Occupational and environmental exposures to industrial chemicals are well known to cause hepatotoxicity and liver injury. However, despite extensive evidence showing that exposure can lead to disease, current research approaches and regulatory policies fail to address the possibility that subtle changes caused by low level exposure to chemicals may also enhance preexisting conditions. In recent years, the conceptual understanding of the contribution of environmental chemicals to liver disease has progressed significantly. Mitochondria are often target of toxicity of environmental toxicants resulting in multisystem disorders involving different cells, tissues, and organs. Here, we review persistent maladaptive changes to mitochondria in response to environmental toxicant exposure as a mechanism of hepatotoxicity. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of toxicant-induced liver disease, rational targeted therapy can be developed to better predict risk, as well as to treat or prevent this disease.

众所周知，职业和环境接触工业化学品会导致肝毒性和肝损伤。然而，尽管大量证据表明接触可能导致疾病，但当前的研究方法和监管政策未能解决低水平接触化学物质引起的微妙变化也可能加剧已有病症的可能性。近年来，人们对环境化学物质对肝病影响的概念性认识取得了显着进展。线粒体通常是环境毒物毒性的目标，导致涉及不同细胞、组织和器官的多系统疾病。在这里，我们回顾了线粒体因环境毒物暴露而发生的持续适应不良变化，作为肝毒性的机制。通过更好地了解介导毒物诱发性肝病发生和进展的机制和危险因素，可以开发合理的靶向治疗以更好地预测风险，以及治疗或预防这种疾病。