Cadmium Toxicity: Oxidative Stress, Inflammation and Tissue Injury

Sandra Concepcion Das, H. Al-Naemi
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引用次数: 27

Abstract

Cadmium is a known environmental pollutant targeting various organs. Often implicated in cadmium toxicology is the formation of reactive oxygen species, overwhelming the free radical scavenging mechanisms and inducing oxidative stress. Acute cadmium intoxication has been shown to reduce antioxidant enzyme activity and induce oxidative stress. However, chronic intoxication has obscure outcomes in oxidative stress while the cell makes adjustments to overcome the toxicant load. Also linked with the occurrence of oxidative stress is inflammation. Stimulation of acute or chronic inflammation is mediated by different cascades. However, key events include activation of transcription factor, NF-κB and release of pro-inflammatory cytokines. Both oxidative stress and inflammation are implicated simultaneously in pathogenesis and induction of multi-organ tissue damage under cadmium exposure. This article reviews the impact of acute and chronic cadmium intoxication on inducing oxidative stress, inflammation and thereby inflicting tissue damage.
镉毒性:氧化应激、炎症和组织损伤
镉是一种已知的环境污染物,可靶向多种器官。镉毒理学中经常涉及的是活性氧的形成,压倒自由基清除机制和诱导氧化应激。急性镉中毒可降低抗氧化酶活性,诱发氧化应激。然而,慢性中毒在氧化应激中有模糊的结果,而细胞做出调整以克服毒物负荷。与氧化应激发生有关的还有炎症。急性或慢性炎症的刺激是由不同的级联介导的。然而,关键事件包括转录因子、NF-κB的激活和促炎细胞因子的释放。氧化应激和炎症同时参与镉暴露下多器官组织损伤的发病和诱导。本文综述了急性和慢性镉中毒对氧化应激、炎症和组织损伤的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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