Effect of aflatoxins on oxidative phosphorylation by rat liver mitochondria.

The in vitro effect of aflatoxins M1, B1 and G1 on oxidative phosphorylation by rat liver mitochondria with succinate as substrate has been studied. All these toxins inhibit the electron transport chain at a 1-10-4 M concentration and the site of inhibition is between cytochrome b and cytochrome c or c1. Aflatoxin M1 (AFM1) uncouples oxidative phosphorylation at a concentration of 1-10-6 M and reduces the ADP:O ratio, whereas aflatoxin B1 (AFB1) at 1-10-6 M concentration uncouples oxidative phosphorulation but does not affect the ADP:O ratio. At a concentration of 1-10-5 M, AFB1 also decreases the ADP:O ratio along with the uncoupling of oxidative phosphorylation. Aflatoxin G1 (AFG1) acts as an uncoupler at a relatively higher concentration of 1-10-4 M. Preincubation of mitochondria with these aflatoxins resulted in inhibition of respiration and uncoupling of rat liver mitochondria.

Effect of dietary protein and hypervitaminosis A or C on tissue peroxidation and erythrocyte lysis of vitamin E deficiency.

Rats were maintained on a vitamin E free diet containing 20% safflower oil for a period of 12 weeks at two dietary protein levels, 20% and 10% casein. Enhanced in vitro tissue lipid peroxidation and lysis of erythrocytes were noticed at both the protein levels. A reduction in body mass and tissue weights were observed in both the protein groups but more so at 20% protein level. Feeding of retinyl palmitate (100 000 IU/100 g body weight) for 4 consecutive days to -E rats inhibited liver and kidney in vitro lipid peroxidation. Ascorbic acid (150 mg/100 g body weight) given orally for 5 days to -E rats inhibited liver brain and kidney in vitro peroxidation. Lysis of erythrocytes from -E rats was further increased by dosing with both the vitamins "A" and "C", the latter being more effective. The stromal enzymes acetyl choline esterase and ATPase were lowered, following the hemolysis profile of the erythrocytes from the different groups. Glutathione content of erythrocytes were unaffected except in -E +C group. In all groups the higher protein level (20%) produced greater lysis as compared to 10% level. It is concluded that 20% protein is more injurious in vitamin E deficiency simultaneously made hypervitaminosis A or C.

Effect of dietary coconut oil and casein and megadoses of vitamin A or C on tissue lipid peroxidation and hemolysis in vitamin E deficiency.

Male rats fed on pellet diet to an average weight of 105 g were placed on a vitamin E deficient diet containing 20% coconut oil for a period of 12 weeks at two dietary protein levels, 20% and 10% casein. Rats on 20% casein diet showed a definite weight loss but not so at the 10% casein level. A marked increase in the liver in vitro lipid peroxidation was observed at both protein levels. Feeding of retinyl palmitate at 100,000 IU/100 g body weight for 4 consecutive days inhibited the liver, brain and kidney in vitro peroxidation; megadoses of ascorbic acid produced less inhibition of the liver peroxidation, but the same degree of inhibition for brain and kidney peroxidation as in vitamin A loaded rats. Both dietary palmitate or ascorbic acid. Acetylcholine esterase and ATPase, two of the membrane enzymes of erythrocytes, were depressed in all the groups. The glutathione content of erythrocytes was increased in rats given ascorbic acid. In all the groups the higher dietary protein levels produced greater loss of body and tissue weights. It is concluded vitamin E deficient diet supplemented with dietary coconut oil (saturated fat) induces increased in vitro lipid peroxidation and oxidative lysis of erythrocytes and that megadoses of vitamin A or C suppress the in vitro lipid peroxidation but enhance the lysis.

Pathways of carbohydrate metabolism in mycobacterium tuberculosis H37Rv1.

Radiorespirometric studies using glucose labelled at 1, 2, 3-4, and 6 positions and enzymatic studies were conducted to determine the primary pathways of glucose dissimilation in Mycobacterium tuberculosis H37Rv. The pattern of 14CO2 recovery was C3-4 greater than C1 greater than C6 = C2. The Embden-Meyerhof pathway was found to be the predominant pathway for glucose oxidation, operative to the extent of 94%. The pentose phosphate pathway accounted for the remaining 6%. Maximum incorporation of 14C into cellular components was from C2 and C6 labelled glucose.