Vitamin E in rats

Turan, B., Hotomaroglu, O., Kilic, M., and Demirel-Yilmaz, E. 1999. Cardiac dysfunction induced by low and high diet antioxidant levels. Comparing selenium and vitamin E in rats. Regul. Pharmacol. Toxicol. 29 142-150. 

Gupta, R.C., Milatovic, D., Zivin, M., Dettbam, W-D. (2000a). Seizure-induced changes in energy metabolites and effects of V-tert-butyl-alpha-phenylnitrone (PBN) and vitamin E in rats. Eur. J. Physiol. 440 R160-2. 

Ross WM, Creighton MO, Inch WR, et al. 1983. Radiation cataract formation diminished by vitamin E in rat lenses in vitro. Exp Eye Res 36 645-653. 

Burton, G.W., Ingold, K.U., Foster, D.O., Cheng, S.C., Webb, A., Hughes, L. and Lusztyk, E. (1988) Comparison of free a-tocopherol and a-tocopheryl acetate as sources of vitamin E in rats and humans. Lipids 23, 834-840. 

Ramirez-Tortosa, C. et al., Anthocyanin-rich extract decreases indices of lipid peroxidation and DNA damage in vitamin E-depleted rats. Free Radic. Biol. Med., 31, 1033, 2001. 

Repeated periods of exercise reduce the likelihood of damage to skeletal muscle during subsequent bouts of the same form of exercise and this appears to be associated with an increase in the activity of muscle SOD (Higuchi et al. 1985), a reduced level of lipid peroxidation products during exercise in trained rats (Alessio and Goldfarb, 1988), and a modification of the concentration of antioxidants and activity of antioxidant enzymes in trained humans (Robertson etal., 1991). Packer and colleagues (Quintanilha etui., 1983 Packer, 1984) have also examined the exercise endurance of animals of modified antioxidant capacity and found that vitamin E-deficient rats have a reduced endurance capacity, while Amelink (1990) has reported that vitamin E-deficient rats have an increased amount of injury following treadmill exercise. 

Sakamoto, W., Fujie, K., Handa, H., Ogihara, T. and Mino, M. (1990). In vivo inhibition of superoxide production and protein kinase C activity in macrophages from vitamin E-treated rats. Intemat. J. Vit. Nutr. Res. 60, 338-342. 

The efficiency of vitamin E in the suppression of free radical-mediated damage induced by iron overload has been studied in animals and humans. Galleano and Puntarulo [46] showed that iron overload increased lipid and protein peroxidation in rat liver. Vitamin E supplementation successfully suppressed these effects and led to an increase in a-tocopherol, ubiquinone-9, and ubiquinone-10 contents in liver. Important results were obtained by Roob et al. [47] who found that vitamin E supplementation attenuated lipid peroxidation (measured as plasma MDA and plasma lipid peroxides) in patients on hemodialysis after receiving iron hydroxide sucrose complex intravenously during hemodialysis session. These findings support the proposal that iron overload enhances free radical-mediated damage in humans. 

Increased succinate-dependent lung mitochondrial oxygen consumption in rats on diet relatively low in vitamin E no significant effect in vitamin E-replete rats at this concentration of ozone... 

The presence of dietary carnosine in vitamin E-deficient rats was found to increase mammary tumor latency, while not affecting tumor incidence (Boissoneault et ah, 1998). Another beneficial effect of carnosine in relation to cancer has recently been reported carnosine was shown to inhibit metastasis of hepatocarcinoma SK-Hep-1 cells (Chung and Hu, 2008). Unlike the effects reported above, carnosine did not affect the viability of these cells but instead the dipeptide inhibited cell migration and invasion. The mechanism responsible apparently involves a decrease... 

Traber, M. G., Kayden, H. ]., Green, J. B., and Green, M. H. (1986). Absorption of water-misdble forms of vitamin E in a patient with cholestasis and in thoracic duct-cannula ted rats. Am.. Clin. Nutr. 44, 914—923. 

To some extent the vitamin E requirement may be lessened by the presence in the diet of synthetic antioxidants and by selenium. Much evidence supports a relationship between the nutritional need for selenium and that for vitamin E. Lack of either causes muscular dystrophy in many animals as well as severe edema (exudative diathesis) in chicks. Since vitamin E-deficient rats have a low selenide (Se2 ) content, it has been suggested that vitamin E protects reduced selenium from oxidation.) Vitamin C (ascorbic acid), in turn, protects vitamin E. 

Grasso P, Abraham R, Hendy R, et al. 1969. The role of dietary silver in the production of liver necrosis in vitamin E-deficient rats. Exp Mol Pathol 11 186-199. 

Shaver SL, Mason KE. 1951. Impaired tolerance to silver in vitamin E deficient rats. Anat Rec 109 382. 

Plasma malondialdehyde-like material, an indicator of lipid peroxidation, is increased in conditions of ischaemia, such as stroke [83, 84] and myocardial infarction [85]. Mitochondria extracted from hearts of vitamin-E-deficient rabbits showed a decreased mitochondrial function and an increased formation of oxygen radicals associated with a reduced superoxide dismutase activity. This was partially reversed by addition of vitamin E in vitro [86]. Measurement of in vitro susceptibility to lipid peroxidation in cardiac muscle from vitamin-E-deficient mice showed a highly significant negative correlation between the concentration of vitamin E and in vitro lipid peroxidation. The results indicate that short-term vitamin E deficiency may expose cardiac muscle to peroxidation injuries [ 87 ]. In rats, treatment for 2 days with isoprenaline increased lipid peroxide activity, as measured by malondialdehyde levels, in the myocardium. Vitamin-E-deficient animals were even more sensitive to this effect, and pretreatment with a-tocopheryl acetate for 2 weeks prevented the effect induced by isoprenaline. The authors [88] propose that free-radical-mediated increases in lipid peroxide activity may have a role in catecholamine-induced heart disease. 

Further evidence for the involvement of vitamin E in arachidonic acid metabolism comes from work by Valentovic, Gairola and Lubawy [146], who showed that vitamin E deficiency in rats increased hepatic lipid peroxidation and decreased aortic PGI2 synthesis. Inhalation of cigarette smoke by the rats increased platelet TXA2 by over 90% and reduced aortic PGI2 by between 26-33%. However, these effects were independent of the presence of vitamin E in the diet. 

Hyperoxia was found to encourage the accumulation of primary and end-products of lipid peroxidation together with a significant lowering of the vitamin E content of rat brain tissue [152]. The consequence of hyperoxia was epileptiform seizures, which were prevented by vitamin E or synthetic antioxidant pre-injection. Other workers [153] have found that protection against hyperoxia is directly related to the level of vitamin E or selenium supplementation. However, some [ 154] have indicated no beneficial effects for vitamin E in reducing oxygen toxicity. 

The vitamin has been shown to be able to protect animals from the lethal effects of anoxia and hypoxia. Rats [189] and rabbits [190] fed on vitamin-E-supple-mented diets survived longer in hypoxia than non-supplemented animals. A similar protective effect has been demonstrated in vitro with cardiac muscle [ 167]. In hypoxic Langendorff-perfused rabbit heart, the presence of vitamin E protected the muscle from the deleterious effects of hypoxia, possibly by improving mitochondrial function [168]. However, in clinical studies, the use of vitamin E in ischaemic heart disease has met with little success [191, 192], although the results have been controversial [193]. 

The functional interrelationship between vitamin C and vitamin E has been known for a number of years (LL). While dietary vitamin E appears to play a role in determining the levels of vitamin C in the plasma and lungs of cigarette smoked rats, the levels of vitamin E in plasma were not significantly altered by the smoke exposure (31). 

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