RESUMEN
The effect of doxorubicin on glucose metabolism was studied in rats with or without the supplementation of α-tocopherol. Rats were treated with doxorubicin, 2 mg/kg body wt. (intravenously), twice a week, for 6 weeks. α-Tocopherol (400 mg/kg body wt.) was co-administered orally for 2 months. Glycolysis was found to be increased with a significant decrease in the activities of tricarboxylic acid cycle enzymes. A significant increase in liver glycogen was noted in doxorubicin treated rats. Activities of glycogen Phosphorylase, glucose-6-phosphate dehydrogenase and glucose-6-phosphatase were found to be decreased. α-Tocopherol co-administration was found to reduce the alterations in the above mentioned enzyme activities. The results are discussed with reference to the drug metabolism, lipid peroxidation and the antioxidant nature of α-tocopherol.
RESUMEN
The effect of estradiol–17ß and progesterone given separately as well as in combination on the rate of hydrogen peroxide formation and lipid peroxidation in the uteri of ovariectomized rats was studied. Estradiol in 3 μg dose per day per animal elicited maximum stimulatory response and progesterone (100 μg), on the other hand, was without any such effect. However, progesterone given along with estradiol completely prevented the effect due to the latter. In the same way, vitamin E, a well known antioxidant was found to be extremelv effective in protecting the uterus from the highly peroxidative action of estradiol–17ß.
RESUMEN
A study on the effect of retinol in vitro on the hemolysis of vitamin Ε deficient rat red blood cells showed that retinol enhanced the lysis of the Ε deficient cells as compared to the lysis of normal cells. The lipid peroxidation present during hydrogen peroxide induced lysis of Ε deficient cells was however markedly inhibited in the presence of retinol without affecting the rate of lysis. In an actively peroxidising system of non-enzymatic lipid peroxidation of rat liver or brain homogenates and of brain lysosomes incubated with human erythrocytes, no lysis was obtained; incorporation of retinol in such systems resulted in lysis but no peroxidation. Hydrogen peroxide generating substances almost completely inhibited the lysis of normal human erythrocytes by retinol, but linoleic acid hydroperoxide and auto-oxidised liver or brain homogenates and ox-brain liposomes increased the lysis. It is concluded that vitamin Ε deficient erythrocyte hemolysis may be augmented by retinol, an anti-oxidant, having a lytic function without the peroxidation of stromal lipids.