College of Wildlife Resources, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
College of Wildlife Resources, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Ecotoxicol Environ Saf. 2019 Sep 15;179:167-174. doi: 10.1016/j.ecoenv.2019.04.062. Epub 2019 Apr 28.
Sub-chronic arsenic (arsenite) exposure-induced oxidative toxicity leads to adverse effects in various organ systems, especially the kidney. Copper sulphate (Cu), known for its extensive uses in agriculture, has also been reported to have pro-oxidation properties. Both of these two potential toxic elements can bio-accumulate through food chain, thus endangering human health. However, their interaction study in the kidney is scanty.
To investigate the synergism effects of Cu in arseniasis-elicited oxidative stress and cascaded renal injury in chickens.
Arsenite intoxication decreased renal antioxidant system along with ATPases. Arsenite exposure also significantly elicited disequilibrium of mitochondrial homeostasis, accompanying by elevated apoptotic and autophagic cell death. The disturbed morphological and ultrastructural changes further corroborated arsenite nephrotoxicity. These anomalies aligned with the findings in Cu groups, which co-administrated with arsenic further deteriorated these pathological changes. This synergism was achieved partially via the inactivation of phosphoinositide-3-kinase/protein kinase b/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway through the activation of P53.
Copper excess and arsenic exposure can function independently or cooperatively to affect oxidative stress, mitochondrial dynamics and programmed cell death. These results highlighted the need to take precautions against copper and arsenic co-exposure when considering their impact in susceptible animals/populations.
亚慢性砷（亚砷酸盐）暴露引起的氧化毒性会导致各种器官系统产生不良反应，尤其是肾脏。硫酸铜（Cu）由于其在农业中的广泛用途而广为人知，也被报道具有促氧化特性。这两种潜在的有毒元素都可以通过食物链进行生物积累，从而危害人类健康。然而，它们在肾脏中的相互作用研究却很少。
研究 Cu 在砷诱导的氧化应激和鸡肾脏损伤级联反应中的协同作用。
亚砷酸盐中毒会降低肾脏的抗氧化系统和 ATP 酶。砷暴露还会显著引起线粒体动态平衡失调，伴随着细胞凋亡和自噬性细胞死亡增加。形态和超微结构的改变进一步证实了亚砷酸盐的肾毒性。这些异常与 Cu 组的发现一致，砷与 Cu 共同给药进一步恶化了这些病理变化。这种协同作用部分是通过激活 P53 使磷酸肌醇 3-激酶/蛋白激酶 B/哺乳动物雷帕霉素靶蛋白（PI3K/AKT/mTOR）通路失活来实现的。
铜过量和砷暴露可以独立或协同作用影响氧化应激、线粒体动力学和程序性细胞死亡。这些结果强调了在考虑铜和砷对易感动物/人群的影响时，需要对它们的共同暴露采取预防措施。
