Accumulation of 8-Oxo-2’-Deoxyguanosine (as a Biomarker of Oxidative DNA Damage) in the Tissues of Aged Hamsters and Change in Antioxidant Enzyme Activities after Single Administration of N-Nitrosobis(2-Oxopropyl) Amine

Abstract

Background: It has been reported that DNA oxidative damage accumulates with age. Two reasons for this phenomenon are the decline in the antioxidant system and the decline in the repair system. It is not clear which of these is the main reason. Objective: To study whether the decline in antioxidant enzyme activities causes the accumulation of DNA oxidative damage, an experimental study was performed with hamsters. Methods: Seventy-four female Syrian golden hamsters were divided into 2 groups: a young group (28 hamsters), and an aged group (46 hamsters). The hamsters in the aged group were kept in our laboratory until they were 18 months old. The levels of 8-oxo-2′-deoxyguanosine (8-oxodG) and the activities of antioxidant enzymes, i.e. catalase, superoxide dismutase (SOD), and glutathione peroxidase (GPx), were measured in both groups. Furthermore, the same parameters were measured in the pancreas and liver following administration of N-nitrosobis(2-oxopropyl)amine (BOP), an inducer of oxidative stress in the hamster pancreas. Results: In the mid brain, cerebellum, lung, heart, spleen and kidney, the 8-oxodG contents in aged hamsters were significantly higher than those in young hamsters. GPx activity decreased with age in the lung, liver and kidney, whereas SOD activity increased in the lung and liver but decreased in the kidney of aged animals. Catalase activity increased in the cerebrum, heart, pancreas and kidney but decreased in the lung and spleen of aged hamsters. When the pancreatic levels of 8-oxodG and antioxidant enzymes were measured after BOP administration, there was no clear-cut relation between the changes in those levels. Conclusions: From these results the increase in 8-oxodG contents in aged hamsters does not seem to be related to the antioxidant system but rather to a possible decline in the repair system against oxidative damage.