BRIEF REPORT: Increased blood oxidative stress in amphetamine users

Abstract

Amphetamine derivatives have been shown to be a potential brain neurotoxin based on the production of free radicals that occurs after administration. The purpose of this study was to examine the lipid peroxidation and antioxidant enzymes in the blood of amphetamine users. The plasma lipid peroxidation was determined and reported as thiobarbituric acid reactive substance and was significantly increased (+21%), whereas the activities of the erythrocyte antioxidant enzymes glutathione peroxidase, catalase, and superoxide dismutase were significantly decreased (-32%, -14% and -31%, respectively) in amphetamine users. These results implicated the potential role of oxidative stress in amphetamine-induced neurotoxicity.

Oxidative stress status in recently abstinent methamphetamine abusers

“…Our finding of enhanced lipid peroxidation is in agreement with previous reports that showed human METH users have higher MDA levels in the brain or in the blood …”

“…In the present study, a persistent reduction of SOD activity suggests a compromised elimination of superoxide radicals in our subjects. This observation is compatible with another study that showed a lower erythrocyte SOD activity in the blood of amphetamine users . The post‐mortem study showed the SOD activity was instead elevated in the brains of METH abusers who tested positive for METH at autopsy .…”

“…In human studies, METH abusers have increased levels of MDA either in the brain or blood . In addition, an alteration of anti‐oxidant parameters has also been observed . These findings collectively support the association between METH use and enhanced oxidative stress.…”

“…There have been only two reports to date describing the systemic oxidative stress in METH abusers. One of them showed increased MDA levels in METH abusers and the other indicated an elevation of oxidative stress by measuring various pertinent indices in the blood of amphetamine users . METH is considered as a more toxic substance than amphetamine due to its cationic lipophilicity.…”

Addictive Drugs and Synaptic Plasticity

“…In addition, cocaine induced a 1.9-fold increase in locomotor activity after overexpression of α-synuclein in the NAc (Boyer and Dreyer, 2007). It is noteworthy that the neurotoxicity induced by the psychostimulants such as amphetamine are mediated by enhanced oxidative stress and these effects are abolished by melatonin (Govitrapong et al, 2010), a main secretory product of pineal gland. Interestingly, a recent report suggested that this melatonin effect is mediated by the reduction of the overexpression of α-synuclein induced by amphetamine (Sae-Ung et al, 2011).…”