Research Information System
TRACE ELEMENTS AND ELECTROLYTES, vol.32, no.4, pp.211-220, 2015 (SCI-Expanded)
Accumulation of cadmium (Cd) which is a wide spread environmental toxin results in toxicity of tissues. Liver is one of the most affected tissues by Cd exposure. Cd exposure induces inflammation in affected tissues. Galectin-3 is an inflammation related molecule, which takes part in cell survival, apoptosis and migration. The present study focused on the role of proinflammatory levels in Cd toxicity and their relationships with galectin-3 levels. Male Wistar rats were exposed to Cd at the dose of 15 ppm for 8 weeks. Inflammatory status in liver was evaluated by measuring the tissue tumor necrosis factor-alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), and interleukin-8 (IL-8) levels. Liver tissue cytochrome c level was used to identify apoptosis. Hypoxia inducible factor (HIF)-1 alpha a and galectin-3 mRNA expression levels were evaluated by RT-PCR. Tissue galectin-3, TNF-alpha, IL-1 beta, and IL-8 levels were evaluated by ELISA. Liver tissue was evaluated histopathologically. A significant increase in galectin-3 tissue level was observed after Cd toxicity, which was accompanied by a significant increase in liver TNF-alpha, IL-1 beta, and IL-8 levels. Cd toxicity resulted in an increase in the cytochrome c levels. Chronic Cd toxicity induced inflammation and apoptosis in rat livers. Cd toxicity led to an increase in galectin-3 production in liver tissues whereas suppresses HIF-1 alpha mRNA expression. The formation of TNF-alpha and IL-8 at the expense of Cd exposure may likely trigger apoptosis and galectin-3 expression increase.