Iron exacerbates aniline-associated splenic toxicity

Our earlier studies have shown that aniline exposure in rats causes time- and dose-dependent accumulation of iron in the spleen, which may exacerbate aniline splenotoxicity by catalyzing free-radical reactions. The present studies were conducted to test whether aniline-induced splenic toxicity could be potentiated by iron overload. For 30 d male Sprague-Dawley rats received the following treatments: 0.5 mmol/kg/ d aniline hydrochloride (AH) by gavage (AH group); 3% carbonyl iron-supplemented diet (IR group); 0.5 mmol/kg/d AH by gavage and iron-supplemented diet (AH + IR group); or no treatments (controls). Treatment-related significant increases in total iron, low molecular weight chelatable iron, lipid peroxidation, and protein oxidation were 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 earlier observations, but were more pronounced in the AH + IR group. The increased toxicity, as evident from greater oxidative stress and morphological changes in the AH + IR group, suggests that iron potentiates the splenic toxicity of aniline.