Laboratory of Drug metabolism and drug toxicity, Department of Pharmacology, pharmacotherapy and toxicology, Faculty of Pharmacy, Dunav 2 str. Sofia -1000, Bulgaria.
Curr Med Chem. 2012;19(33):5677-82. doi: 10.2174/092986712803988929.
Cocaine belongs to the group of psychostimulants and together with amphetamines has been recognized as one of the most significant examples of drug abuse. Cocaine abuse is due to intense feelings of euphoria, friendliness, empathy, and hyperactivity, which result from its potent inhibitory effects on presynaptic dopamine and noradrenaline re-uptake. Misuse of cocaine can induce severe toxic effects, including neurotoxicity, cardiotoxicity, hepatotoxicity. There are a number of data, both experimental and clinical, regarding its hepatotoxic effects, associated with lipid peroxidation-induced oxidative damage. The oxidative metabolism of cocaine to reactive oxygen species (ROS) like nitrogen peroxide and superoxide anion radicals are thought to be responsible for the cocaine associated liver injury. This review summarizes the present information on cocaine hepatic biotransformation and the possible role of its oxidative metabolism in cocaine-induced hepatic injury.
可卡因属于苯丙胺类兴奋剂，与安非他命一起被认为是药物滥用的最重要例子之一。可卡因滥用是由于其强烈的欣快感、友好、同理心和多动，这是由于它对突触前多巴胺和去甲肾上腺素再摄取的强烈抑制作用。可卡因的滥用会引起严重的毒性作用，包括神经毒性、心脏毒性、肝毒性。有许多关于其肝毒性作用的实验和临床数据，与脂质过氧化诱导的氧化损伤有关。可卡因氧化代谢产生的活性氧（ROS），如氮氧化物和超氧阴离子自由基，被认为是导致可卡因相关肝损伤的原因。这篇综述总结了可卡因肝生物转化的现有信息，以及其氧化代谢在可卡因诱导肝损伤中的可能作用。
