The Effects of High Doses of Vitamin E on Histological Alteration in Liver of Male Pups From Rat

Background and aim: vitamin e is an integral element of the liver's major lipid-soluble plasma lipoproteins and antioxidants. vitamin e is a nutrient that has both antioxidant and non-antioxidant properties. as an antioxidant, it inhibits ldl cholesterol, vitamin e plays an important role in protecting oxidative stress and trapping free radicals in lipid membranes, degrading and enhancing ros-related lipid peroxidation in the plasma membrane it is mutagenic and carcinogenic, it prevents both in vitro and in vivo conditions. and exerts a protective effect against oxidative-related diseases. vitamin e can maintain liver cell morphological stability and cell membrane integrity, and improve necrosis. research has shown that vitamin e can effectively mitochondrial morphology, network. endoplasmic reticulum and restore the activity of antioxidant enzymes (cat, sod and gsh-px). in addition, vitamin e inhibits mitochondrial ros production by enhancing mitochondrial membrane potential and improving mitochondrial function. among the non-antioxidant properties of vitamin e can be the administration of prostacyclin, reducing inflammation and reducing cell adhesion molecules. vitamin e protects cells and subcellular structures from oxidative damage by reducing lpo products. when vitamin e was used alone, hepatic lpo decreased and gsh levels increased. vitamin e as a protection against toxicity increased gsh and tas levels and reduced mda, tos and xo levels compared to control groups. vitamin e can decrease plasma corticosterone in mice exposed to stress. vitamin e can also reduce adipose tissue lipolysis by interfering with the glucocorticoid response, because glucocorticoids stimulate lipolysis. glucocorticoid receptor signal transduction has also been implicated in the expression of irs2, pdk4, angptl4 and ppargc1a genes. vitamin e significantly reduced the settings of ppargc1a, pdk4, irs2 and cpt2 and tended to lower the levels of angptl4 and slc22a5 mrna genes. vitamin e supplements prevent the increase in circulating fatty acids (ffa) and induce inflammation in the liver. vitamin e alters the liver transcriptional response to synthesis and inflammation of fat and cholesterol. camp-dependent pathways of catecholamine are important activators of lipolysis as well as transcriptional regulators of irs2 and ppargc1a. the potential inhibitory effect of vitamin e on camp signaling begins with inhibition of the upstream regulator of creb.considering the above and the usefulness of vitamin e, consuming large amounts of vitamin e may have negative effects.methods: adult male and female wistar rats weighing 220 g were used, divided into six experimental groups, and received oral gavage doses of vitamin e and oil from day zero of gestation until 28 days after birth. they received. and a number of offspring were anesthetized on day 28 after birth and liver was removed for histopathological evaluation and activity of antioxidant enzymes, mda, gpx, sod, catalase assay and stored at -80 ° c. microtomes were cut to about 5 microns in thickness and stained by h&e method and studied by light microscopy (magnification 400). data were analyzed by spss software at the significant level (p≤0.05).results: in this study, significant reductions in mda oxidative enzymes were observed in vitamin e groups compared to the control group (p <0.05).as well as gpx levels, catalase increased significantly compared to controls (p <0.05). and in histopathological studies, the number of hepatic hepatocytes in doses of 400, 800, 1200, and vitamin e increased significantly compared to the control, nave, and oily groups (p <0.05).and relatively little damage was observed at a dose of 1200.conclusion: the study looked at antioxidant enzymes and found that low-dose vitamin e had a positive effect on oxidative stress and decreased free radicals, as well as reducing the toxicity of ros-induced liver cells caused by high doses of vitamin e. it also reduces damage to liver cells, lobules and hepatocytes.