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Vitamin allergic response

Populations that are unusually susceptible to toxic effects of silver exposure are those that have a dietary deficiency of vitamin E or selenium, or that may have a genetically based deficiency in the metabolism of these essential nutrients. Individuals with damaged livers may also be more susceptible to the effects of silver exposure. In addition, populations with high exposures to selenium may be more likely to develop argyria. Furthermore, some individuals may exhibit an allergic response to silver. [Pg.64]

Vitamin B12 is virtually nontoxic, even at high oral or injected doses excessive amounts are rapidly excreted. However, occasionally allergic responses to injected vitamin B12 occur (Fisher 1973), and adverse reactions to the combined administration of large injected doses of vitamin B12 and of oral vitamin C have been reported (Schrauzer 1979). Vitamin B12 is required for methionine biosynthesis and functions in conjunction with folic acid as the intermediate carrier of the methyl group. In its coenzyme form (5 -deoxyadenosylcobala-min), it is required for the conversion of methylmalonyl-CoA to succinyl-CoA. (Friedrich 1987). Bacteria utilize vitamin Bjj or its coenzyme in certain dehydrases, deaminases, and in methane biosynthesis. [Pg.832]

In the body, the ester link of procaine is hydrolyzed, yielding p-aminobenzoic acid (PABA) and N,h/-diethyl-aminoethanol (DEAE), an analog of DMAE. It is PABA (Figure 3.11) that is responsible for the large majority of allergic reactions to procaine it is excreted rapidly by the kidneys. PABA is most often used as a sunscreen, but is sometimes called vitamin B-x , although it is not essential for humans and the body cannot synthesize folate from PABA. According to some authors, the Aslan method relies solely on the combined action of PABA and DEAE/DMAE. It is assumed that the action of PABA is due to its anti-free-radical properties. [Pg.20]

Liden S (1975) Alphosyl sensitivity and propyl gallate. Contact Dermatitis 1 257-258 Liden S, Goransson K (1975) Contact allergy to dibenzthion. Contact Dermatitis 1 258 Lindgren S, Groth O, Molin L (1976) Allergic contact response to vitamin A acid. Contact Dermatitis 2 212-217... [Pg.372]

As outlined by de Weck (1971) in one of his basic contributions to our understanding of drug reactions, the ability of a simple chemical to induce an immune response, and consequently allergic reactions, rests on its ability to form those macromolecular conjugates in vivo or on the presence in the final pharmaceutical preparation of substances with chemical reactivity towards body constituents. For this to occur, it is either necessary that the vitamins possess some intrinsic chemical reactivity, contain some reactive decomposition product or byproduct, or that a reactive species is metabolically created in vivo (the reactive metabolite). [Pg.664]

Lindgren S, Groth O, Molin L (1976) Allergic contact response to vitamin A acid. Contact Dermatitis 2 212-217... [Pg.687]

Bucca, C., Rolla, G., Oliva, A., and Farina, J. C., 1990, Effect of vitamin C on histamine bronchial responsiveness of patients with allergic rhinitis, Ann. Allergy 65 311-314. [Pg.207]


See other pages where Vitamin allergic response is mentioned: [Pg.2714]    [Pg.2714]    [Pg.246]    [Pg.449]    [Pg.272]    [Pg.657]    [Pg.665]    [Pg.368]    [Pg.303]    [Pg.74]    [Pg.123]    [Pg.48]    [Pg.1843]    [Pg.50]    [Pg.254]    [Pg.255]    [Pg.666]    [Pg.667]    [Pg.674]    [Pg.684]    [Pg.224]    [Pg.24]    [Pg.182]    [Pg.3]   
See also in sourсe #XX -- [ Pg.832 ]




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Allergic response

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