Effect of ethanol and low dietary copper on perinatal and postweanling copper utilization in the rat

Graduation date: 1989The hypotheses of this research were (1) to test if\ud the antagonistic effect of ethanol on liver copper could\ud be seen within a short period when ethanol ingestion,\ud low dietary copper and high metabolic demand represented\ud by either pregnancy plus lactation or rapid growth are\ud simultaneously present and (2) to test if ethanol\ud ingestion would exaggerate a marginal dietary copper\ud status to an obvious copper deficiency.\ud Pregnant rats were fed liquid diets containing\ud either 0.75 (low) or 3.75 (control) mg copper/L with or\ud without 30% of kcal from ethanol throughout gestation\ud and the first 15 days of lactation. Maternal ethanol\ud intake failed to exaggerate a marginal copper status to\ud a copper deficient anemia in both dams and pups as\ud estimated by concentrations of hemoglobin and liver iron\ud and oxidase activity of the copper-metalloenzyme\ud ceruloplasmin. However, maternal ethanol intake did depress maternal liver copper concentration when diet\ud copper was low (interactive effect P<0.05). This effect\ud was specific for liver because other tissue copper\ud concentration was unaffected by ethanol. Although\ud ethanol depressed total pup liver copper concentration\ud regardless of dietary copper level, the interactive\ud effect seen in maternal liver was reflected in copper\ud content of the pup liver metallothionein fraction eluted\ud from a Sephadex G-75 column. At least part of the\ud depressive effect of ethanol on pup liver copper can be\ud explained by elevated pup serum corticosterone (r=-0.61,\ud P