Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study has been done to determine the effect of vitamin E deficiency on the functions of splenic lymphocytes and alveolar macrophages (AM) in rats. Vitamin E deficiency did not cause any changes of body weight, spleen and thymus weights, and numbers of splenocytes and AM compared with those of control rats. And also, we could not find any significant changes of lymphocyte responses to mitogens (PHA, Con A, and LPS) and natural killer cell (NK) activity except for AM function in vitamin E-deficient rats. In vitamin E-deficient rats, AM showed a higher phagocytosis than that of control rats. After in vitro treatment with a macrophage-activating factor (MAF) for 4 h at 37 degrees C, AM from control rats showed a greater enhancement (167%) of phagocytic activity compared with that of AM from vitamin E-deficient rats. When the effect of MAF prepared from splenic lymphocytes of rats from control or vitamin E-deficient rats on phagocytosis of AM was studied, MAF from control rats showed an about 150% increase of phagocytic activity in a 1/250 dilution of MAF. However, MAF from vitamin E-deficient group had almost no effect on phagocytosis of AM in the same dilution of MAF as control rats. These results may suggest that vitamin E deficiency induces the higher phagocytic function of AM responsible for host defense in the lung, but their enhancement is not due to the activation by MAF from lymphocytes.
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PMID:Effects of vitamin E deficiency on the functions of splenic lymphocytes and alveolar macrophages. 269 18

Feeding a vitamin E-deficient diet increases pathology in hearts of mice infected with a myocarditic coxsackievirus B3 (CVB3/20). Hearts from infected mice fed a vitamin E-deficient diet rich in highly unsaturated fat (menhaden oil) exhibited more severe pathology than hearts from infected mice fed a vitamin E-deficient diet based largely on saturated fat (lard). Furthermore, a cloned and sequenced amyocarditic coxsackievirus B3 (CVB3/0), which caused little or no pathology in the hearts of vitamin E-supplemented mice, induced extensive cardiac pathology in vitamin E-deficient mice. In infected mice, both mitogen and antigen responses were depressed by vitamin E deficiency, although neutralizing antibody responses were unaffected. Natural killer cell responses were comparable in infected mice fed a lard-based diet with or without supplemented vitamin E. However, a menhaden oil-based diet, whether supplemented with vitamin E or not, significantly depressed natural killer cell activity in infected mice compared with mice fed the lard-based diet. Coxsackievirus B3/0 recovered from the heart of a vitamin E-deficient donor mouse, passaged one time onto HeLa cells, caused significant heart damage when passed back into vitamin E-supplemented recipient mice, demonstrating that the amyocarditic CVB3/0 had changed to a virulent phenotype. Enhanced virulence was also seen with CVB3/20 virus similarly passaged in a vitamin E-deficient donor. Our work demonstrates the important role of host nutritional antioxidant status in determining the severity of certain viral infections.
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PMID:Vitamin E deficiency intensifies the myocardial injury of coxsackievirus B3 infection of mice. 812 Jun 53