Du Jun, Li Zhengqing, Cao Xianhong, Qi Qiurong, Wang Luqi, Liu Ping, Chen Yifei, Hu Guoliang, Guo Xiaoquan, Gao Xiaona
Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, China.
Department of Animal Science, Jiangxi Biological Vocational College, Nanchang 330200, China.
Antioxidants (Basel). 2024 Aug 13;13(8):980. doi: 10.3390/antiox13080980.
Nickel and chromium are both common heavy metals that pose serious environmental and health hazards. However, the exact mechanism by which nickel and/or chromium cause renal injury is unclear. Therefore, we explored the molecular mechanisms of renal injury caused by nickel and/or chromium poisoning from the perspective of mitochondrial dynamics and the Nrf2 antioxidant pathway. In this study, eighty 6-week-old C57BL/6J mice were randomly divided into four groups: control (Con, untreated), nickel (Ni, 110 mg/L Ni), chromium (Cr, 50 mg/L Cr), and combined nickel-chromium (Ni + Cr, 110 mg/L Ni, 50 mg/L Cr). The results showed that chronic nickel and/or chromium exposure inhibited body weight gain and impaired kidney function and structure in mice. Chronic nickel and/or chromium exposure led to the disruption of mitochondrial dynamics and thus induced oxidative stress. On the other hand, the Nrf2 antioxidant pathway may play an important regulatory role in mitigating oxidative stress-induced oxidative damage in kidney. The present study partially elucidated the molecular mechanism of renal injury induced by nickel and/or chromium exposure in mice and the regulatory role of the Nrf2 pathway in inducing oxidative injury from the perspective of mitochondrial dynamics. This provides a theoretical basis for the development of prevention and control strategies, and environmental protection measures.
镍和铬都是常见的重金属，会对环境和健康造成严重危害。然而，镍和/或铬导致肾损伤的确切机制尚不清楚。因此，我们从线粒体动力学和Nrf2抗氧化途径的角度探讨了镍和/或铬中毒所致肾损伤的分子机制。在本研究中，80只6周龄的C57BL/6J小鼠被随机分为四组：对照组（Con，未处理）、镍组（Ni，110 mg/L镍）、铬组（Cr，50 mg/L铬）和镍铬联合组（Ni + Cr，110 mg/L镍，50 mg/L铬）。结果表明，慢性镍和/或铬暴露会抑制小鼠体重增加，并损害其肾功能和结构。慢性镍和/或铬暴露会导致线粒体动力学紊乱，从而诱导氧化应激。另一方面，Nrf2抗氧化途径可能在减轻氧化应激诱导的肾脏氧化损伤中发挥重要的调节作用。本研究部分阐明了镍和/或铬暴露诱导小鼠肾损伤的分子机制以及Nrf2途径在诱导氧化损伤方面的调节作用，从线粒体动力学角度为防控策略和环境保护措施的制定提供了理论依据。
