Oxidative stress markers and apoptosis in the prostate of diabetic rats and the influence of vitamin C treatment

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Processo FAPESP: 06/03873-1

Processo FAPESP: 08/05341-2

Processo FAPESP: 08/00542-0

Processo FAPESP: 09/05078-2

Processo FAPESP: 09/06885-9

Negative consequences of diabetes on the prostate such as involution are associated with diminished testosterone, insulin deficiency, and hyperglycemia. The contributions of oxidative damage, which usually increases with diabetes, are unknown for these alterations. This study evaluated the impact of streptozotocin-induced diabetes on the biomarkers of the antioxidant system of rat ventral prostate, the influence of vitamin C supplementation on these biomarkers, and on the balance between cell proliferation and death. Diabetes (D) was induced in Wistar male rats by streptozotocin (5?mg/100?g b.w., i.p.). Control animals (C) were injected with a vehicle. Vitamin C (150?mg/kg b.w./day) supplementation was introduced by gavage in diabetes (D?+?V) as well as control (C?+?V) groups. Thirty days after diabetes onset, the rats were killed and the ventral prostates were analyzed using light microscopy, immunocytochemistry, and biochemical assays for biomarkers of oxidative stress. In comparison to control groups, the levels of circulating testosterone, proliferating, and androgen receptor-positive cells decreased in diabetic groups regardless of vitamin C treatment whereas apoptosis was increased. The levels of superoxide dismutase and glutathione peroxidase did not change, but the levels of glutathione-S-transferase (GST) were increased in diabetic prostate. Vitamin C supplementation normalized GST activity and recovered the apoptotic rates in the prostate. In conclusion, GST is a good indicator of compensatory oxidant defense in the prostate at earlier stages of diabetes and vitamin C improves its activity and attenuates apoptosis in the gland. J. Cell. Biochem. 113: 22232233, 2012. (c) 2012 Wiley Periodicals, Inc.