Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: December 1, 2003
Publication Date: March 24, 2004
Citation: Johnson, W.T., Demars, L.C. 2004. Copper deficiency induces heme oxygenase-1 in rat heart and liver [abstract]. The Federation of American Societies for Experimental Biology Journal. 18:A914-A915. Technical Abstract: The induction of HO-1 can be stimulated by a variety of non-heme agents that generate reactive oxygen species (ROS). Copper (Cu) deficiency increases oxidative stress in rats and is known to increase total hepatic HO activity. However, it is not known whether increased hepatic HO activity during copper deficiency represents induction of HO-1 or whether Cu deficiency can induce HO-1 in non-hepatic tissues. Accordingly, HO-1 induction in liver and hearts of rats fed either Cu-deficient (0.3 mg Cu/kg) or Cu-adequate (6 mg Cu/kg) diet was assessed by immunoblotting and real-time PCR. Optical densities (mean±SEM) for hepatic HO-1 determined by scanning densitometry of the Western blots were higher (P<0.05, one-tail t-test) in Cu-deficient rats (0.17±0.02, N=12) compared to control rats (0.11±0.02, N=12). HO-1 mRNA was also elevated 3-fold in livers of Cu-deficient rats (P<0.05, one-tail t-test). Optical densities for cardiac HO-1 also were higher (P<0.05, one-tail t-test) in Cu-deficient rats (0.10±0.01, N=12) compared to control rats (0.05±0.005, N=12) and HO-1 mRNA was elevated 2-fold (P<0.05, one-tail t-test) in hearts of Cu-deficient rats. Elevation of HO-1 protein and mRNA in liver and heart indicates that induction of HO-1 by Cu-deficiency is not limited to liver and suggests that oxidative stress in liver and heart is sufficient to induce stress proteins such as HO-1.