Author
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Saari, Jack |
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Dahlen, Gwen |
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Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only Publication Acceptance Date: 4/18/1998 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Severe dietary copper (Cu) deficiency causes anemia, the rapid development of which suggests hemolysis. Because of reduced activity of Cu-dependent superoxide dismutase, hemolysis by peroxidation has been suggested. However, another possible candidate is erythrocyte nitric oxide (NO), which could, by itself or via conversion to peroxynitrite, cause membrane damage and hemolysis. Forty-two rats were fed a Cu-adequate (6 ug Cu/g diet) or a Cu-deficient diet (<0.5 ug Cu/g diet) and water alone or water that contained the NO precursor L-arginine (7.5 g/L) or the NO synthase inhibitor L-NAME (0.7 g/L). After 5 wks, rats fed Cu-deficient diet and water alone had a reduced liver Cu concentration and anemia (p<0.05). Urine nitrate/nitrite (NOX), an index of NO production, was elevated by Cu deficiency (p<0.05). No effect of arginine feeding was found. L-NAME treatment inhibited NO production and anemia (p<0.05). We conclude that increased NO production may contribute to Cu-deficiency-induced anemia. Dietary Cu-ad Cu-ad+ Cu-ad+ Cu-def Cu-def+ Cu-def+ Group Arginine L-NAME Arginine L-NAME Liver Cu, 12.2+/-1.1 12.8+/-1.3 13.9+/-2.0 1.1+/-0.2 1.7+/-0.7 2.3+/-1.6 ug/g Hct,% 41+/-1 42+/-1 41+/-3 27+/-5 29+/-5 36+/-8 Urine NOX, 3.0+/-2.7 2.5+/-3.0 0.5+/-0.5 5.6+/-2.2 5.6+/-2.9 0.5+/-0.7 umol/day |
