Role of manganese and vitamin E deficiency in mouse paralysis

¹ Department of Physiology, University of Minnesota Medical School, Minneapolis, Minnesota

Inbred C₃H male mice in 20 groups of 10 each were studied to identify the trace mineral element essential to the prevention of "paralysis" in vitamin E deficiency. Cobalt, copper, manganese, and zinc were studied by employing several possible combinations of omissions and additions. Highly purified vitamin E-deficient diets were employed and -tocopheryl acetate added as the source of vitamin E. It was found that in vitamin E deficiency a concomitant lack of Mn invariably resulted in 100% incidence of early paralysis. Lack of no other element had this effect. After onset of symptoms, additions of vitamin E or Mn, or both, did not reverse the damage, but life spans were increased. The mechanisms of the effect of Mn in protecting against early onset of paralysis in the mouse has not been explained. Body weights were higher in Mn-fed, E-deficient mice than in groups lacking Mn but receiving other minerals.