The Therapeutic Role of Glutathione in Oxidative Stress and Oxidative DNA Damage Caused by Hexavalent Chromium

Hexavalent chromium Cr (VI) causes various toxic and carcinogenic effects. The main carcinogenic effect is observed in the pulmonary system through inhalation route. Reduction of Cr (VI) to Cr (V, IV, and III) reactive intermediates within the cells by intracellular reducing agents such as glutathione is an important event leading to oxidative stress and oxidative DNA damage. This study evaluated the effects of intraperitoneal administration of Cr (VI) and GSH on total oxidant status (TOS), total antioxidant capacity (TAC), oxidative stress index, and oxidative DNA damage by evaluating the level of 8-hydroxy-2I-deoxyguanosine (8-OHdG) in Swiss-Albino mice. Seventy two mice were divided into 6 groups and treated intraperitoneally as follow: control (saline), group GSH (30 mg/kg GSH) groups of Cr-20 (20 mg/kg, K2Cr2O7), Cr-30 (30 mg/kg K2Cr2O7), Cr-20 + GSH (20 mg/kg K2Cr2O7 + 30 mg/kg GSH), Cr-30 + GSH (30 mg/kg K2Cr2O7 + 30 mg/kg GSH). Total oxidant capacities of Cr-20 and Cr-30 were increased compared to control, Cr-20 + GSH, and Cr-30 + GSH. TOS levels in Cr-20 + GSH and Cr-30 + GSH were lower than in Cr-20 and Cr-30. No difference in TAC was observed among the groups. 8-Hydroxy-2I-deoxyguanosine levels were increased in groups Cr-20 and Cr-30 compared with control and groups Cr-20 + GSH and Cr-30 + GSH. No difference was determined in 8-OHdG levels among control, groups GSH, Cr-20 + GSH and Cr-30 + GSH. Results indicate that Cr (VI) given i.p. route causes increased oxidative stress and oxidative DNA damage in the blood of Swiss-Albino mice. Administration of GSH via i.p. route protects from oxidative stress and DNA damage.