The Long Way to Objectify Organ Damage Related to Cocaine Abuse: Oxidative Stress is the Main Culprit
Margherita Neri, Stefania Bello, Natascha Pascale, Cristoforo Pomara, Irene Riezzo, Emanuela Turillazzi and Vittorio Fineschi
Affiliation: Department of Forensic Pathology, Ospedale Colonnello D'Avanzo, Viale degli Aviatori 1, 71100 Foggia, Italy.
Keywords: Antioxidant defense, apoptosis, cocaine-metabolism, cocaine-toxicity, lipid peroxidation, oxidative stress.
Cocaine is one of the principal drugs of abuse, it is an illegal psychostimulant, and the chronic consumption of
cocaine causes damage in a range of body organs. Cocaine is known to undergo metabolism through multiple enzymatic
pathways leading to the formation of several highly reactive species, which have been proposed to exert a direct toxic
effect in the organs. All its metabolites may be involved in the activation of redox cycles, the depletion or decrease of
antioxidant enzymes and the consequent generation of reactive oxygen species (ROS) leading to oxidative stress (OS)
events, the lipid peroxidation and disruption of cellular activity, and consequently cocaine-induced organs damage.
However, the exact mechanisms of cocaine-mediated toxicity in all the organs are not fully understood.
This review provides extensive evidence in support of the hypothesis that oxidative metabolites play important roles
comprising oxidative stress, defined as a disturbance of redox signaling and control that can cause malfunction in organs
such as the brain, heart, liver, kidney and skin.
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