Abstract:
Cellular response to stress leads to production of heat shock proteins (Hsps) that are protective against various perturbations including stress, infection and inflammation. The liver is a victim to many body disturbances including intoxications and systemic diseases. Stemming on the ability of Hsps to protect an array of perturbations in various body systems, it is justifiable to explore their protective potency to the rat model of carbon tetrachloride (CTC)-induced hepatic toxicity. The current study therefore aimed at testing whether prior induction of Hsp90 could protect the liver against CTC. Rats were exposed to zinc sulphate (ZS) to induce Hsp90 then CTC for 8, 24, 48 or 72 hr. At the end of treatment, rats were sacrificed, autopsied, liver samples taken and fixed in formalin and routinely processed. Sectioned tissues were stained with hematoxylin and eosin or anti-Hsp90 monoclonal antibodies to assess morphological changes and Hsp90 expression respectively. CTC induced damage to the liver that was reduced by ZS. The ZS-mediated reduction of CTC-induced hepatic damage matched with ZS-induced over-expression of Hsp90. It is concluded that over-expression of Hsp90 is beneficial against CTC-induced hepatotoxicity.
