Vitamin induced” deficiency

Anand et al. 1987). The authors hypothesized that the ocular effects associated with endosulfan may be a result of prolonged hypertension (although no data on blood pressure were presented, and there is no other information to indicate that chronically administered endosulfan induces hypertension) or an endosulfan-induced vitamin A deficiency (which was observed in this study). Although the rabbit may represent a uniquely sensitive species, the possibility that long-term exposure of persons at hazardous waste sites to endosulfan may result in adverse effects on ocular tissues cannot be eliminated. 

Shvedova, A.A. et al. (2007) Vitamin E deficiency enhances pulmonary inflammatory response and oxidative stress induced by single-walled carbon nanotubes in C57BL/6 mice. Toxicology and Applied Pharmacology, 221 (3), 339-348. 

The conducted experiments confirm the h)q5othesis that topically applied vitamin A is taken up fast into deeper cell layers and exerts pharmacological activity on mucous membranes. For the first time, we evidently demonstrated that squamous epithelial changes induced by vitamin A deficiency of OVX-rats are totally reversed in to a fully healthy... 

Chopra, D. P., and Joiakim, A. P. (1991). Differences in lectin binding in squamous metaplasia induced by benzo(a)pyrene and vitamin A deficiency in hamster tracheal explants. 

Pyridoxine is indicated in vitamin B deficiency, for the treatment of some pyridoxine responsive anemia s and for isoniazid-induced neuropathy. It may relieve symptoms of pellagra when niacin fails. Long-term administration of large doses may produce neurotoxicity manifesting itself in progressive peripheral sensory neuropathy. 

VII.a.2.2. Treatment. Treatment of established vitamin D deficiency requires much larger doses of vitamin D, such as calciferol tablets of 1 mg (40,000 units) daily. Newer but more expensive preparations such as alfa-calcidol and calcitriol are very effective, and are particularly valuable in patients with renal failure who are unable to hydroxylate calciferol. Patients treated with pharmacological doses of vitamin D preparations must be monitored by checking serum calcium at regular intervals because of the risk of inducing hypercalcaemia. This should always be suspected if patients develop thirst, nausea or vomiting. The newer hydroxylated preparations have a shorter effective half-life, and therefore problems of overdosage are quicker to resolve once identified. 

Altered vitamin A homeostasis, primarily manifested as decreased hepatic storage of vitamin A, is another established effect of PBBs in animals. Vitamin A is essential for normal growth and cell differentiation, particularly differentiation of epithelial cells, and some PBB-induced epithelial lesions resemble those produced by vitamin A deficiency. Because it is the primary storage site for vitamin A, the liver has a major role in retinol metabolism. Esterification of dietary vitamin A, hydrolysis of stored vitamin A, mobilization and release into the blood of vitamin A bound to retinol-binding protein, and much of the synthesis of retinol-binding protein occurs in the liver. 

Van Vleet JF. 1977. Protection by various nutritional supplements against lesions of selenium-vitamin E deficiency induced in ducklings fed tellurium or silver. Am J Vet Res 38 1393-1398. 

Van Vleet JF. 1982. Amounts of twelve elements required to induce selenium-vitamin E deficiency. Am J Vet Res 43 851-857. 

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. 

Tissue reserves of retinoids in the healthy adult are sufficiently large to require long-term dietary deprivation to induce deficiency. Vitamin A deficiency occurs more commonly in chronic diseases affecting fat absorption, such as biliary tract or pancreatic insufficiency, sprue, Crohn s disease involving the terminal ileum, and portal cirrhosis deficiency may also occur following partial gastrectomy or during extreme, chronic dietary inadequacy. 

Flodstrom S, Busk L, Kronevi T, et al. 1991. Modulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin and phenobarbital-induced promotion of hepatocarcinogenesis in rats by the type of diet and vitamin A deficiency. Fund Appl Toxicol 16 375-391. 

There is little in the literature relative to vitamin A and colon cancer in human populations. Experimental animal studies, however, strongly suggest that vitamin A deficiency may have a role in this type of cancer. We have shown that a deficiency of vitamin A increased DMH-induced tumors and shortened the lag time for induction, compared to normally supplemented controls (72). More recently (73) we have confirmed a protective role for vitamin A in colon carcinogenesis (Table XVII). Furthermore, we have shown (74) that vitamin A deficiency can result in colon tumors in rats given aflatoxin (AFB ) which is normally a liver carcinogen (Table XVIII). The colon tumors associated with the hepatocarcinogen AFB.. appear to be a result of differences in metabolism and binding of AFB or its metabolite ) to colon DNA under conditions of vitamin A deficiency (75). 

Table I summarizes the status of vitamin E and Se in various tissues obtained from rats subjected to altered vitamin E and/or Se nutrition. It is evident from the Table that the animals fed on vitamini E and/or Se-deficient diets showed marked decrease in tissue levels of vitamin E and/or Se respectively. This indicates that the diets employed in these experiments induced desirable deficiency states of vitamin and/or Se. In general, vitamin E levels were affected more in microsomes than in cytosols under vitamin E-deficiency states.

No specific information was located regarding nutritional factors that might influence the absorption or toxicity of DEHP. Because DEHP might exert toxic effects on the testes through depletion of zinc or vitamin E, and both zinc and vitamin E deficiencies are not uncommon in preterm infants due to side effects of parenteral nutrition, depletion of these substances could increase the potential for DEHP-induced testicular toxicity (Chan et al. 1999 Obladen et al. 1998 Roth et al. 1988). DEHP could also exacerbate zinc and vitamin E deficiencies that occur in preterm infants from other causes (FDA 200lh). 

Both p-carotene and vitamin A can inhibit growth in a large range of human cancer cell lines (Krinsky, 1993 Niles, 2000). Several animal studies have shown that vitamin A deficiency promotes the development of spontaneous and chemically-induced tumors, whereas dietary supplementation with vitamin A can prevent chemically-induced tumor development (Niles, 2000). Likewise, p-carotene protects against tumor development in animal models (Krinsky, 1993 Cooper, 2004 Russell, 2004). Nevertheless, P-carotene is preferred for human studies because blood and tissue levels increase in proportion to dietary intake, whereas vitamin A level does not increase in a linear manner because of homeostatic regulation high levels of vitamin A are toxic (Cooper, 2004). 

MPTP toxicity has also been reported to be significantly increased by vitamin E deficiency (Ola). In addition, MPTP induces lipid peroxidation in the substantia nigra in vitamin E-deficient mice (A5) pretreatment with an MAO inhibitor prior to MPTP administration is protective from its parkinsonian-inducing effect (S16). 

The first report of an experimentally-induced deficiency was by Doisy (1) who fed two subjects a formula diet that was deficient in vitamin K. One of the subjects developed a slight reddening of the hair, a scaly, transient dermatitis, depressed vitamin K-dependent clotting factors, and hypocholesterolemia. The symptoms were unresponsive to vitamin K but disappeared when a normal diet was resumed. When Doisey recalculated his purified diet, he realized that he had inadvertently omitted the manganese. The diet had contained a manganese level of only 0.34 mg/day and apparently had produced a manganese deficiency. 

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