Arsenic (As) and antimony (Sb) are known as an environmental contaminant with cardiotoxicity properties. The endoplasmic reticulum (ER) is the largest calcium reservoir in the cell, and its calcium homeostasis disorder plays a vital role in endoplasmic reticulum stress (ERS) and apoptosis. The objective of this study was to investigate whether As and Sb induced apoptosis via endoplasmic reticulum stress (ERS) linked to calcium homeostasis disturbance. In this study, thirty-two adult mice were gavage-fed daily with As₂O₃ (4 mg/kg), SbCl₃ (15 mg/kg) and co-treat with SbCl₃ (15 mg/kg) and As₂O₃ (4 mg/kg) daily for 60 days. It was observed that As or/and Sb caused histopathological lesions and ER expansion of the heart. Meanwhile, the gene expression of ER Ca²⁺ release channels (RyR2 and IP3R) and calmodulin-dependent protein kinase II (CaMKII) increased while the levels of mRNA and protein of ER Ca²⁺ uptake channel (SERCA2) downregulated significantly compared to the controls. Then, As or/and Sb induced ERS and triggered the ER apoptotic pathway by activating unfolded protein response (UPR)-associated genes ((PERK, ATF6, IRE1, XBP1, JNK, GRP78), and apoptosis-related genes (Caspase12, Caspase3, p53, CHOP). Above indicators in As + Sb group became more severe than that of As group and Sb group. Overall, our results proved that the cardiotoxicity caused by As or/and Sb might be concerning disturbing calcium homeostasis, which induced apoptosis through the ERS pathway.

Eight new 4-hydroxy-2-pyridone alkaloids arthpyrones D–K (1–8), along with two known analogues apiosporamide (9) and arthpyrone B (10), were isolated from a deep-sea-derived fungus Arthrinium sp. UJNMF0008. The structures of the isolated compounds were elucidated on the basis of spectroscopic methods with that of 1 being established by chemical transformation and X-ray diffraction analysis. Compounds 1 and 2 bore an ester functionality linking the pyridone and decalin moieties first reported in this class of metabolites, while 3 and 4 incorporated a rare natural hexa- or tetrahydrobenzofuro[3,2-c]pyridin-3(2H)-one motif. Compounds 3–6 and 9 exhibited moderate to significant antibacterial activity against Mycobacterium smegmatis and Staphylococcus aureus with IC₅₀ values ranging from 1.66–42.8 μM, while 9 displayed cytotoxicity against two human osteosarcoma cell lines (U2OS and MG63) with IC₅₀ values of 19.3 and 11.7 μM, respectively.

This study revealed for the first time the dynamic changes of the bacterial community during the fermentation of traditional Chinese fish sauce (TCFS) using high-throughput sequencing. In the early phase of TCFS fermentation, Shewanella (approximately 90%) within Proteobacteria was the dominant bacteria. Then, Halanaerobium (3%–86%) within Firmicutes rapidly replaced Shewanella as the dominant genus until the 12th month. Lactococcus (3.31%) and Bacillus (45.56%) belonging to Firmicutes were detected abundantly in the 3rd and 9th months after fermentation, respectively. In the late phase (12–15 months), Tetragenococcus within Firmicutes replaced Halanaerobium as the most dominant bacteria (29.54%). Many other genera including Pseudomonas, Psychrobacter, Tissierella, Carnobacterium and Gallicola were abundantly present in the 15th month after fermentation. Furthermore, the relationships between the bacterial community and major functional substances of TCFS, including amino nitrogen (AAN), free amino acids (FAAs), total soluble nitrogen (TSN), and trimethylamine (TMA), were investigated by partial least squares regression (PLSR). Tetragenococcus was positively correlated with the formation of TMA, while Halanaerobium showed the opposite result, suggesting that Tetragenococcus might be a good starter for TCFS fermentation. These results contribute to our knowledge about bacterial participation in the process of TCFS fermentation and will help improve the quality of fermented seafood.

Arsenic (As) and antimony (Sb) are commonly accumulated environmental pollutants that often coexist in nature and cause serious widespread biological toxicity. To investigate the nephrotoxicity induced by As and Sb in detail, we explored the mechanism by which As and Sb cotreatment induced autophagy and pyroptosis in vivo and in vitro. In this study, mice were treated with 4 mg/kg arsenic trioxide (ATO) or/and 15 mg/kg antimony trichloride (SbCl₃) by intragastric intubation for 60 days. TCMK-1 cells were treated with ATO (12.5 μM), SbCl₃ (25 μM) or a combination of As and Sb for 24 h. The results of the in vivo experiment demonstrated that As or/and Sb exposure could induce histopathological changes in the kidneys, and increase the levels of biochemical indicators of nephrotoxicity. In addition, As and Sb can co-induce oxidative stress, which further activate autophagy and pyroptosis. In an in vitro experiment, As and/or Sb coexposure increased ROS generation and decreased MMP. Moreover, the results of related molecular experiments further confirmed that As and Sb coactivated autophagy and pyroptosis. In conclusion, our results indicated that As and Sb co-exposure could cause autophagy and pyroptosis via the ROS pathway, and these two metals might have a synergistic effect on nephrotoxicity.