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Effects of vitamin E deficiency on the functions of splenic lymphocytes and alveolar macrophages

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 c...

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Bibliographic Details
Published in:Journal of Nutritional Science and Vitaminology 1989, Vol.35(5), pp.419-430
Main Authors: Moriguchi, S. (Tokushima Univ. (Japan). School of Medicine), Kobayashi, N, Kishino, Y
Format: Article
Language:English
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Summary: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°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.
ISSN:0301-4800
1881-7742
DOI:10.3177/jnsv.35.419