DIETARY COPPER DEFICIENCY REDUCES HEAT-SHOCK PROTEIN EXPRESSION IN CARDIOVASCULAR TISSUES

Dietary copper deficiency impairs cardiovascular function by depressio n of catecholamine metabolism, and alteration of the structure and fun ction of cardiac mitochondria. Heat shock proteins (HSPs) are a group of cellular homeostatic proteins that are induced in vascular tissue b y catecholaminergic transmission after exposure to stress. We investig ated the effects of dietary copper deficiency on the induction and acc umulation of HSPs in several cardiovascular tissues. Stress-induced le vels of aortic HSP70 mRNA were reduced in copper-deficient (CuD) rats when compared with copper-adequate (CuA) controls. Cocaine-induced HSP 70 mRNA accumulation was not different between CuA and CuD rats, sugge sting that reduced HSP70 levels in restrained CuD animals may result f rom altered catecholaminergic neurotransmission. The level of HSP60 mR NA was specifically reduced in the atria of CuD rats, which may be ass ociated with altered mitochondrial structure and function. These resul ts describe a novel relationship between dietary copper deficiency and the expression of highly conserved cellular stress response proteins. Loss of these essential homeostatic proteins in vascular tissue may c ontribute to the impairment of cardiovascular function known to accomp any copper deficiency.