Iron exacerbates aniline-associated splenic toxicity

Our earlier studies have shown that aniline exposure in rats causes time- a nd dose-dependent accumulation of iron in the spleen, which may exacerbate aniline splenotoxicity by catalyzing free-radical reactions. The present st udies were conducted to test whether aniline-induced splenic toxicity could be potentiated by iron overload. For 30 d male Sprague-Dawley rats receive d the following treatments: 0.5 mmol/kg/d aniline hydrochloride (AH) by gav age (AH group); 3% carbonyl iron-supplemented diet (IR group); 0.5 mmol/kg/ d AH by gavage and iron-supplemented diet (AN + IR group); or no treatments (controls). Treatment-related significant increases in total iron, low mol ecular weight chelatable iron, lipid peroxidation, and protein oxidation we re observed in the spleens of all the groups compared to control. However, these changes were much greater in the combined AH + IR group. The aniline- induced morphological changes in the spleen were consistent with our earlie r observations, but were more pronounced in the AH + IR group. The increase d toxicity, as evident from greater oxidative stress and morphological chan ges in the AH + IR group, suggests that iron potentiates the splenic toxici ty of aniline.