Cocaine-induced cardiovascular disorders such as hypertension, thrombosis, myocardial dysfunction, cardiac dysrhythmias
and endocarditis have received widespread attention in the context of cocaine abuse. The number of sudden deaths from cardiac causes,
including myocardial infarction, ventricular tachyarrhythmia or aortic dissection, is also increasing. This manuscript will highlight the recent
employment of study about cocaine cardiotoxicity and oxidative stress. Evidence has revealed that cardiac oxidative stress is a
prominent early event of cocaine administration, which severely compromises the cardiac antioxidant cellular system and causes cardiac
antioxidant cellular system injuries. Oxidative damage such as peroxidation of membrane phospholipids and depletion of nonenzymatic
antioxidants such as glutathione have been found in the myocardium of chronic cocaine-treated animals and in patients. The data indicate
that cocaine administration compromised the heart's antioxidant defense system. About the mechanisms involved in the cellular damage,
the evidence that cocaine causes apoptosis in the heart comes from in vivo study. In animals model after short-term and long term-cocaine
administration, the investigators demonstrates the role of Reactive Oxygen Species as a trigger of cardiac injury induced by cocaine. Cocaine
also increased infiltration of inflammatory cells in the heart, and apoptotic cells were predominantly found near inflammatory cells.
The role of oxidative stress in cocaine-induced apoptosis in the heart is wide studied and documented.
Keywords: Antioxidant enzymes, apoptosis, cardiotoxicity, cocaine related-death, oxidative stress, reactive oxygen species, Cocaine-induced, cardiovascular disorders, hypertension, myocardial dysfunction
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