Citation

Vitcheva V. Curr. Med. Chem. 2012; 19(33): 5677-5682.

Affiliation

Department of Pharmacology, pharmacotherapy and toxicology Faculty of Pharmacy; "Dunav"2 str. Sofia -1000; Bulgaria. vesselavitcheva@yahoo.com.

Copyright

(Copyright © 2012, Bentham Science Publishers)

DOI

unavailable

PMID

22856658

Abstract

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.

Language: en