophagy in KK-1 cells and C57BL/6 mice ovaries. Therefore, oxidative stress plays an important role in female toxicity induced by MC-LR.

ACS Style

Haohao Liu; Xiaofeng Zhang; Shenshen Zhang; Hui Huang; Jinxia Wu; Yueqin Wang; Le Yuan; Chuanrui Liu; Xin Zeng; Xuemin Cheng; Donggang Zhuang; Huizhen Zhang. Oxidative Stress Mediates Microcystin-LR-Induced Endoplasmic Reticulum Stress and Autophagy in KK-1 Cells and C57BL/6 Mice Ovaries. Frontiers in Physiology 2018, 9, 1058 .

AMA Style

Haohao Liu, Xiaofeng Zhang, Shenshen Zhang, Hui Huang, Jinxia Wu, Yueqin Wang, Le Yuan, Chuanrui Liu, Xin Zeng, Xuemin Cheng, Donggang Zhuang, Huizhen Zhang. Oxidative Stress Mediates Microcystin-LR-Induced Endoplasmic Reticulum Stress and Autophagy in KK-1 Cells and C57BL/6 Mice Ovaries. Frontiers in Physiology. 2018; 9 ():1058.

Chicago/Turabian Style

Haohao Liu; Xiaofeng Zhang; Shenshen Zhang; Hui Huang; Jinxia Wu; Yueqin Wang; Le Yuan; Chuanrui Liu; Xin Zeng; Xuemin Cheng; Donggang Zhuang; Huizhen Zhang. 2018. "Oxidative Stress Mediates Microcystin-LR-Induced Endoplasmic Reticulum Stress and Autophagy in KK-1 Cells and C57BL/6 Mice Ovaries." Frontiers in Physiology 9, no. : 1058.

Journal article
Published: 09 June 2018 in Toxins
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Microcystin-leucine arginine (MC-LR), a cyclic heptapeptide produced by cyanobacteria, is a strong reproductive toxin. Studies performed in rat Sertoli cells and Chinese hamster ovary cells have demonstrated typical apoptosis after MC-LR exposure. However, little is known on how to protect against the reproductive toxicity induced by MC-LR. The present study aimed to explore the possible molecular mechanism underlying the anti-apoptosis and protective effects of resveratrol (RES) on the co-culture of Sertoli–germ cells and rat testes. The results demonstrated that MC-LR treatment inhibited the proliferation of Sertoli–germ cells and induced apoptosis. Furthermore, sirtuin 1 (SIRT1) and Bcl-2 were inhibited, while p53 and Ku70 acetylation, Bax expression, and cleaved caspase-3 were upregulated by MC-LR. However, RES pretreatment ameliorated MC-LR-induced apoptosis and SIRT1 inhibition, and downregulated the MC-LR-induced increase in p53 and Ku70 acetylation, Bax expression, and caspase-3 activation. In addition, RES reversed the MC-LR-mediated reduction in Ku70 binding to Bax. The present study indicated that the administration of RES could ameliorate MC-LR-induced Sertoli–germ cell apoptosis and protect against reproductive toxicity in rats by stimulating the SIRT1/p53 pathway, suppressing p53 and Ku70 acetylation and enhancing the binding of Ku70 to Bax.

ACS Style

Haohao Liu; Shenshen Zhang; Chuanrui Liu; Jinxia Wu; Yueqin Wang; Le Yuan; Xingde Du; Rui Wang; Phelisters Wegesa Marwa; Donggang Zhuang; Xuemin Cheng; Huizhen Zhang. Resveratrol Ameliorates Microcystin-LR-Induced Testis Germ Cell Apoptosis in Rats via SIRT1 Signaling Pathway Activation. Toxins 2018, 10, 235 .

AMA Style

Haohao Liu, Shenshen Zhang, Chuanrui Liu, Jinxia Wu, Yueqin Wang, Le Yuan, Xingde Du, Rui Wang, Phelisters Wegesa Marwa, Donggang Zhuang, Xuemin Cheng, Huizhen Zhang. Resveratrol Ameliorates Microcystin-LR-Induced Testis Germ Cell Apoptosis in Rats via SIRT1 Signaling Pathway Activation. Toxins. 2018; 10 (6):235.

Chicago/Turabian Style

Haohao Liu; Shenshen Zhang; Chuanrui Liu; Jinxia Wu; Yueqin Wang; Le Yuan; Xingde Du; Rui Wang; Phelisters Wegesa Marwa; Donggang Zhuang; Xuemin Cheng; Huizhen Zhang. 2018. "Resveratrol Ameliorates Microcystin-LR-Induced Testis Germ Cell Apoptosis in Rats via SIRT1 Signaling Pathway Activation." Toxins 10, no. 6: 235.

Article
Published: 18 April 2018 in Journal of Mechanical Science and Technology
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This paper focuses on the singularity-free optimization for the working path of a 3SPS+1PS type parallel mechanism which is used for the simulation of hip joint motion. Kinematic and dynamic models of the test mechanism were set up with the vector method and the principle of virtual power, respectively. Based on the Jacobian matrix, the kinematic and dynamic performance evaluation indices were defined. The working path of the test mechanism traverses the singular surface twice. Optimization was conducted with the attitude of the virtual reference coordinate system as the design variable, the mean value of the motion transmission performance index and the mean value and the standard deviation of the driving force in the working path as the optimization objectives, and the reachable workspace as the constraint condition. The equivalent working path of the test mechanism after optimization had no singularity. Moreover, the motion transmission performance improved evidently and the driving force changed smoothly.

ACS Style

Huizhen Zhang; Gang Cheng; Xianlei Shan; Yang Li. Singularity-free path optimization of the parallel test mechanism for artificial hip joints. Journal of Mechanical Science and Technology 2018, 32, 1775 -1786.

AMA Style

Huizhen Zhang, Gang Cheng, Xianlei Shan, Yang Li. Singularity-free path optimization of the parallel test mechanism for artificial hip joints. Journal of Mechanical Science and Technology. 2018; 32 (4):1775-1786.

Chicago/Turabian Style

Huizhen Zhang; Gang Cheng; Xianlei Shan; Yang Li. 2018. "Singularity-free path optimization of the parallel test mechanism for artificial hip joints." Journal of Mechanical Science and Technology 32, no. 4: 1775-1786.

Original research article
Published: 08 November 2016 in Frontiers in Physiology
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Microcystin-LR (MC-LR) is a ubiquitous peptide that exhibits strong reproductive toxicity, although the mechanistic basis for such toxicity remains largely unknown. The present study was conducted to investigate the mechanisms underlying the adverse effects of exposure to MC-LR in Chinese hamster ovary (CHO) cells. The results showed that MC-LR inhibited the in vitro proliferation of CHO cells significantly, with an IC50 of 10 μg/mL. Moreover, MC-LR-treated CHO cells revealed strong induction of cell cycle arrest and apoptosis. Additionally, exposure of CHO cells to MC-LR resulted in excess reactive oxygen species production and intracellular calcium release, with resultant endoplasmic reticulum stress (ERs). There was also extensive accumulation of autophagic vacuoles with the highest concentration of MC-LR used (10 μg/mL). Furthermore, the expression of ERs (GRP78, ATF-6, PERK, IRE1, CHOP) and autophagy (Beclin1 and LC3II) proteins was increased, with concomitantly reduced expression of LC3I suggesting that ERs and autophagy were induced in CHO cells by MC-LR treatment. Conversely, pretreatment of CHO cells with 4-Phenyl butyric acid, the ERs inhibitor reduced the MC-LR-induced apoptotic cell death and cellular autophagy as evidenced by the reduced expression of Beclin1 and LC3II. Similarly, MC-LR treatment in combination with an autophagy inhibitor (3-methyladenine) increased apoptotic cell death compared with MC-LR alone, and induced ERs via upregulating ERs proteins. The overall results indicated that activation of ERs and autophagy are both associated with MC-LR-induced apoptosis in CHO cells. ERs may be a trigger of autophagy in this process.

ACS Style

Shenshen Zhang; Chuanrui Liu; Yang Li; Mustapha U. Imam; Hui Huang; Haohao Liu; Yongjuan Xin; Huizhen Zhang. Novel Role of ER Stress and Autophagy in Microcystin-LR Induced Apoptosis in Chinese Hamster Ovary Cells. Frontiers in Physiology 2016, 7, 527 .

AMA Style

Shenshen Zhang, Chuanrui Liu, Yang Li, Mustapha U. Imam, Hui Huang, Haohao Liu, Yongjuan Xin, Huizhen Zhang. Novel Role of ER Stress and Autophagy in Microcystin-LR Induced Apoptosis in Chinese Hamster Ovary Cells. Frontiers in Physiology. 2016; 7 ():527.

Chicago/Turabian Style

Shenshen Zhang; Chuanrui Liu; Yang Li; Mustapha U. Imam; Hui Huang; Haohao Liu; Yongjuan Xin; Huizhen Zhang. 2016. "Novel Role of ER Stress and Autophagy in Microcystin-LR Induced Apoptosis in Chinese Hamster Ovary Cells." Frontiers in Physiology 7, no. : 527.

Article
Published: 09 September 2016 in Journal of Patient Safety
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To investigate adverse events (AEs) at baseline in a Chinese general hospital using the Institute for Healthcare Improvement (IHI) Global Trigger Tool (GTT) and discuss the feasibility of this tool to detect AEs in China. A total of 10 inpatient records from the hospital were sampled randomly half a month in 2014. The records were reviewed to identify AEs according to the second edition of the IHI GTT for measuring AEs. Triggers and AEs were analyzed using Microsoft Excel 2007. Statistical analyses were performed using IBM SPSS software, version 19.0. A review of 240 patient records identified 51.0% (26/51) triggers in the worksheet, and 33.3% (17/51) were associated with AEs. A total of 70 AEs were identified in 54 patients, including 65.7% (46/70) category E AEs, which represent temporary harm requiring intervention, and 34.3% (24/70) category F AEs, which represent temporary harm requiring initial or prolonged hospitalization. The average rate of AEs per 1000 patient-days was 32.1 ± 20.9. The average rate of AEs per 100 admissions was 29.2 ± 16.1. The average rate of admissions with an AE was 22.5% ± 13.9%. The most significant characteristic of patients with AEs was longer hospital stay. More than one fifth of adult inpatients in the current study experienced at least one AE resulting in temporary harm, most commonly caused by surgical operations and medication. With some modifications, the IHI GTT is a feasible and effective tool for detecting the overall status of AEs in a Chinese hospital.

ACS Style

Xiao-Di Xu; Yi-Jie Yuan; Li-Ming Zhao; Zhao Li-Ming; Hui-Zhen Zhang; Hua Wu. Adverse Events at Baseline in a Chinese General Hospital: A Pilot Study of the Global Trigger Tool. Journal of Patient Safety 2016, 16, 269 -273.

AMA Style

Xiao-Di Xu, Yi-Jie Yuan, Li-Ming Zhao, Zhao Li-Ming, Hui-Zhen Zhang, Hua Wu. Adverse Events at Baseline in a Chinese General Hospital: A Pilot Study of the Global Trigger Tool. Journal of Patient Safety. 2016; 16 (4):269-273.

Chicago/Turabian Style

Xiao-Di Xu; Yi-Jie Yuan; Li-Ming Zhao; Zhao Li-Ming; Hui-Zhen Zhang; Hua Wu. 2016. "Adverse Events at Baseline in a Chinese General Hospital: A Pilot Study of the Global Trigger Tool." Journal of Patient Safety 16, no. 4: 269-273.