Journal
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Volume 228, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2021.112954
Keywords
NiCl2; Kidney; Oxidative stress; Apoptosis; Autophagy
Categories
Funding
- Sichuan Science and Technology Program (Science and Technology Department of Sichuan Province, Chengdu, China) [2020YJ0113, 2019YFQ0012, 2018NZ0002]
- National key research and development project [2018YFD0501800]
- Sichuan beef cattle innovation team of National modern agricultural industrytechnology system (Sichuan Provincial Department of Agriculture and Rural Affairs, Chengdu, China) [SCCXTD-2020-13]
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The study found that nickel-mediated renal injury is associated with oxidative stress-induced apoptosis and autophagy. NAC, as an effective antioxidant, can suppress nickel-induced oxidative stress and alleviate kidney damage.
As an extensively environmental pollution, Nickel (Ni) represents a serious hazard to human health. The present study focused on exploring the mechanism of Ni-mediated nephrotoxicity, such as apoptosis, autophagy and oxidative stress. In the current work, NiCl2 treatment could induce kidney damage. Meanwhile, NiCl2 treatment elevated ROS production and MDA content and suppressed the antioxidant activity, which was characterized by reducing T-AOC, CAT, SOD activity and GSH content. For investigating the role of oxidative stress on NiCl2mediated nephrotoxicity, N-acetyl cysteine (NAC, effective antioxidant and free radical scavenger) was cotreated with NiCl2. The results showed that NAC significantly suppressed the NiCl2-mediated oxidative stress and mitigated NiCl2-induced the kidney damage. Then, whether oxidative stress-induced autophagy and apoptosis were involved in NiCl2-induced nephrotoxicity was explored. The findings demonstrated that NAC relieved NiCl2-induced autophagy and reversed the activation of Akt/AMPK/mTOR pathway. Concurrently, the results indicated that NAC attenuated NiCl2-induced apoptosis, as evidenced by reduction of apoptotic cells and cleaved-caspase-3/- 8/- 9 together with cleaved-PARP protein levels. To sum up, our findings suggested that NiCl2-mediated renal injury was associated with oxidative stress-induced apoptosis and autophagy. This study provides new theoretical basis for excess Ni exposure nephrotoxic researches.
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