Open AccessThe Protective Role of Glutathione, Cysteine and Vitamin C against Oxidative DNA Damage Induced in Rat Kidney by Potassium Bromate
Author(s) -
Sai Kimie,
Umemura Takashi,
Takagi Atsuya,
Hasegawa Ryuichi,
Kurokawa Yuji
Publication year - 1992
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1992.tb02350.x
Subject(s) - potassium bromate , chemistry , glutathione , lipid peroxidation , vitamin c , kidney , oxidative stress , endocrinology , antioxidant , medicine , pharmacology , thiol , vitamin e , biochemistry , enzyme , catalysis
The roles of glutathione (GSH), cysteine, vitamin C., liposome‐encapsulated superoxide dismutase (L‐SOD) and vitamin E in preventing oxidative DNA damage and cytotoxicity in the rat kidney after administration of potassium bromate (KBrO 3 ) to male F344 rats were investigated by measuring 8‐hydroxydeoxyguanosine (8‐OH‐dG), an oxidative DNA product, lipid peroxidation (LPO) levels and relative kidney weight (RKW). Combined pre‐ and posttreatment of animals with 2 × 800 mg/kg GSH i.p. inhibited the increase of 8‐OH‐dG, LPO levels and RKW caused by 80 mg/kg KBrO 3 i.p. administration. In contrast, pretreatment with 0.3 ml/kg diethylmaleate (DEM) i.p., a depletor of tissue GSH, was associated with elevation of 8‐OH‐dG, LPO levels and RKW after a 20 mg/kg KBrO 3 i.p. treatment, which itself caused no change. Administration of KBrO 3 itself reduced renal non‐protein thiol levels, but this was inhibited by the two doses of exogenous GSH. Combined treatment with DEM and KBrO 3 lowered the non‐protein thiol level in the kidney more than did DEM treatment alone. Protective effects against the oxidative damage caused by KBrO 3 were also observed for pre‐ and posttreatment with 400 mg/kg cysteine i.p., another sulfhydryl compound, and daily i.g. application of 200 mg/kg vitamin C for 5 days. However, no influence was evident after pre‐ and posttreatment with 18,000 U/kg L‐SOD i.p. or daily i.g. 100 mg/kg of vitamin E for 5 days. The results suggest that intracellular GSH plays an essential protective role against renal oxidative DNA damage and nephrotoxicity caused by KBrO 3 .