Potential role of some oxidant/antioxidant status parameters in prefrontal cortex of rat brain in an experimental psychosis model and the protective effects of melatonin

Abstract

OBJECTIVES: The etiology of schizophrenia is unknown. However, some of the neuropathological changes in schizophrenia may be the result of increased free radical-mediated or reactive oxygen species (ROS) mediated neurotoxicity. Melatonin is a hormone produced especially at night in the pineal gland; additionally is a highly important antioxidant. The aim of this study is to indicate the contribution effect of the neuropathophysiology of schizophrenia and protective effects of melatonin against this oxidative damaged. MK-801 induced selective neurotoxicity has been proposed as an animal model for psychosis.

MATERIALS AND METHODS: 21 healthy adult and male Wistar albino rats were divided into three groups. MK-801 was given intraperitoneally for 5 days in experimental psychosis group. Melatonin was given to the treatment group for 6 days by intraperitoneally. In control group, saline was given in the same way. At the 7th day of the experiments, rats were killed by decapitation. Brains were removed and prefrontal part of the brain was divided for biochemical analyses.

RESULTS: Some antioxidant enzymes, malondialdehyde and protein carbonyl analyses were made by spectrophotometric methods. SOD, GSH-Px, XO activities and malondialdehyde, protein carbonyl and NO levels were found to be increased significantly in prefrontal cortex of MK-801 group (p < 0.0001) compared to the control group. In melatonin treated rats, prefrontal tissue malondialdehyde and protein carbonyl levels were decreased significantly in comparison with MK-801 group (p < 0.0001).

CONCLUSIONS: MK-801 may induce oxidative stress in prefrontal cortex of rats. This experimental study provides some evidences for the protective effects of melatonin on MK-801-induced changes in prefrontal rat cortex.