Peculiarities of leukotrienes metabolism in vitamin E deficiency in rats

Some changes take place in the spectrum of fatty acid, cholesterol and individual phospholipids' composition in the rat liver, under E-hypovitaminosis, that can play a considerable role in the cell damage. The level of cysteinyl leucotriene decreases in the blood and liver under E-hypovitaminosis and it rises to the control level under vitamin E correction. This demonstrates the influence of tocopherol on 5-LO pathway arachidonic acid.     

Possible interrelationship between gluconeogenesis and ketogenesis in the liver

Effeects of various ketogenic substrates on gluconeogenesis from lactate were examined. D,L-3-Hydroxybutyrate (5 mM) stimulated gluconeogenesis by 41%, the effect being the same as that of 5 mM acetate (49%). No stimulating effect of acetoacetate was observed; conversely, acetoacetate (up to 40 mM) partially or completely abolished the observed stimulating effects of acetate, oleate, and 3-hydroxybutyrate. The results suggest that, in intact liver cells, pyruvate is transported into mitochondria in exchange for acetoacetate and that an interrelationship between gluconeogenesis and ketogenesis at the level of mitochondrial pyruvate carrier may exist in the liver.     

Effect of selenium deficiency and vitamin E deficiency on glutathione metabolism in isolated rat hepatocytes

Selenium deficiency and vitamin E deficiency both affect xenobiotic metabolism and toxicity. In addition, selenium deficiency causes changes in the activity of some glutathione-requiring enzymes. We have studied glutathione metabolism in isolated hepatocytes from selenium-deficient, vitamin E-deficient, and control rats. Cell viability, as measured by trypan blue exclusion, was comparable for all groups during the 5-h incubation. Freshly isolated hepatocytes had the same glutathione concentration regardless of diet group. During the incubation, however, the glutathione concentration in selenium-deficient hepatocytes rose to 1.4 times that in control hepatocytes. The selenium-deficient cells also released twice as much glutathione into the incubation medium as did the control cells. Total glutathione (intracellular plus extracellular) in the incubation flask increased from 47.7 +/- 8.9 to 152 +/- 16.5 nmol/10(6) selenium-deficient cells over 5 h compared with an increase from 46.7 +/- 7.1 to 92.0 +/- 17.4 nmol/10(6) control cells and from 47.7 +/- 11.7 to 79.5 +/- 24.9 nmol/10(6) vitamin E-deficient cells. This overall increase in glutathione concentration suggested that glutathione synthesis was accelerated by selenium deficiency. The activity of gamma-glutamylcysteine synthetase was twice as great in selenium-deficient liver supernatant (105,000 X g) as in vitamin E-deficient or control liver supernatant (105,000 X g). Hemoglobin-free perfused livers were used to determine the form of glutathione released and its route. Selenium-deficient livers released 4 times as much GSH into the caval perfusate as did control livers. Plasma glutathione concentration in selenium-deficient rats was found to be 2-fold that in control rats, suggesting that increased GSH synthesis and release is an in vivo phenomenon associated with selenium deficiency.     

Relationships between biotin and vitamin B12. Effects of biotin and vitamin B12 on folic acid metabolism

1. The effects of dietary biotin compared with vitamin B₁₂ on the total content and on the distribution of the various folate derivatives in the liver of rats given a biotin-free diet have been studied. The effect of both vitamins on the conversion in vitro of folic acid into citrovorum factor in the same experimental conditions was also examined. 2. In biotin-treated rats as well as in vitamin B₁₂-treated rats the total content of folic acid-active substances measured microbiologically by Pediococcus cerevisiae, Streptococcus faecalis and Lactobacillus casei is significantly higher than that in biotin-deficient rats. The liver distribution of various folate derivatives in the three groups of animals is also markedly modified. 3. The amount of citrovorum factor formed in systems with liver homogenate of rats receiving biotin or vitamin B₁₂ is higher than that with liver homogenates of deficient rats. 4. The results obtained demonstrate the influence of biotin in the metabolism of folic acid, and the similar actions at this level of both biotin and vitamin B₁₂. These results are discussed in relation to the participation of the two vitamins in the metabolism of C₁ units, as a biochemical interpretation of the relationships between vitamin B₁₂ and biotin.