Gaolong Zhong

TL;DR: Findings provide strong evidence that excess Cu can trigger autophagy and apoptosis via the mitochondrial pathway by inducing oxidative stress in rat kidneys.

TL;DR: In this paper, a total of sixty 4-week-old mice were divided into four groups and treated with 4 ǫ/kg arsenic trioxide (ATO) or/and 15 õ/kg antimony (Sb) for 60 days, and the results demonstrated that biochemical indicators of hepatotoxicity were upregulated in all treated groups.

TL;DR: Zhang et al. as discussed by the authors investigated the influence of arsenic trioxide (ATO) on the gut-liver axis and consequent hepatotoxicity in waterfowl and found that ATO-exposure induced intestinal damage, liver inflammatory cell infiltration and vesicle steatosis.

TL;DR: Zhang et al. as discussed by the authors explored the mechanism by which As and Sb cotreatment induced autophagy and pyroptosis in vivo and in vitro, and they showed that As or Sb exposure could induce histopathological changes in the kidneys, and increase the levels of biochemical indicators of nephrotoxicity.

TL;DR: It is suggested that Msr can protect broiler hepatocytes against ATO-induced oxidative stress and NAC-mediated reversal of oxidative damage may represent a strategy to mitigate potential economic losses associated with arsenic poisoning in the poultry industry.