Vitamin oxygen radical formation

Ellis et al. [72] recently studied the effects of short- and long-term vitamin C therapy in the patients with chronic heart failure (CHF). It was found that oxygen radical production and TBAR product formation were higher in patients with CHF than in control subjects. Both short-term (intravenous) and long-term (oral) vitamin C therapy exhibited favorable effects on the parameters of oxidative stress in patients the treatments decreased oxygen radical formation and the level of lipid peroxidation and improved flow-mediated dilation in brachial artery. However, there was no correlation between changes in endothelial function and oxidative stress. 

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. 

Fig. 4. Mechanism of lipid peroxidation and its inhibition by vitamin E. Lipid peroxidation is initiated by generating a relatively nnreactive carbon-centered radical upon hydrogen abstraction by a hydroxyl radical (1). The fast formation (2) of the more reactive peroxyl radicals (ROO) ensures rapid attack of any peroxidizable substrate either by abstraction of a hydrogen atom (3a) or addition to a double bond (3b). The propagation is teiminated by mutual elimination of peroxyl radicals (4) or by suppression of free-radical formation in the presence of a-tocopherol (a-TOH) (5a). The tocopheryl radical is believed to be neutralized by ascorbic acid (AscAH) (5b) and radical oxygen, and a-tocopherol then re-enters the inhibition cycle.

Ascorbic acid—vitamin C—is an essential nutrient that the human body cannot manufacture from other compounds. It is needed for the formation of collagen, the protein that makes up connective tissue, and is essential to muscles, bones, cartilage, and blood vessels. It is a strong antioxidant, preventing damage from oxygen free radicals. 

It is possible that steric factors prevent the formation of the bridging peroxide species in the case of vitamin Bj2,. (55), however, other cases have been reported (59) in which oxygenation proceeds no further than the formation of mononuclear peroxo radicals (i.e. first stage above). 

In vitro studies have shown that homocysteine can undergo autoxidation, leading to the formation of oxygen free radicals (30-32). Homocysteine is involved in oxidative modification of low-density lipoprotein in vitro (33). Increased lipid peroxidation in humans with hyperhomocysteinemia has been reported (34,35). However, vitamin supplementation that resulted in substantial reduction of tHcy concentrations did not normalize either the homocysteine redox status or the increased lipid peroxidation in CAD patients (35,36). 

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