Vitamins deleterious effects

Nakamura, T. et al., Vitamin C abrogates the deleterious effect of UVB radiation on cutaneous immunity by a mechanism that does not depend on TNF-a, J. Invest. Dermatol. 109, 20-24, 1997. 

Phytic acid, although restricted to a more narrow range of food products, mainly grains, complexes a broader spectrum of minerals than does oxalic acid. Decreased availability of P is probably the most widely recognized result of excessive intakes of phytic acid, yet Ca. Cu, Zn, Fe. and Mn are also complexed and rendered unavailable hy this compound. High intakes of both calcium and vitamin D help to offset ihe deleterious effects of oxalates. 

If vitamins are added to a product to make a nutritional claim, it is critical that shelf-life studies are undertaken to prove that the overages added are sufficient to ensure that the label claims can be met at the end of product shelf life. This is important as none of the vitamins are fully stable in a soft drink environment and some, for instance vitamin C, are very quickly lost in the presence of oxygen. The addition of the fat-soluble vitamins to a soft drink also offers a formulation challenge to ensure that they are fully dispersed and that there are no problems with neck ringing during storage. Trace metals, particularly the transition elements, can also have a deleterious effect on vitamin shelf life, and sometimes metal scavengers, such as EDTA or phosphate salts, are added to improve the shelf life. 

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]. 

There is controversy about whether the long-term use of Cl-hydroxylated vitamin D analogues in non-dialysed patients with chronic renal insufficiency is associated with an impairment of glomerular filtration rate (SEDA-9, 639) (49). Treatment with these drugs should be restricted to patients with severe renal osteodystrophy. A proper dose should be administered in order to avoid a deleterious effect on renal function. Serum calcium and creatinine concentrations should be monitored carefully. The treatment should be withdrawn if hypercalcemia develops. 

Pathological syndromes may result in muscular spasm, as seen in the exertional myopathies, or weakness, as seen in hyperkalemic periodic paralysis (HYPP). Similarly, infectious diseases may result in muscular rigidity (C. tetani infection (tetanus)) or paralysis (C. botulinum intoxication (botulism)). Overt rhabdomyolysis may result from the ingestion of the coccidiostats monensin, rumensin and lasalocid, or one of a number of plant mycotoxins. Dietary deficiencies of selenium or vitamin E have also been described as having severe deleterious effects on skeletal muscle health. 

Balchum et al. (1971) have provided evidence supporting the concept that the peroxidation or ozonization of unsaturated fatty acids in biological membranes is a primary mechanism of the deleterious effects of 03. The hypothesis is based on the tendency of 03 to react with the ethylene groups of unsaturated fatty acids, resulting in the formation of free radicals. The free radicals can, in the presence of molecular oxygen, cause peroxidation of unsaturated fatty acids. In support of this hypothesis is the evidence that after 03 exposure there was a relative decrease in unsaturated fatty acids as compared to saturated fatty acids, and the more unsaturated the fatty acid, the greater the loss. Furthermore, a deficiency of vitamin E increases the toxicity of 03 for the rat (Goldstein et al. 1970). 

Carotenoids are 40-carbon compounds made up of eight isoprene units. Carotenoids serve as light absorbing molecules in photosynthesis and also protect certain tissues from the deleterious effects of light. Beta-carotene is the precursor of vitamin A (which does not occur in plants). Beta-carotene occurs abundantly in the liver oils of fish and is extracted from that matrix commercially. Nutritionists recommend tomatoes, carrots, and green vegetables in daily quantities in order that carotenoids can be converted into vitamin A, a compound necessary for vision and other vital functions. 

Respiratory decline, characteristic of vitamin E-deficient liver tissue during the prenecrotic phase of dietary necrotic liver degeneration, consists of the breakdown of respiration in vitro, after brief, initial periods of normal oxygen consumption. The phenomenon is observed with liver slices and also homogenates, but not with isolated mitochondria from the livers of animals during the latent phase of the disease. Respiratory decline is not related to the rate of peroxide formation in the homogenate. Combination experiments disclosed that miorosomes exert a deleterious effect on the... 

Vitamin E prevents the deleterious effect of polyunsaturated fatty acids on the storage of vitamin A in the liver of rats (Moore, 1939) and chicks (Dam et al., 1952b) and protects essential fatty acids fed in suboptimal amounts to rats (Hove and Harris, 1946). In these cases, as well as in the prevention of ceroid formation, vitamin E apparently functions as an antioxidant. 

Long term experiments involving 13c substitution in mice have been attempted, with Inconclusive results on the possible deleterious effects of the isotope (38). These animals were fed on a diet of performed l c materials derived from laboratory synthesis, together with added vitamins, etc. of isotopically normal content. 

In 1939, Giorgy isolated from liver a vitamin called vitamin H, which prevented the development of the deleterious effects observed after the administration of avidin. After several years, the biochemists succeeded in relating these isolated findings and demonstrating that bios, vitamin R, and vitamin H are all the same compound, the official name of which became biotin. Du Vigneaud established that biotin is the A-cis-hexahydro-2-keto-l H-thieno (3,4) imidazole-4-valeric acid, an optically active monocarboxylic acid. Biotin is found in a bound form in many animal and plant tissues [72]. 

Certain compounds are able to react with free radicals to form a stable compound which is harmless. Vitamin E is especially effective in this respect and its antioxidant activity is promoted by vitamin C, /3-carotene and certain other lipid-soluble antioxidants. On the other hand, iron and copper salts have a deleterious effect. The ability of )8-carotene to scavenge free radical intermediates is not related to its role as provitamin A but depends on the large number of double bonds in the molecule. 

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