This page has only limited features, please log in for full access.
Methylmercury (MeHg) exposure and its harmful effects on the developing brain continue to be a global environmental health concern. Decline in mitochondrial function is central to the toxic effects of MeHg and pathogenesis of mitochondria-related diseases including Parkinson's disease (PD). LRRK2 (Leucine-rich repeat kinase 2) mutation is one of the most common genetic risk factors for PD. In this study, we utilize an acute toxicity model of MeHg exposure in the model organism Caenorhabditis elegans (C. elegans) to compare lifespan, developmental progression, mitochondrial membrane potential and reactive oxygen species (ROS) between the wild-type N2 strain, wild-type LRRK2 transgenic strain (WLZ1), and mutant LRRK2(G2019S) transgenic strain (WLZ3). Additionally, the expression levels of skn-1 and gst-4 were investigated. Our results show that acute MeHg exposure (5 and 10 µM) caused a significant developmental delay in the N2 and WLZ3 worms. Notably, the worms expressing wild-type LRRK2 were resistant to 5 µM MeHg- induced developmental retardation. ROS levels in response to MeHg exposure were increased in the N2 worms, but not in the WLZ1 or WLZ3 worms. The mitochondrial membrane potential was decreased in the N2 worms but increased in the WLZ1 and WLZ3 worms following MeHg exposure. Furthermore, MeHg exposure increased the expression of skn-1 in N2, but not in WLZ1 worms. Although skn-1 expression was increased in the WLZ3 worms following MeHg exposure, gst-4 expression was not induced. Both skn-1 and gst-4 had higher basal expression levels in LRRK2s transgenic than wild-type N2 worms. Knocking down of skn-1 with feeding RNAi had a significant developmental effect in WLZ1 worms; however, the effect was not found in WLZ3 worms. These results suggest that mitochondrial dysfunction and a defect in the SKN-1 signaling in the LRRK2 G2019S worms contribute to the severe developmental delay, establishing a modulatory role of LRRK2 mutation in MeHg-induced acute toxicity.
Tao Ke; Joao B. T. Rocha; Alexey A. Tinkov; Abel Santamaria; Aaron B. Bowman; Michael Aschner. The Role of Human LRRK2 in Acute Methylmercury Toxicity in Caenorhabditis elegans. Neurochemical Research 2021, 1 -12.
AMA StyleTao Ke, Joao B. T. Rocha, Alexey A. Tinkov, Abel Santamaria, Aaron B. Bowman, Michael Aschner. The Role of Human LRRK2 in Acute Methylmercury Toxicity in Caenorhabditis elegans. Neurochemical Research. 2021; ():1-12.
Chicago/Turabian StyleTao Ke; Joao B. T. Rocha; Alexey A. Tinkov; Abel Santamaria; Aaron B. Bowman; Michael Aschner. 2021. "The Role of Human LRRK2 in Acute Methylmercury Toxicity in Caenorhabditis elegans." Neurochemical Research , no. : 1-12.
Metals are actively involved in multiple catalytic physiological activities. However, metal overload may result in neurotoxicity as it increases formation of reactive oxygen species (ROS) and elevates oxidative stress in the nervous system. Mitochondria are a key target of metal-induced toxicity, given their role in energy production. As the brain consumes a large amount of energy, mitochondrial dysfunction and the subsequent decrease in levels of ATP may significantly disrupt brain function, resulting in neuronal cell death and ensuing neurological disorders. Here, we address contemporary studies on metal-induced mitochondrial dysfunction and its impact on the nervous system.
Hong Cheng; Bobo Yang; Tao Ke; Shaojun Li; Xiaobo Yang; Michael Aschner; Pan Chen. Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders. Toxics 2021, 9, 142 .
AMA StyleHong Cheng, Bobo Yang, Tao Ke, Shaojun Li, Xiaobo Yang, Michael Aschner, Pan Chen. Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders. Toxics. 2021; 9 (6):142.
Chicago/Turabian StyleHong Cheng; Bobo Yang; Tao Ke; Shaojun Li; Xiaobo Yang; Michael Aschner; Pan Chen. 2021. "Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders." Toxics 9, no. 6: 142.
Methylmercury (MeHg) is a global pollutant and potent neurotoxin. In humans, MeHg damages the central nervous system (CNS), causing irreversible neuronal shrinkage, and neuronal loss. Most chelators for clinical mercury detoxification are thiol-containing agents. N,N ‘bis-(2-mercaptoethyl) isophthalamide (NBMI) is a lipophilic thiol agent synthesized from natural chemicals. NBMI has high affinity for mercury, cadmium and lead, and can decrease their concentrations in polluted water. However, the efficacy of NBMI for MeHg toxicity has yet to be evaluated in intact animals. Here we used the nematode Caenorhabditis elegans (C. elegans) to test the efficacy of NBMI in attenuating MeHg toxicity in vivo in the whole organism. The results showed that NBMI reduced both the acute toxicity (125 μM MeHg, 1 h) and chronic (5 μM MeHg, 24 h) MeHg toxicity. Co-treatment with NBMI achieved maximal efficacy against MeHg toxicity, however delayed treatment 6 days after initiation of exposure was also effective at reducing neurotoxicity. Co-treatment of NBMI reduced the worms’ death rate, structural damage in DAergic neurons, and restored antioxidant response levels. While this study provides proof of principle for the therapeutic value of NBMI in MeHg toxicity, future studies are needed to address the cellular and molecular mechanisms and translatability of these effects to humans and other animals.
Tao Ke; Julia Bornhorst; Tanja Schwerdtle; Abel Santamaría; Félix Alexandre Antunes Soare; João B. T. Rocha; Marcelo Farina; Aaron B. Bowman; Michael Aschner. Therapeutic Efficacy of the N,N′ Bis-(2-Mercaptoethyl) Isophthalamide Chelator for Methylmercury Intoxication in Caenorhabditis elegans. Neurotoxicity Research 2020, 38, 133 -144.
AMA StyleTao Ke, Julia Bornhorst, Tanja Schwerdtle, Abel Santamaría, Félix Alexandre Antunes Soare, João B. T. Rocha, Marcelo Farina, Aaron B. Bowman, Michael Aschner. Therapeutic Efficacy of the N,N′ Bis-(2-Mercaptoethyl) Isophthalamide Chelator for Methylmercury Intoxication in Caenorhabditis elegans. Neurotoxicity Research. 2020; 38 (1):133-144.
Chicago/Turabian StyleTao Ke; Julia Bornhorst; Tanja Schwerdtle; Abel Santamaría; Félix Alexandre Antunes Soare; João B. T. Rocha; Marcelo Farina; Aaron B. Bowman; Michael Aschner. 2020. "Therapeutic Efficacy of the N,N′ Bis-(2-Mercaptoethyl) Isophthalamide Chelator for Methylmercury Intoxication in Caenorhabditis elegans." Neurotoxicity Research 38, no. 1: 133-144.
Manganese (Mn) is the twelfth most abundant element on the earth and an essential metal to human health. Mn is present at low concentrations in a variety of dietary sources, which provides adequate Mn content to sustain support various physiological processes in the human body. However, with the rise of Mn utility in a variety of industries, there is an increased risk of overexposure to this transition metal, which can have neurotoxic consequences. This risk includes occupational exposure of Mn to workers as well as overall increased Mn pollution affecting the general public. Here, we review exposure due to air pollution and inhalation in industrial settings; we also delve into the toxic effects of manganese on the brain such as oxidative stress, inflammatory response and transporter dysregulation. Additionally, we summarize current understandings underlying the mechanisms of Mn toxicity.
Mahfuzur R. Miah; Omamuyovwi M. Ijomone; Comfort O.A. Okoh; Olayemi K. Ijomone; Grace T. Akingbade; Tao Ke; Bárbara Krum; Airton Da Cunha Martins Jr; Ayodele Akinyemi; Nicole Aranoff; Felix Alexandre Antunes Soares; Aaron B. Bowman; Michael Aschner. The effects of manganese overexposure on brain health. Neurochemistry International 2020, 135, 104688 -104688.
AMA StyleMahfuzur R. Miah, Omamuyovwi M. Ijomone, Comfort O.A. Okoh, Olayemi K. Ijomone, Grace T. Akingbade, Tao Ke, Bárbara Krum, Airton Da Cunha Martins Jr, Ayodele Akinyemi, Nicole Aranoff, Felix Alexandre Antunes Soares, Aaron B. Bowman, Michael Aschner. The effects of manganese overexposure on brain health. Neurochemistry International. 2020; 135 ():104688-104688.
Chicago/Turabian StyleMahfuzur R. Miah; Omamuyovwi M. Ijomone; Comfort O.A. Okoh; Olayemi K. Ijomone; Grace T. Akingbade; Tao Ke; Bárbara Krum; Airton Da Cunha Martins Jr; Ayodele Akinyemi; Nicole Aranoff; Felix Alexandre Antunes Soares; Aaron B. Bowman; Michael Aschner. 2020. "The effects of manganese overexposure on brain health." Neurochemistry International 135, no. : 104688-104688.
The neurotransmitter dopamine is a neuromodulator in the positive and negative regulation of brain circuits. Dopamine insufficiency or overload has been implicated in aberrant activities of neural circuits that play key roles in the pathogenesis of neurological and psychiatric diseases. Dopaminergic neurons are vulnerable to environmental insults. The neurotoxin methylmercury (MeHg) produces dopaminergic neuron damage in rodent as well as in Caenorhabditis elegans (C. elegans) models. Previous studies have demonstrated the utility of C. elegans as an alternative and complementary experimental model in dissecting out mechanism of MeHg-induced dopaminergic neurodegeneration. However, a sensitive pathological change that marks early events in neurodegeneration induced by environmental level of MeHg, is still lacking. By establishing a chronic exposure C. elegans model, for the first time, we have shown the propensity of MeHg (5 μM, 10 days) to induce bright puncta of dat-1::mCherry aggreagtes in the dendrites of cephalic (2 CEPs) dopaminergic neurons in a dose- and time-dependent manner, while these changes were not found in other dopaminergic neurons: anterior deirids (2 ADEs) and posterior deirids (2 PDEs), cholinergic neurons (2 AIYs) or glutamatergic neurons (2 PVDs). The bright puncta appear as an aggregation of mCherry proteins accumulating in dendrites. Further staining shows that the puncta were not inclusions in lysosome, or amyloid protein aggregates. In addition, features of the puncta including enlarged sphere shape (0.5–2 μm diameters), bright and accompanying with the shrinkage of the dendrite suggest that the puncta are likely composed of homologous mCherry molecules packaged at the dendritic site for exportation. Moreover, in the glutathione S-transferase 4 (gst-4) transcriptional reporter strain and RT-PCR assay, the expression levels of gst-4 and tubulins (tba-1 and tba-2) genes were not significantly modified under this chronic exposure paradigm, but gst-4 did show significant changes in an one day exposure paradigm. Collectively, these results suggest that CEP dopaminergic neurons are a sensitive target of MeHg, and the current exposure paradigm could be used as a model to investigate mechanism of dopaminergic neurotoxicity.
Tao Ke; Aristidis Tsatsakis; Abel Santamaría; Félix Alexandre Antunes Soare; Alexey A. Tinkov; Anca Oana Docea; Anatoly Skalny; Aaron B. Bowman; Michael Aschner. Chronic exposure to methylmercury induces puncta formation in cephalic dopaminergic neurons in Caenorhabditis elegans. NeuroToxicology 2020, 77, 105 -113.
AMA StyleTao Ke, Aristidis Tsatsakis, Abel Santamaría, Félix Alexandre Antunes Soare, Alexey A. Tinkov, Anca Oana Docea, Anatoly Skalny, Aaron B. Bowman, Michael Aschner. Chronic exposure to methylmercury induces puncta formation in cephalic dopaminergic neurons in Caenorhabditis elegans. NeuroToxicology. 2020; 77 ():105-113.
Chicago/Turabian StyleTao Ke; Aristidis Tsatsakis; Abel Santamaría; Félix Alexandre Antunes Soare; Alexey A. Tinkov; Anca Oana Docea; Anatoly Skalny; Aaron B. Bowman; Michael Aschner. 2020. "Chronic exposure to methylmercury induces puncta formation in cephalic dopaminergic neurons in Caenorhabditis elegans." NeuroToxicology 77, no. : 105-113.
Manganese (Mn) overexposure is a public health concern due to its widespread industrial usage and the risk for environmental contamination. The clinical symptoms of Mn neurotoxicity, or manganism, share several pathological features of Parkinson’s disease (PD). Biologically, Mn is an essential trace element, and Mn in the brain is preferentially localized in astrocytes. This review summarizes the role of astrocytes in Mn-induced neurotoxicity, specifically on the role of neurotransmitter recycling, neuroinflammation, and genetics. Mn overexposure can dysregulate astrocytic cycling of glutamine (Gln) and glutamate (Glu), which is the basis for Mn-induced excitotoxic neuronal injury. In addition, reactive astrocytes are important mediators of Mn-induced neuronal damage by potentiating neuroinflammation. Genetic studies, including those with Caenorhabditis elegans (C. elegans) have uncovered several genes associated with Mn neurotoxicity. Though we have yet to fully understand the role of astrocytes in the pathologic changes characteristic of manganism, significant strides have been made over the last two decades in deciphering the role of astrocytes in Mn-induced neurotoxicity and neurodegeneration.
Tao Ke; Marta Sidoryk-Wegrzynowicz; Edward Pajarillo; Asha Rizor; Félix Alexandre Antunes Soares; Eunsook Lee; Michael Aschner. Role of Astrocytes in Manganese Neurotoxicity Revisited. Neurochemical Research 2019, 44, 2449 -2459.
AMA StyleTao Ke, Marta Sidoryk-Wegrzynowicz, Edward Pajarillo, Asha Rizor, Félix Alexandre Antunes Soares, Eunsook Lee, Michael Aschner. Role of Astrocytes in Manganese Neurotoxicity Revisited. Neurochemical Research. 2019; 44 (11):2449-2459.
Chicago/Turabian StyleTao Ke; Marta Sidoryk-Wegrzynowicz; Edward Pajarillo; Asha Rizor; Félix Alexandre Antunes Soares; Eunsook Lee; Michael Aschner. 2019. "Role of Astrocytes in Manganese Neurotoxicity Revisited." Neurochemical Research 44, no. 11: 2449-2459.
The organic form of mercurial complex, methylmercury (MeHg), is a neurotoxin that bioaccumulates in the food web. Studies in model organisms, such as Caenorhabditis elegans (C. elegans), provide powerful insights on the role of genetic factors in MeHg-induced toxicity. C. elegans is a free living worm that is commonly cultured in nematode growth medium (NGM) agar plates seeded with bacteria. The bacteria have broad impact on C. elegans biology, including development, reproduction and lifespan, as well as metabolism of experimental chemicals. We hypothesized that MeHg toxicity in C. elegans could be modified by the bacterial food. Using a C. elegans wild-type (WT) strain and transgenic reporter strains, we found that bacterial food reduced the chronic toxicity of MeHg in C. elegans in a dose- and live-status-dependent manner. The MeHg-induced death rate in C. elegans was highest in fasted worms, followed by dehydrated dead bacteria, dead bacteria and live bacteria fed worms. Among the different bacterial foods, dehydrated dead bacteria fed worms were most sensitive to the toxicity of MeHg. The distinct bacteria food (dehydrated dead bacteria food) attenuated oxidative stress and development delay in C. elegans exposed to MeHg. The FOXO transcriptional factor DAF16 was not changed by MeHg but modified by the distinct bacteria food. Independent of MeHg treatment, daf-16 expression in fed worms migrated from the intestine to muscle. We conclude that, in chronic exposure studies in C. elegans, the effects of bacteria on toxicological outcomes should be considered.
Tao Ke; Michael Aschner. Bacteria affect Caenorhabditis elegans responses to MeHg toxicity. NeuroToxicology 2019, 75, 129 -135.
AMA StyleTao Ke, Michael Aschner. Bacteria affect Caenorhabditis elegans responses to MeHg toxicity. NeuroToxicology. 2019; 75 ():129-135.
Chicago/Turabian StyleTao Ke; Michael Aschner. 2019. "Bacteria affect Caenorhabditis elegans responses to MeHg toxicity." NeuroToxicology 75, no. : 129-135.
Mercury (Hg) exposure remains a major public health concern due to its widespread distribution in the environment. Organic mercurials, such as MeHg, have been extensively investigated especially because of their congenital effects. In this context, studies on the molecular mechanism of MeHg-induced neurotoxicity are pivotal to the understanding of its toxic effects and the development of preventive measures. Post-translational modifications (PTMs) of proteins, such as phosphorylation, ubiquitination, and acetylation are essential for the proper function of proteins and play important roles in the regulation of cellular homeostasis. The rapid and transient nature of many PTMs allows efficient signal transduction in response to stress. This review summarizes the current knowledge of PTMs in MeHg-induced neurotoxicity, including the most commonly PTMs, as well as PTMs induced by oxidative stress and PTMs of antioxidant proteins. Though PTMs represent an important molecular mechanism for maintaining cellular homeostasis and are involved in the neurotoxic effects of MeHg, we are far from understanding the complete picture on their role, and further research is warranted to increase our knowledge of PTMs in MeHg-induced neurotoxicity.
Tao Ke; Filipe Marques Gonçalves; Cinara Ludvig Gonçalves; Alessandra Antunes dos Santos; João B.T. Rocha; Marcelo Farina; Anatoly Skalny; Aristidis Tsatsakis; Aaron B. Bowman; Michael Aschner. Post-translational modifications in MeHg-induced neurotoxicity. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 2018, 1865, 2068 -2081.
AMA StyleTao Ke, Filipe Marques Gonçalves, Cinara Ludvig Gonçalves, Alessandra Antunes dos Santos, João B.T. Rocha, Marcelo Farina, Anatoly Skalny, Aristidis Tsatsakis, Aaron B. Bowman, Michael Aschner. Post-translational modifications in MeHg-induced neurotoxicity. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 2018; 1865 (8):2068-2081.
Chicago/Turabian StyleTao Ke; Filipe Marques Gonçalves; Cinara Ludvig Gonçalves; Alessandra Antunes dos Santos; João B.T. Rocha; Marcelo Farina; Anatoly Skalny; Aristidis Tsatsakis; Aaron B. Bowman; Michael Aschner. 2018. "Post-translational modifications in MeHg-induced neurotoxicity." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1865, no. 8: 2068-2081.
A visual detection system for lead(ii) comprised of SiO2nanoparticles, decorated electrospun polydiacetylene–glycine nanofibrous strip and a smartphone.
Yan Li; Lihuan Wang; Yanan Wen; Bin Ding; Gang Sun; Tao Ke; Jingyuan Chen; Jianyong Yu. Constitution of a visual detection system for lead(ii) on polydiacetylene–glycine embedded nanofibrous membranes. Journal of Materials Chemistry A 2015, 3, 9722 -9730.
AMA StyleYan Li, Lihuan Wang, Yanan Wen, Bin Ding, Gang Sun, Tao Ke, Jingyuan Chen, Jianyong Yu. Constitution of a visual detection system for lead(ii) on polydiacetylene–glycine embedded nanofibrous membranes. Journal of Materials Chemistry A. 2015; 3 (18):9722-9730.
Chicago/Turabian StyleYan Li; Lihuan Wang; Yanan Wen; Bin Ding; Gang Sun; Tao Ke; Jingyuan Chen; Jianyong Yu. 2015. "Constitution of a visual detection system for lead(ii) on polydiacetylene–glycine embedded nanofibrous membranes." Journal of Materials Chemistry A 3, no. 18: 9722-9730.
Cold adaptation is a body's protective response to cold stress. Mild chronic intermittent cold (CIC) exposure has been used to generate animal models for cold adaptation studies. However, the effects of mild CIC exposure on vital organs are not completely characterized. In the present study, we exposed rats to mild CIC for two weeks, and then measured the body weights, the weights of brown adipose tissue (BAT), the levels of ATP and reactive oxygen species (ROS) in the brains, livers, hearts, muscles and BATs. Rats formed cold adaptation after exposure to CIC for two weeks. Compared to rats of the control group that were hosted under ambient temperature, rats exposed to mild CIC showed a lower average body weight, but a higher weight of brown adipose tissue (BAT). Rats exposed to CIC for two weeks also exhibited higher levels of ATP and ROS in all examined organs as compared to those of the control group. In addition, we determined the expression levels of cold-inducible RNA binding protein (Cirbp) and thioredoxin (TRX) in rat tissues after 2 weeks of CIC exposure. Both Cirbp and TRX were increased, suggesting a role of these two proteins for establishment of cold adaptation. Together, this study reveals the effects of mild CIC exposure on vital organs of rats during CIC exposure.
Xiaohui Wang; Honglei Che; Wenbin Zhang; Jiye Wang; Tao Ke; Rui Cao; Shanshan Meng; Dan Li; Ouyang Weiming; Jingyuan Chen; Wenjing Luo. Effects of Mild Chronic Intermittent Cold Exposure on Rat Organs. International Journal of Biological Sciences 2015, 11, 1171 -1180.
AMA StyleXiaohui Wang, Honglei Che, Wenbin Zhang, Jiye Wang, Tao Ke, Rui Cao, Shanshan Meng, Dan Li, Ouyang Weiming, Jingyuan Chen, Wenjing Luo. Effects of Mild Chronic Intermittent Cold Exposure on Rat Organs. International Journal of Biological Sciences. 2015; 11 (10):1171-1180.
Chicago/Turabian StyleXiaohui Wang; Honglei Che; Wenbin Zhang; Jiye Wang; Tao Ke; Rui Cao; Shanshan Meng; Dan Li; Ouyang Weiming; Jingyuan Chen; Wenjing Luo. 2015. "Effects of Mild Chronic Intermittent Cold Exposure on Rat Organs." International Journal of Biological Sciences 11, no. 10: 1171-1180.
A portable, sensitive and selective colorimetric strip for naked-eye recognition of Pb2+utilizing solid-phase polydiacetylene embedded electrospun polyacrylonitrile nanofibers.
Yan Li; Lihuan Wang; Xia Yin; Bin Ding; Gang Sun; Tao Ke; Jingyuan Chen; Jianyong Yu. Colorimetric strips for visual lead ion recognition utilizing polydiacetylene embedded nanofibers. Journal of Materials Chemistry A 2014, 2, 18304 -18312.
AMA StyleYan Li, Lihuan Wang, Xia Yin, Bin Ding, Gang Sun, Tao Ke, Jingyuan Chen, Jianyong Yu. Colorimetric strips for visual lead ion recognition utilizing polydiacetylene embedded nanofibers. Journal of Materials Chemistry A. 2014; 2 (43):18304-18312.
Chicago/Turabian StyleYan Li; Lihuan Wang; Xia Yin; Bin Ding; Gang Sun; Tao Ke; Jingyuan Chen; Jianyong Yu. 2014. "Colorimetric strips for visual lead ion recognition utilizing polydiacetylene embedded nanofibers." Journal of Materials Chemistry A 2, no. 43: 18304-18312.
Creating a sensitive and selective method that can provide simple, practical, and high throughput determination of lead ions (Pb2+) has proved extremely challenging. This work responds to this challenge by designing, fabricating, and evaluating a portable sensor strip for naked-eye chromatic assaying of trace amount of Pb2+. The sensor design is then realized utilizing electrospun nylon-6/polyvinylidene fluoride (N6/PVDF) nanofibers/nets (NFN) membranes assemble L-glutathione-conjugated Au nanoparticle probes ([email protected]), which can aggregate to trigger a vivid color change of pink to purple upon incubation with Pb2+. Benefiting from large surface areas, high porosity, and Steiner tree networks structure of the NFN membranes, the strips exhibited excellent stability, rapid response (10 min), wide detection range (10–500 μg/dL) and low naked-eye detection limit of 10 μg/dL. Additionally, the sensing responses are visualized quantitatively by employing a chromatic framework that translates measured spectra into numeric color values directly related to color perception. Furthermore, the NFN-based strip displayed excellent selectivity to other possible metal cations. The result clearly demonstrated that this is a promising sensing system which could act as a first step toward remediation of lead poisoning in future.
Yan Li; Bin Ding; Gang Sun; Tao Ke; Jingyuan Chen; Salem S. Al-Deyab; Jianyong Yu. Solid-phase pink-to-purple chromatic strips utilizing gold probes and nanofibrous membranes combined system for lead (II) assaying. Sensors and Actuators B: Chemical 2014, 204, 673 -681.
AMA StyleYan Li, Bin Ding, Gang Sun, Tao Ke, Jingyuan Chen, Salem S. Al-Deyab, Jianyong Yu. Solid-phase pink-to-purple chromatic strips utilizing gold probes and nanofibrous membranes combined system for lead (II) assaying. Sensors and Actuators B: Chemical. 2014; 204 ():673-681.
Chicago/Turabian StyleYan Li; Bin Ding; Gang Sun; Tao Ke; Jingyuan Chen; Salem S. Al-Deyab; Jianyong Yu. 2014. "Solid-phase pink-to-purple chromatic strips utilizing gold probes and nanofibrous membranes combined system for lead (II) assaying." Sensors and Actuators B: Chemical 204, no. : 673-681.
Yan Xu; Honglei Che; Mingchao Liu; Tao Ke; Yueyun Ma; Jingyuan Chen; Xiaoke Hao. [Changes and regulatory mechanism of tight junction proteins in in vitro model of lead-induced blood-brain barrier injury]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 2013, 29, 1 .
AMA StyleYan Xu, Honglei Che, Mingchao Liu, Tao Ke, Yueyun Ma, Jingyuan Chen, Xiaoke Hao. [Changes and regulatory mechanism of tight junction proteins in in vitro model of lead-induced blood-brain barrier injury]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology. 2013; 29 (11):1.
Chicago/Turabian StyleYan Xu; Honglei Che; Mingchao Liu; Tao Ke; Yueyun Ma; Jingyuan Chen; Xiaoke Hao. 2013. "[Changes and regulatory mechanism of tight junction proteins in in vitro model of lead-induced blood-brain barrier injury]." Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 29, no. 11: 1.
Acute mountain sickness (AMS) refers to the cerebral abnormalities typically triggered by exposure to hypobaric hypoxia at high altitude. Although AMS is not often life threatening, it can seriously impact health quality and decrease productivity. Thus, detection of potential susceptibility to AMS has become important for people arriving at high-altitude plateaus for the first time, including laborers and military staff. The aim of this review was to examine techniques which efficiently assess the susceptibility to AMS prior to exposure to high altitude.
Han Song; Tao Ke; Wen-Jing Luo; Jing-Yuan Chen. Non-high altitude methods for rapid screening of susceptibility to acute mountain sickness. BMC Public Health 2013, 13, 902 -902.
AMA StyleHan Song, Tao Ke, Wen-Jing Luo, Jing-Yuan Chen. Non-high altitude methods for rapid screening of susceptibility to acute mountain sickness. BMC Public Health. 2013; 13 (1):902-902.
Chicago/Turabian StyleHan Song; Tao Ke; Wen-Jing Luo; Jing-Yuan Chen. 2013. "Non-high altitude methods for rapid screening of susceptibility to acute mountain sickness." BMC Public Health 13, no. 1: 902-902.
Ke, Tao, Jiye Wang, Erik R. Swenson, Xiangnan Zhang, Yunlong Hu, Yaoming Chen, Mingchao Liu, Wenbin Zhang, Feng Zhao, Xuefeng Shen, Qun Yang, Jingyuan Chen, and Wenjing Luo. Effect of acetazolamide and gingko biloba on the human pulmonary vascular response to an acute altitude ascent. High Alt Med Biol 14:162–167, 2013.—Acetazolamide and gingko biloba are the two most investigated drugs for the prevention of acute mountain sickness (AMS). Evidence suggests that they may also reduce pulmonary artery systolic pressure (PASP). To investigate whether these two drugs for AMS prevention also reduce PASP with rapid airlift ascent to high altitude, a randomized controlled trial was conducted on 28 healthy young men with acetazolamide (125 mg bid), gingko biloba (120 mg bid), or placebo for 3 days prior to airlift ascent (397 m) and for the first 3 days at high altitude (3658 m). PASP, AMS, arterial oxygen saturation (Sao2), mean arterial pressure (MAP), heart rate (HR), forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), and peak expiratory flow (PEF) were assessed both at 397 m and 3658 m. HR, PEF, and PASP increased with altitude exposure (p<0.05), and SaO2 decreased (p<0.05). PASP with acetazolamide (mean at 3658 m, 26.2 mm Hg; incremental change, 4.7 mm Hg, 95% CI., 2.6–6.9 mm Hg) was lower than that with ginkgo biloba (mean at 3658 m, 33.7 mm Hg, p=0.001; incremental change, 13.1 mm Hg, 95%CI., 9.6–16.5 mm Hg, p=0.002), and with placebo (mean at 3658 m, 34.7 mm Hg, p<0.001; 14.4 mm Hg, 95% CI., 8.8–20.0 mm Hg, p=0.001). The data show that a low prophylactic dosage of acetazolamide, but not gingko biloba, mitigates the early increase of PASP in a quick ascent profile.
Tao Ke; Jiye Wang; Erik R. Swenson; Xiangnan Zhang; Yunlong Hu; Yaoming Chen; Mingchao Liu; Wenbin Zhang; Feng Zhao; Xuefeng Shen; Qun Yang; Jingyuan Chen; Wenjing Luo. Effect of Acetazolamide and Gingko Biloba on the Human Pulmonary Vascular Response to an Acute Altitude Ascent. High Altitude Medicine & Biology 2013, 14, 162 -167.
AMA StyleTao Ke, Jiye Wang, Erik R. Swenson, Xiangnan Zhang, Yunlong Hu, Yaoming Chen, Mingchao Liu, Wenbin Zhang, Feng Zhao, Xuefeng Shen, Qun Yang, Jingyuan Chen, Wenjing Luo. Effect of Acetazolamide and Gingko Biloba on the Human Pulmonary Vascular Response to an Acute Altitude Ascent. High Altitude Medicine & Biology. 2013; 14 (2):162-167.
Chicago/Turabian StyleTao Ke; Jiye Wang; Erik R. Swenson; Xiangnan Zhang; Yunlong Hu; Yaoming Chen; Mingchao Liu; Wenbin Zhang; Feng Zhao; Xuefeng Shen; Qun Yang; Jingyuan Chen; Wenjing Luo. 2013. "Effect of Acetazolamide and Gingko Biloba on the Human Pulmonary Vascular Response to an Acute Altitude Ascent." High Altitude Medicine & Biology 14, no. 2: 162-167.
The effect of lead (Pb) on spatial memory and hippocampal long-term potentiation (LTP) as a key risk factor has been widely recognized and the oxidative damage has been proposed as a possible mechanism of lead neurotoxicity. Selenium (Se) is a nutritionally essential trace element with known antioxidant potential. In this study we investigated the effect and the underlying mechanisms of Se supplementary on Pb induced cognition and synaptic plasticity impairment. Lactating Sprague-Dawley rats (SD rats) were randomly divided to four groups: 0ppm lead acetate (Pb); 0ppm Pb and 0.2ppm sodium selenite (Se); 100ppm Pb; 100ppm Pb and 0.2ppm Se. Lactating rats were treated with or without Pb and/or Se throughout lactation until weaning. The levels of hippocampal LTP, the spatial memory, the apoptosis of hippocampal neurons, the levels of lactate dehydrogenase (LDH) release, and the serum level of superoxide dismutase (SOD) and malondialdehyde (MDA) were assayed. It had been observed that in Pb group the spatial memory, the induce level of LTP, the serum SOD level decreased, the LDH release level, the neurons apoptosis level, the serum MDA level increased, while in the Se supplements groups, the spatial memory, the induce level of LTP increased significantly. Compared with the Pb group, Se supplements shown down regulated the level of LDH, the neurons apoptosis and the serum MDA, and up regulated the level of serum SOD. We could draw the conclusion that Se supplements could alleviate toxic effect of lead on hippocampal LTP and spatial memory. The treated with selenium around 0.2ppm may protect against spatial memory dysfunction induced by lead exposure.
Ming-Chao Liu; Yan Xu; Yao-Ming Chen; Juan Li; Fang Zhao; Gang Zheng; Jin-Fei Jing; Tao Ke; Jing-Yuan Chen; Wen-Jing Luo. The effect of sodium selenite on lead induced cognitive dysfunction. NeuroToxicology 2013, 36, 82 -88.
AMA StyleMing-Chao Liu, Yan Xu, Yao-Ming Chen, Juan Li, Fang Zhao, Gang Zheng, Jin-Fei Jing, Tao Ke, Jing-Yuan Chen, Wen-Jing Luo. The effect of sodium selenite on lead induced cognitive dysfunction. NeuroToxicology. 2013; 36 ():82-88.
Chicago/Turabian StyleMing-Chao Liu; Yan Xu; Yao-Ming Chen; Juan Li; Fang Zhao; Gang Zheng; Jin-Fei Jing; Tao Ke; Jing-Yuan Chen; Wen-Jing Luo. 2013. "The effect of sodium selenite on lead induced cognitive dysfunction." NeuroToxicology 36, no. : 82-88.
High-altitude hypoxia impedes cognitive performance. It is not well known whether the prophylactic use of acetazolamide for altitude sickness can influence cognitive performance at high altitude. When ascending to high altitude locations, one may face medical risks, including cognitive impairment, which may significantly hinder climbing abilities or exploratory behavior. Effective prophylactic drugs have rarely been reported. Because acetazolamide is commonly used to treat acute mountain sickness (AMS), we assessed the potential effects of acetazolamide on cognitive performance during high-altitude exposure. Twenty-one volunteers aged 22–26 years were randomized to receive a 4-day treatment of acetazolamide (125 mg Bid, n = 11) or placebo (n = 10) before and after air travel from Xianyang (402 m) to Lhasa (3561 m). Neuropsychological performance was assessed using the digit symbol substitution test (DSST), paced auditory serial addition test (PASAT), operation span task, and free recall test at 6, 30, and 54 h after arrival at Lhasa. The Lake Louise Score (LLS) was used to diagnose AMS. At high altitude, acetazolamide impaired rather than improved neuropsychological measures of concentration, cognitive processing speed, reaction time, short-term memory, and working memory, which were assessed by DSST, PASAT, and operation span task at 6 and 30 h after arrival (p < 0.05). However, the prophylactic use of acetazolamide was found to reduce the incidence of AMS compared to the placebo (p < 0.05). In conclusion, acetazolamide impairs neuropsychological function, at least in part, shortly after the ascent to high altitude.
Jiye Wang; Tao Ke; Xiangnan Zhang; Yaoming Chen; Mingchao Liu; Jingyuan Chen; Wenjing Luo. Effects of acetazolamide on cognitive performance during high-altitude exposure. Neurotoxicology and Teratology 2013, 35, 28 -33.
AMA StyleJiye Wang, Tao Ke, Xiangnan Zhang, Yaoming Chen, Mingchao Liu, Jingyuan Chen, Wenjing Luo. Effects of acetazolamide on cognitive performance during high-altitude exposure. Neurotoxicology and Teratology. 2013; 35 ():28-33.
Chicago/Turabian StyleJiye Wang; Tao Ke; Xiangnan Zhang; Yaoming Chen; Mingchao Liu; Jingyuan Chen; Wenjing Luo. 2013. "Effects of acetazolamide on cognitive performance during high-altitude exposure." Neurotoxicology and Teratology 35, no. : 28-33.
Accidental deaths due to exposure to extremely low natural temperature happen every winter. Exposure to extreme cold causes injury of multiple organs. However, early responses of the bodies to acute extreme cold exposure remain incompletely understood. In this study, we found that hepatic glycogen was rapidly reduced in rats exposed to -15°C, and the key enzymes required for glycogenesis were upregulated in the livers of the cold-exposed rats. In line with the rapid consumption of glycogen, acute cold exposure induced a transient elevation of cellular ATP level, which lasted about one hour. The ATP level went back to basal level after two hours of cold exposure. Four hours of cold exposure resulted in cellular ATP depletion and cell apoptosis. The dynamic change of cellular ATP levels was well associated with Akt activation in cold-exposed liver cells. The activation of Akt was required for cold exposure-induced ATP elevation. Blockade of Akt activation diminished the transient increase of intracellular ATP content and exacerbated cell apoptosis during acute cold exposure. These results suggest that Akt activation plays a pivotal role in maintaining cellular bioenergy balance and promoting liver cell survival during acute cold exposure.
Jiye Wang; Yaoming Chen; Wenbin Zhang; Gang Zheng; Shanshan Meng; Honglei Che; Tao Ke; Jingrun Yang; Jingyuan Chen; Wenjing Luo. Akt Activation Protects Liver Cells from Apoptosis in Rats during Acute Cold Exposure. International Journal of Biological Sciences 2013, 9, 509 -517.
AMA StyleJiye Wang, Yaoming Chen, Wenbin Zhang, Gang Zheng, Shanshan Meng, Honglei Che, Tao Ke, Jingrun Yang, Jingyuan Chen, Wenjing Luo. Akt Activation Protects Liver Cells from Apoptosis in Rats during Acute Cold Exposure. International Journal of Biological Sciences. 2013; 9 (5):509-517.
Chicago/Turabian StyleJiye Wang; Yaoming Chen; Wenbin Zhang; Gang Zheng; Shanshan Meng; Honglei Che; Tao Ke; Jingrun Yang; Jingyuan Chen; Wenjing Luo. 2013. "Akt Activation Protects Liver Cells from Apoptosis in Rats during Acute Cold Exposure." International Journal of Biological Sciences 9, no. 5: 509-517.
Manganese is a common environmental and occupational pollutant. Excessive intake of manganese can cause toxicity known as manganism. Recently it has been demonstrated that unusual expression of cell cycle proteins and aberrant cell cycle progression in the central nervous system are involved in the pathogenesis of neurodegenerative diseases. The present studies were initiated to investigate whether p21 are induced after manganese exposure and its potential effects in vitro, with particular attention being given to understand the underlying regulatory mechanism of p21 induction by manganese in this process. We found that manganese induced DAergic cells injury and upregulation of p21 levels in nigrostriatal regions. Treatment of the PC12 cells with manganese resulted in a time- and concentration-dependent loss of cell viability. Analysis of cell cycle profile indicated that manganese blocked cell cycle progression by arresting the cell cycle at G2/M phase. Moreover, manganese treatment resulted in an increase in the mRNA and protein levels of p21, but did not have the same effect on other related factors. Silencing p21 by RNA interference showed a marked reversal of both G2/M arrest and the decrease in cell viability induced by manganese. Manganese did not stabilize the p21 protein and mRNA, and caused a marked increase in p21 mRNA levels together with an increase in its promoter activity, indicating a transcriptional mechanism. Overall, the in vivo and in vitro data suggest that exposure to manganese can increase p21 levels. An altered cell cycle status of PC12 cells can be induced by manganese through p21 up-regulation, and the induction of p21 occurs at the transcriptional level via promoter activation and mRNA induction.
F. Zhao; J.-B. Zhang; T.-J. Cai; X.-Q. Liu; M.-C. Liu; T. Ke; J.-Y. Chen; W.-J. Luo. Manganese induces p21 expression in PC12 cells at the transcriptional level. Neuroscience 2012, 215, 184 -195.
AMA StyleF. Zhao, J.-B. Zhang, T.-J. Cai, X.-Q. Liu, M.-C. Liu, T. Ke, J.-Y. Chen, W.-J. Luo. Manganese induces p21 expression in PC12 cells at the transcriptional level. Neuroscience. 2012; 215 ():184-195.
Chicago/Turabian StyleF. Zhao; J.-B. Zhang; T.-J. Cai; X.-Q. Liu; M.-C. Liu; T. Ke; J.-Y. Chen; W.-J. Luo. 2012. "Manganese induces p21 expression in PC12 cells at the transcriptional level." Neuroscience 215, no. : 184-195.
Mitochondrial impairment is hypothesized to contribute to cell injury during cold stress. Mitochondria fission and fusion are closely related in the function of the mitochondria, but the precise mechanisms whereby these processes regulate cell injury during cold stress remain to be determined. HEK293 cells were cultured in a cold environment (4.0+/-0.1 degrees C) for 2, 4, 8, or 12h. Western blot analyses showed that these cells expressed decreased fission-related protein Drp1 and increased fusion-related protein Mfn2 at 4h; meanwhile, electron microscopy analysis revealed large and long mitochondrial morphology within these cells, indicating increased mitochondrial fusion. With silencing of Mfn2 but not of Mfn1 by siRNA promoted cold-stress-induced cell death with decreased ATP production in HEK293 cells. Our results show that increased expression of Mfn2 and mitochondrial fusion are important for mitochondrial function as well as cell survival during cold stress. These findings have important implications for understanding the mechanisms of mitochondrial fusion and fission in cold-stress-induced cell injury.
Wenbin Zhang; Yaomin Chen; Qun Yang; Honglei Che; Xiangjun Chen; Ting Yao; Fang Zhao; Mingchao Liu; Tao Ke; Jingyuan Chen; Wenjing Luo. Mitofusin-2 protects against cold stress-induced cell injury in HEK293 cells. Biochemical and Biophysical Research Communications 2010, 397, 270 -276.
AMA StyleWenbin Zhang, Yaomin Chen, Qun Yang, Honglei Che, Xiangjun Chen, Ting Yao, Fang Zhao, Mingchao Liu, Tao Ke, Jingyuan Chen, Wenjing Luo. Mitofusin-2 protects against cold stress-induced cell injury in HEK293 cells. Biochemical and Biophysical Research Communications. 2010; 397 (2):270-276.
Chicago/Turabian StyleWenbin Zhang; Yaomin Chen; Qun Yang; Honglei Che; Xiangjun Chen; Ting Yao; Fang Zhao; Mingchao Liu; Tao Ke; Jingyuan Chen; Wenjing Luo. 2010. "Mitofusin-2 protects against cold stress-induced cell injury in HEK293 cells." Biochemical and Biophysical Research Communications 397, no. 2: 270-276.