Female NZB/W mice beginning at both 6 wk and 6 mo of age were fed four different levels of dietary zinc: 100 ppm zinc (control), 9 ppm zinc (marginal deficiency), 5 ppm zinc (moderate deficiency), and 2.5 ppm (severe deficiency). In addition, because dietary deprivation of zinc is associated with inanition, a group of mice were fed the control diet but in amounts equal to the intake of mice fed 5 ppm zinc. Mice who entered the study at 6 wk and were fed 100 ppm zinc developed typical murine lupus characterized by anti-dsDNA antibodies, proteinuria, glomerulonephritis, and a 50% mortality at 9 mo of age. Mice fed 9 ppm zinc did not significantly deviate from this pattern. However, mice fed 5 and 2.5 ppm zinc experienced a significant delay in the appearance as well as lower titers of antibodies to dsDNA, reduced proteinuria and prolonged life span, with 90% survival at 10 mo of age. Although caloric restriction consistent with the decreased food intake observed in mice fed 5 ppm zinc also resulted in significant delay in the progression of autoimmune disease, the magnitude of pathology observed in pair-fed controls was significantly greater than that of zinc-deprived mice. Mice who entered the study at 6 mo of age all had established disease upon initiation of the diets. Zinc deprivation under such conditions delayed the rise in titers of antibodies to dsDNA and reduced the observed proteinuria, glomerulonephritis, and resultant mortality. Nonetheless, these changes were not as dramatic as those produced by the initiation of dietary manipulation at an earlier age. The results in both groups correlated well with alterations in plasma zinc levels, and they underscore dietary intervention as a possible means of modulating disease activity in systemic lupus erythematosus.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Immunology|
|State||Published - 1982|
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