Expression of iron metabolism genes as markers of organ toxicity

Abstract

Aim. An increasing number of toxicants in the environment causes harmful effects on organism, resulting in broad range of metabolic disturbances, including iron metabolism. Perturbations in iron homeostasis may lead to the development of various pathological states, including organ injury and carcinogenesis. In this study, we investigated the effect of liver toxicant, bis-(2-ethylhexyl) phtalete (DEHP), and kidney toxicant, aristolochic acid (AA), on tissue-specific iron metabolism in rats. Methods. Gene expression in the livers and kidneys of Fischer 344 rats was determined by quantitative reverse transcription-PCR. Results. DEHP treatment increased the expression of liver toxicity and DNA damage marker genes, and iron-related genes, Ftl1, Fth1, Slc40a1, and decrease the expression of miR-122 and Hamp in the livers, but not in the kidneys. In contrast, AA increased the expression of kidney toxicity and DNA damage markers, and iron homeostasis genes, Ftl1, Fth1, Slc40a1 in the kidneys. Conclusions. Our results indicate an existence of organ-specific changes in the expression of iron metabolism genes in rats treated with DEHP and AA, respectively. These changes were accompanied by increasing of DNA damage and toxicity markers in the liver of DEHP-treated rats and in the kidneys of rats treated with AA.
 Keywords: toxicity, iron metabolism, liver, kidney.