Comparison of Melatonin Effect on Oxidant Status and Antioxidant Capacity in Liver and Heart of Young and Aged Rats

Abstract

Oxidative stress is involved in several pathologic conditions such as metabolic or cardiovascular disease, and in aging. Oxidative damage of biomolecules increases with age. Melatonin is the main neurohormone of the pineal gland and specific antioxidants may act against age-related oxidative damage. This study investigated the effects of administration of melatonin on aging-related parameters such as total oxidant status (TOS), hydrogen peroxide (H2O2) and lipid hydroperoxide (LOOH) levels and total antioxidant capacity (TAC) in the heart and liver in a rat model of aging. Young (3-month-old) and aged (24-month-old) male Wistar rats were divided into control and melatonin-treated groups. Melatonin was given for 21 days (10 mg/kg/day). At the end of the treatment period, TOS, TAC, H2O2, and LOOH levels were measured. H2O2 in the liver, but not in the heart, was found to be increased in aged rats. Melatonin treatment diminished H2O2 in the heart of both group of rats compared with those of untreated control rats. Melatonin treatment also led to a decrease in H2O2 in the liver of aged rats. LOOH were found to be increased in both tissues of aged rats whereas melatonin treatment decreased LOOH levels in heart and liver tissues of aged rats. In the young rats melatonin also inhibited LOOH in liver. TAC in heart and liver was not found to be statistically different between young and aged rats. In young rats, melatonin treatment resulted in an increase in TAC that was associated with increased H2O2. In the liver and heart of the rats, TOS was increased with age and was ameliorated by melatonin treatment. Our results demonstrate that there is no dramatic overall decline in the antioxidant system with age. However, total oxidant status increased with age. Melatonin has a restorative effect on oxidative status.