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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #57186
Title: HIGH-DOSE VITAMIN E SUPPLEMENTATION HAS NO EFFECT ON ETHANOL-INDUCED PATHOLOGICAL LIVER INJURY

Author
item SADRZADEH S M H - NEW ENGLAND DEACONESS
item MEYDANI MOHSEN - TUFTS-HNRCA
item KHETTRY U - NEW ENGLAND DEACONESS
item NANJI A A - NEW ENGLAND DEACONESS

Submitted to: Journal of Pharmacology and Experimental Therapeutics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/8/1995
Publication Date: N/A
Citation: N/A

Interpretive Summary: The effect of a dose of vitamin E 100 times higher than the required level on alcohol toxicity in rats was studied. Rats were fed the high vitamin E diet along with 42% of calories as alcohol (the amount equivalent of 3-5 drinks in humans) for 30 days using a stomach tube. Alcohol feeding resulted in liver injury. Rats fed normal diets showed liver injuries where the extent of injury was inversely correlated with the concentration of vitamin E in liver, i.e. liver with a higher level of vitamin E had lower injury. Large doses of vitamin E did not protect the liver of rats from alcohol injury. Moreover, in this group, the higher the level of vitamin E in the liver, the more injury was assessed in the liver injury. Therefore, the large dose of vitamin E not only does not protect against alcoholic liver injury but it also may exacerbate the problem.

Technical Abstract: The effect of alpha-tocopherol supplementation on ethanol-induced liver damage was studied. The intragastric feeding rat model was used in this study. Both normal and alpha-tocopherol supplemented animals (3123 IU/kg body weight) were fed liquid diet and ethanol for one month. In pair-fed animals, ethanol was isocalorically replaced by dextrose. The blood ethanol level in the ethanol-fed groups was between 150-350 mg/dL. Lipid peroxidation was assessed by measuring live thiobarbituric acid reactive substances (TBARS) and conjugated dienes. Liver damage was assessed by light microscopy. Overall chronic ethanol treatment resulted in increase in TBARS and conjugated dienes in both normal (60% and 35%, p<0.01, respectively) and alpha-tocopherol supplemented groups (50% and 47%, p<0.01, respectively). In animals receiving either dextrose or ethanol and regular diet, there was a significant inverse correlation between liver alpha-tocopherol and TBARS (r=0.88, p<0.01) and conjugated dienes (r=-0.75, p<0.05). In contrast, in the vitamin E supplemented rats a significant positive correlation was observed between liver alpha-tocopherol, TBARS (r=0.78, p<0.01) and conjugated dienes (r=0.87, p<0.01). Of major significance is that alpha-tocopherol supplementation had no effect on ethanol-induced pathological changes in the liver. In conclusion, these results show that in the intragastric feeding model, alpha-tocopherol supplementation had no protective effect on ethanol-induced liver damage.