title: Oxidative stress markers and apoptosis in the prostate of diabetic rats and the influence of vitamin C treatment.
abstract: 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.
authors.affiliation: Department of Cell Biology, Institute of Biology-UNICAMP, Campinas, São Paulo, Brazil.
authors.forename: Marina Guimarães
authors.initials: MG
authors.lastname: Gobbo
authors.forename: Daniele Lisboa
authors.initials: DL
authors.lastname: Ribeiro
authors.forename: Sebastião Roberto
authors.initials: SR
authors.lastname: Taboga
authors.forename: Eduardo Alves
authors.initials: EA
authors.lastname: de Almeida
authors.forename: Rejane Maira
authors.initials: RM
authors.lastname: Góes
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001205:Ascorbic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D015415:Biomarkers; D049109:Cell Proliferation / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D005979:Glutathione Peroxidase / Q000096:biosynthesis; D005982:Glutathione Transferase / Q000096:biosynthesis; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D011467:Prostate / Q000378:metabolism* / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D011944:Receptors, Androgen / Q000378:metabolism; D013311:Streptozocin / Q000009:adverse effects / Q000494:pharmacology; D013482:Superoxide Dismutase / Q000096:biosynthesis; D013739:Testosterone / Q000097:blood
chemical_list: D015415:Biomarkers; D011944:Receptors, Androgen; D013739:Testosterone; D013311:Streptozocin; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D001205:Ascorbic Acid