Date of Award
Joan C. Edwards School of Medicine
Type of Degree
Chronic alcohol abuse is the third leading cause of preventable death in the United States. Ethanol metabolism causes liver injury through alterations in hepatic metabolic state, redox status, and acetaldehyde adduct formations. Increased iron absorption is associated with chronic ethanol consumption and may play a role in ethanol induced oxidative stress. We tested the hypothesis that normal labile iron in the liver plays a role in ethanol related pathological stress, using C57/Bl6 mice pair-fed Lieber-DeCarli liquid ethanol diets for 11 and 22 weeks. Normal iron group mice received 55mg/kg iron as ferric citrate, whereas the low iron groups received 5mg/kg. Our findings indicate that chronic ethanol treatment did not result in discernible differences in oxidant stress from the controls as measured by 4-HNE residue formation and histological analysis of liver sections. Additionally, DNA methylation status was unchanged and there were no differences in glutathione and SAMe indicating no apparent impact on the methionine cycle. Analysis of hepatic proteins ferritin and transferrin receptor by western blot confirmed the expected response to the differences in dietary iron. Global protein acetylation was increased by ethanol treatment and further stimulated in animals fed the low iron diets. Overall, this study has identified novel interactions between iron deficiency and ethanol exposure.
Alcohol - Physiological effect - Research.
Alcoholic liver diseases.
Ethanol - pharmacology.
Thornton, Jesse A., "Role of iron in ethanol derived hepatic stress" (2013). Theses, Dissertations and Capstones. 727.