Glutathione and MDA in tissues of rats treated with ochratoxin A

Ochratoxin A (OTA) is a mycotoxin produced by Penicillium and Aspergillus moulds. It contaminates cereals, cereal products, coffee, nuts, meat, milk and other commodities like wine, beer and cheese. Studies on laboratory and domestic animals have shown that OTA is nephrotoxic, carcinogenic, genotoxic, and immunotoxic. One of the possible mechanisms of OTA toxicity is the production of free radicals and consequent oxidative stress. In this study oxidative stress in plasma and different tissues of rats treated with OTA was investigated by measuring the levels of glutathione (GSH) with spectrophotometric method and malondialdehyde (MDA) with HPLC method. Adult male Wistar rats in groups by six were treated orally with NaHCO3 (control group), 250 g OTA/kg b.w. and 500 g OTA/kg b.w. every day for eight days. Animals were sacrificed 24 hours after the last treatment and plasma, liver, kidney and brain tissues were collected and frozen until analyzed. Concentrations of GSH measured in kidney of controls (196.2 nmol/g) and treated animals (190.5 and 201.9 nmol/g in animals treated with 250 g OTA/kg b.w. and 500 g OTA/kg b.w, respectively) was not statistically significant. Although kidney is the target organ of OTA toxicity, the lack of the effect of OTA treatment on kidney GSH concentration may be explained with the relatively short time of exposure. In liver of animals given 0, 250, 500 g OTA/kg b.w, GSH concentrations were 89.2, 71.5 and 62.4 nmol/g tissue, respectively, and in plasma 11.0, 7.3 and 8.5 µmol/L, respectively. The effect of OTA on plasma GSH concentration is probably the consequence of effect of OTA on liver, the most important detoxifying organ. Contrary to expectations, OTA treatment caused slight increase of GSH in brain tissue of rats. The concentration of MDA, which is the final product of lipid peroxidation, in brain and plasma was significantly higher in OTA- treated animals than in controls, confirming that OTA increases lipid peroxidation.