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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #37397
Title: EFFECT OF CHRONIC ETHANOL FEEDING ON PLASMA AND LIVER ALPHA-AND GAMMA- TOCOPHEROL LEVELS IN NORMAL AND VITAMIN E-DEFICIENT RATS. RELATIONSHIP TO LIPID PERIOXIDATION

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

Submitted to: Biochemical Pharmacology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/18/1994
Publication Date: N/A
Citation: N/A

Interpretive Summary: Vitamin E deficiency is associated with liver injury in response to alcohol intake. To determine the effect of alcohol on blood and liver levels of 2 vitamin E compounds, alpha- and gamma-tocopherol, we fed normal and vitamin E-deficient rats a liquid diet and alcohol for one month. In normal rats, the decrease in the tocopherols in liver was greater than the concomitant decrease in blood levels with gamma-tocopherol suffering greater decreases in both blood and liver. In vitamin E-deficient rats, alcohol had no effect on the tocopherols in blood but significantly decreased liver concentrations suggesting that in both groups of rats, the liver tocopher- ols are utilized to defend against stress and damage from alcohol. We have shown that vitamin E-deficient animals are more susceptible to alcohol- induced liver damage compared to those of normal rats. We also showed an inverse correlation between the levels of certain toxins in the liver and alpha- and gamma-tocopherol. Therefore it seems logical to assume that alcohol consumption in vitamin E-deficient animals is associated with greater severity of liver injury.

Technical Abstract: The effect of chronic ethanol intake on alpha- (a) and gamma- (g) tocopherol levels in serum and liver in rats was studied. Normal and vitamin E- (E) deficient animals were fed a liquid diet and ethanol for 1 mo. In pair-fed animals, dextrose was isocalorically replaced by ethanol. Blood ethanol level was between 150 and 250 mg/dl. Liver peroxidation was measured as thiobarbituric acid reactive substances (TBARS). Plasma alanine amino transferase (ALT) was increased by 3-fold in E-deficient rats compared to normal rats. Plasma a- and g-tocopherol were decreased in normal rats by 23.3% and 65%, respectively, (p<0.01). Liver a- and g-tocopherol were also decreased by 51.7% and 76%, respectively (p<0.01). E-deficient animals had significantly lower mean plasma a-tocopherol (5,670 vs. 530 ng/ml, p<0.01) and ethanol feeding did not further decrease the levels. The liver a- and g-tocopherol were decreased by 58.8% and 56.5% (p<0.01) respectively, beyond the already low levels of this group. There was an inverse correlation between liver TBARS and liver a-tocopherol (r=-0.59, p<0.05) and g-tocopherol (r=-0.65, p<0.02). Ethanol feeding decreased the plasma and liver g-tocopherol more than a-tocopherol in both normal and E-deficient animals. Ethanol feeding, while markedly decreasing both a- and g-tocopherol in livers of normal and E-deficient rats, only decreases plasma levels of tocopherols in normal rats. The higher ALT in E-deficient animals and inverse correlation between TBARS and a- and g-tocopherol suggest that enhanced lipid peroxidation is associated with greater severity of liver injury induced by ethanol in E-deficient rats.