β-Glucan protects against chronic nicotine-induced oxidative damage in rat kidney and bladder

In this study, we investigated the protective effect of β-glucan against nicotine induced oxidative damage in urinary bladder and kidney tissues. Wistar albino rats were injected i.p. with nicotine hydrogen bitartarate (0.6 mg/kg daily for 21 days) or saline. β-Glucan (50 mg/kg, p.o.) was administered alone or with nicotine injections for 21 days. After decapitation, the urinary bladder and kidney tissues were taken for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, and myeloperoxidase (MPO) activity. Tissue samples were also examined histologically. In serum samples MDA, GSH, BUN, creatinine, TNF-α levels and LDH activity were analyzed. Chronic nicotine administration caused a significant decrease in GSH levels and increases in MDA levels and MPO activity in kidney and bladder tissues, suggesting oxidative organ damage, which was also histologically verified. Furthermore, β-glucan restored the reduced GSH levels, while it significantly decreased MDA levels and MPO activity. Renal function tests, LDH and TNF-α levels, which were increased significantly due to nicotine administration, were decreased with β-glucan treatment. The present data suggest that β-glucan supplementation effectively counteracts the chronic nicotine toxicity and attenuates oxidative damage of bladder and kidney tissues possibly by its antioxidant effects.