Hepatic Antioxidant Effect of Paroxetine in Rats Exposed to Chronic Restraint Model

Depressed mood, with its accompanying mental and physical stresses, could affect the progression and severity of several diseases e.g. hypertension, myocardial infarction, gastritis, peptic ulcer. The present animal study was done to investigate the potential antioxidant effect of paroxetine, as a selective serotonin reuptake inhibitor, to protect against chronic restraint stress-induced oxidative damage in the liver. Thirty albino rats were divided into 3 equal groups. Group 1 was control, non-stressed non-treated group. Group 2 was exposed to chronic restraint model by placing them in wire mesh cages exactly fit to their size for 6 hours daily for 21 days. Group 3 were also exposed to chronic restraint model for 21 days while they were administered by paroxetine 1 mg/kg/day ip during the restraint period. At the end of the study, liver transaminases were determined by commercial kits. The hepatic levels of glutathione peroxidase, catalase and thiobarbituric acid reactive substance were also determined by spectrophotometric methods. Glutathione repletion ability by hepatic cells with and without paroxetine treatment was also determined in all tested groups. The results showed a significant (p<0.05) increase in serum levels of transaminases and liver anti-oxidant enzymes while levels of thiobarbituric acid reactive substance were significantly (p<0.05) reduced in paroxetine-treated group compared with non-stressed non-treated control rats. Glutathione repletion ability was also significantly (p<0.05) increased in treated group to a level comparable to the control non-stressed non-treated values.