Oxidative stress-mediated apoptosis and autophagy involved in Ni-induced nephrotoxicity in the mice
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....
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2021
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oai:doaj.org-article:0379a3e5384a47de9d096b7bc4d752542021-11-04T04:25:51ZOxidative stress-mediated apoptosis and autophagy involved in Ni-induced nephrotoxicity in the mice0147-651310.1016/j.ecoenv.2021.112954https://doaj.org/article/0379a3e5384a47de9d096b7bc4d752542021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S0147651321010666https://doaj.org/toc/0147-6513As 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 NiCl2-mediated nephrotoxicity, N-acetyl cysteine (NAC, effective antioxidant and free radical scavenger) was co-treated 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.Hongrui GuoHeng YinZhicai ZuoZhuangzhi YangYue YangLing WeiHengmin CuiHuidan DengXia ChenJian ChenYanqiu ZhuPing OuyangYi GengZongjun DuHuaqiao TangFengyuan WangJing FangElsevierarticleNiCl2KidneyOxidative stressApoptosisAutophagyEnvironmental pollutionTD172-193.5Environmental sciencesGE1-350ENEcotoxicology and Environmental Safety, Vol 228, Iss , Pp 112954- (2021) |
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| topic |
NiCl2 Kidney Oxidative stress Apoptosis Autophagy Environmental pollution TD172-193.5 Environmental sciences GE1-350 |
| spellingShingle |
NiCl2 Kidney Oxidative stress Apoptosis Autophagy Environmental pollution TD172-193.5 Environmental sciences GE1-350 Hongrui Guo Heng Yin Zhicai Zuo Zhuangzhi Yang Yue Yang Ling Wei Hengmin Cui Huidan Deng Xia Chen Jian Chen Yanqiu Zhu Ping Ouyang Yi Geng Zongjun Du Huaqiao Tang Fengyuan Wang Jing Fang Oxidative stress-mediated apoptosis and autophagy involved in Ni-induced nephrotoxicity in the mice |
| description |
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 NiCl2-mediated nephrotoxicity, N-acetyl cysteine (NAC, effective antioxidant and free radical scavenger) was co-treated 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. |
| format |
article |
| author |
Hongrui Guo Heng Yin Zhicai Zuo Zhuangzhi Yang Yue Yang Ling Wei Hengmin Cui Huidan Deng Xia Chen Jian Chen Yanqiu Zhu Ping Ouyang Yi Geng Zongjun Du Huaqiao Tang Fengyuan Wang Jing Fang |
| author_facet |
Hongrui Guo Heng Yin Zhicai Zuo Zhuangzhi Yang Yue Yang Ling Wei Hengmin Cui Huidan Deng Xia Chen Jian Chen Yanqiu Zhu Ping Ouyang Yi Geng Zongjun Du Huaqiao Tang Fengyuan Wang Jing Fang |
| author_sort |
Hongrui Guo |
| title |
Oxidative stress-mediated apoptosis and autophagy involved in Ni-induced nephrotoxicity in the mice |
| title_short |
Oxidative stress-mediated apoptosis and autophagy involved in Ni-induced nephrotoxicity in the mice |
| title_full |
Oxidative stress-mediated apoptosis and autophagy involved in Ni-induced nephrotoxicity in the mice |
| title_fullStr |
Oxidative stress-mediated apoptosis and autophagy involved in Ni-induced nephrotoxicity in the mice |
| title_full_unstemmed |
Oxidative stress-mediated apoptosis and autophagy involved in Ni-induced nephrotoxicity in the mice |
| title_sort |
oxidative stress-mediated apoptosis and autophagy involved in ni-induced nephrotoxicity in the mice |
| publisher |
Elsevier |
| publishDate |
2021 |
| url |
https://doaj.org/article/0379a3e5384a47de9d096b7bc4d75254 |
| work_keys_str_mv |
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