Prakash Chandra, Soni Manisha, Kumar Vijay
Department of Biochemistry, Maharshi Dayanand University, Rohtak, 124001, Haryana, India.
J Appl Toxicol. 2016 Feb;36(2):179-88. doi: 10.1002/jat.3256. Epub 2015 Oct 29.
Arsenic is a toxic metalloid present ubiquitously on earth. Since the last decade, it has gained considerable attention due to its severe neurotoxic effects. Arsenic can cross the blood-brain barrier and accumulate in different regions of the brain suggesting its role in neurological diseases. Arsenic exposure has been associated with reactive oxygen species generation, which is supposed to be one of the mechanisms of arsenic-induced oxidative stress. Mitochondria, being the major source of reactive oxygen species generation may present an important target of arsenic toxicity. It is speculated that the proper functioning of the brain depends largely on efficient mitochondrial functions. Multiple studies have reported evidence of brain mitochondrial impairment after arsenic exposure. In this review, we have evaluated the proposed mechanisms of arsenic-induced mitochondrial oxidative stress and dysfunction. The understanding of molecular mechanism of mitochondrial dysfunction may be helpful to develop therapeutic strategies against arsenic-induced neurotoxicity. The ameliorative measures undertaken in arsenic-induced mitochondrial dysfunction have also been highlighted.
砷是一种有毒类金属，在地球上广泛存在。自上一个十年以来，由于其严重的神经毒性作用，它受到了相当大的关注。砷能够穿过血脑屏障并在大脑的不同区域蓄积，这表明它在神经疾病中发挥作用。砷暴露与活性氧的产生有关，这被认为是砷诱导氧化应激的机制之一。线粒体作为活性氧产生的主要来源，可能是砷毒性的一个重要靶点。据推测，大脑的正常功能很大程度上依赖于线粒体的有效功能。多项研究报告了砷暴露后脑线粒体损伤的证据。在本综述中，我们评估了砷诱导线粒体氧化应激和功能障碍的推测机制。对线粒体功能障碍分子机制的理解可能有助于制定针对砷诱导神经毒性的治疗策略。同时也强调了针对砷诱导线粒体功能障碍所采取的改善措施。
