Accumulation of the wide spread environmental toxin cadmium in tissues results in toxicity. Cadmium (Cd) exposure induces inflammation and apoptosis in the effected tissues. Midkine (MK) is a heparin-binding growth factor. Its expression is induced in tissues as a result of stress. After cadmium toxicity, MK expression is increased in liver cells. The present study was focused to evaluate the MK expression differences in liver, kidney and heart in a chronic Cd toxicity model and their relationships between tissue damage stage relevance and apoptosis.

Male Wistar rats were exposed to Cd at the dose of 15 ppm for 8 weeks. MK levels were measured in kidney, heart and liver tissue. The relationship between tissue midkine levels and apoptosis was evaluated with tissue caspase-3 levels. Tissue MK levels were measured by ELISA and confirmed by MK mRNA expressions. Highest Cd level was in the liver. A significant increase in caspase-3 tissue levels was seen after Cd toxicity, this was accompanied with a significant increase in the MK mRNA expressions. Tissue midkine levels were significantly increased in Cd group. Apoptosis was more prominent in liver tissues than kidney and heart. MK levels increased 3, 1.7, 1.3X folds in liver, kidney and heart respectively.

Chronic Cd administration induces inflammation and apoptosis in rat liver, kidney and hearts. MK might be important for the internal tissue prevention mechanisms against Cd toxicity.