ABSTRACT Acrylamide (AA), is an important industrial compound, formed during food processing under high temperature. Due to its potential carcinogenic effect, it has been recognized as a human health concern. In this study, we investigated the role of oxidative stress in acrylamide’s genotoxicity and protective role of L- carnitine (LCA) in human lymphocytes. The micronucleus test (MNT) was used to monitor AA genotoxicity after 20h exposure to concentrations of 0.25,50 and 100 mM. Furthermore we evaluated oxidative stress markers, such as reactive oxygen species (ROS), lipid peroxidation (LPO) and glutathione (GSH) content. In MNT, It has been found that AA at high concentrations (50 and 100 µM) significantly increased the micronuclei (MN) frequencies. On the one hand, AA exposure induced ROS formation, LPO and also GSH oxidation in treated lymphocytes. On the other hand, pretreatment with LCA (100 and 200µM) inhibited AA-induced oxidative stress which subsequently led to decreasing of the micronuclei (MN) frequencies in human lymphocytes. In overall, the clastugenic effect of acrylamide was confirmed. Also, it has been observed that LCA prevented AA genotoxicity via amelioration of oxidative stress in human lymphocytes. Therefore, oxidative stress suggested as an important factor involved in acrylamide-induced genotoxicity.
ABSTRACT Methamphetamine (METH) is widely abused in worldwide. METH use could damage the dopaminergic system and induce cardiotoxicity via oxidative stress and mitochondrial dysfunction. Edaravone, a sedative-hypnotic agent, is known for it's antioxidant properties. In this study we used edaravone for attenuating of METH-induced cardiotoxicity in rats. The groups (six rats in each group) were as follows: control, METH (5 mg/kg IP) and edaravone (5, 10 and 20 mg/kg, IP) was administered 30 min before METH. After 24 hours, animals were killed, heart tissue was separated and mitochondrial fraction was isolated and oxidative stress markers were measured. Edaravone significantly (p<0.05) protected the heart against lipid peroxidation by inhibition of reactive oxygen species (ROS) formation. Edaravone also significantly (p<0.05) increased the levels of heart glutathione (GSH). METH administration significantly (p<0.05) disrupted mitochondrial function that edaravone pre-treatment significantly (p<0.05) inhibited METH-induced mitochondrial dysfunction. Protein carbonyl level also increased after METH exposure, but was significantly (p<0.05) decreased with edaravone pre-treatment. These results suggested that edaravone is able to inhibition of METH-induced oxidative stress and mitochondrial dysfunction and subsequently METH-induced cardiotoxicity. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH toxicity and cardio degenerative disease.