Antibody pyridoxine

CNS toxicity occurs because isoniazid has structural similarities to pyridoxine (vitamin Be) and can inhibit its actions. This toxicity is dose-related and more common in slow acetylators. Manifestations include peripheral neuropathy, optic neuritis, ataxia, psychosis and seizures. The administration of pyridoxine to patients receiving INH does not interfere with the tuberculostatic action of INH but it prevents and can even reverse neuritis. Hematological effects include anaemia which is also responsive to pyridoxine. In some 20% of patients antinuclear antibodies can be detected but only in a minority of these patients drug-induced lupus erythematosus becomes manifest. 

Frisoni GB, De Leo D, Rozzini R, et al Psychic correlates of sleep symptoms in the elderly. Int J Geriatr Psychiatry 7 891-898, 1992 Fritschy J, Benke D, Mertens S, et al 5 types of type A GABA receptors identified in neurons by double and triple immunofluorescence staining with subunit specific antibodies. Proc Natl Acad Sci USA 89 6726-6730, 1992 Frye CA, Duncan JE Progesterone metabolites effective at the GABAa receptor complex attenuate pain sensitivity in rats. Brain Res 643 194-203, 1994 Erye CA, Cuevas CA, Crystal S, et al Diet and estrous cycle influence pain sensitivity in rats. Pharmacol Biochem Behav 45 255-260, 1993 Erye PE, Arnold LE Persistent amphetamine-induced compulsive rituals response to pyridoxine (B6). Biol Psychiatry 16 583-587, 1981... 

Deficiency of vitamin B6 (pyridoxine) causes gradual disappearance of the lymphatic system, depressed number of B lymphocytes in peripheral blood, and impaired activity of antibodies and IL-2 (Szponar and Respondek 1998) (Table 2.2.4). Vitamin D3 can produce an immunosupressive effect. The recent literature data suggest that one of metabolites of this vitamin, 1,2,5-dihydroxy D3, by affecting a specific receptor present on monocytes and lymphocytes, can inhibit their proliferation. This effect occurs via retardation of the production of mRNA for GM CSF, IL-2, and IFN-7. At the same time, it has been demonstrated that deficiency of vitamin D3 in food caused impaired cellular-type tolerance (Szponar and Respondek 1998). 

Table I summarizes the effects of the various deficiencies of the vitamin B complex upon the response to a variety of antigenic stimuli in different test animals. It is the reviewers opinion that, with the exception of the criticisms already made, this table represents the results of well-controlled, adequate experiments. It is quite apparent that the individual members of the vitamin B complex play a very important role in determining antibody response. Their absence may produce a marked impairment in antibody production. Generalizations on this subject are dangerous, but it would appear that pyridoxine, pantothenic acid, and folic acid deficiencies show the most consistent deleterious effects upon antibody production. It is also apparent that the effects of the individual deficiencies may vary widely depending upon the antigen employed.

There is considerable basis for linking pyridoxine to amino acid metabolism, and the participation of this vitamin in antibody production may be related to such a function. However, in a recent review, Beaton et al. (1954) suggest that pyridoxine is not essential for protein synthesis or maintenance in the rat and that its effect on amino acid metabolism is of a secondary nature. A role for pantothenic acid in protein synthesis has not yet been demonstrated. A relationship between pantothenic acid and peptide bond formation is suggested by the observation of Chantrenne (1944) that coenzyme A, the coenzyme derivative of pantothenic acid, is... 

The possible functions of pantothenic acid, pyridoxine, or folic acid in the mechanisms involved in the release of antibody from their sites of formation were further investigated as follows (Ludovici et al., 1951b). Rats were immunized with human erythrocytes while on the deficient diets and their initial titers determined. Four days later the animals were injected intraperitoneally with the respective vitamin and maintained on an adequate control diet for the remainder of the experiment. Antibody titers were determined periodically thereafter. The effect of the... 

Figure 1. Effect of Repeated Antigenic Stimuli upon Antibody Response in Pyridoxine-deficient and Control Rats. Injections of Diphtheria Toxoid Given at Times Indicated by the Arrows. Animals were Fed the Pyridoxine-deficient or the Control Diet during the Entire Course of the Study, and were on Experiment for Four Weeks Prior to the First Toxoid Injection, Figures on the Ordinate Represent Reciprocal Titers. Used by Permission, from Axelrod (1958), Copyright by the American Society for Clinical Nutrition, Inc,...

Effect of Pyridoxine-deficiency upon Circulating Antibody Response to Alum-precipated Diphtheria Toxoid ... 

The development of a method suitable for the study of antibody synthesis by individual cells has facilitated investigations of antibody synthesis at the cellular level (Jerne and Nordin, 1963). With this procedure, we have demonstrated a dramatic reduction in the number of antibody-forming cells in the spleens of pyridoxine-deficient rats immunized with sheep erythrocytes (Figure 6) (Kumar and Axelrod, 1968). This decreased cellular immune response was independent of the inanition associated with the deficiency and was... 

Studies on the mechanism of action of pantothenic acid at the cellular level were conducted similarly to those described for pyridoxine deficiency and can be summarized as follows (Lederer et al., 1975) 1) a marked reduction in splenic antibody-forming... 

Investigations on the mode of action of pyridoxine and pantothenic acid have demonstrated a marked reduction in the production of antibody-forming cells following antigenic stimulation in both deficiency states. The metabolism of antigen appeared to be normal. However, these two vitamins seem to function at different loci in the development of the immune process. Whereas pyridoxine appears to be necessary for the production of units from serine... 

Axelrod, A. E, and Hopper, S. (1960) Effects of pantothenic acid, pyridoxine and thiamine deficiencies upon antibody formation to influenza virus PR-8 in rats, J. Nutr., 72 325. 

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