Evidence for the influence of vitamin C on age- and heat exposure-dependent deterioration of biochemical function in rat's liver and kidney

Molecular mechanisms responsible for age-dependent deterioration of biochemical functions have not been completely revealed as yet. We studied the role of ascorbic acid food supplementation in young and aged acute heat-exposed rats. The duration of heat exposure (40±0.5 °C) for heat-exposed Wistar rats, at the age of 35 days and 22–24 months, was approximately 2 h. In the aged heat-unexposed animals cholesterol and triglycerides were considerably high, whereas tissues ascorbic acid, glutathione and methylglyoxal were significantly low. Administration of vitamin C reverted these age-associated differences to the status comparable to young rats. The role of vitamin C supplementation was almost the same in young heat-exposed animals. In this direction in young rats suppression of LTC4 synthesis is evident during acute heat exposure as a result of vitamin C treatment. The importance of vitamin C treatment for young heat-exposed rats is in the protection of apoptosis, if it is determined across the LTC4 changes. In contrary, in old heat-exposed rats, vitamin C does not suppress the apoptotic processes. The results suggest that oxidative and apoptotic processes in the liver and the kidney as a result of the acute heat exposure is presumably subject of ascorbic acid deficiency.