Increased Apoptosis and Free Radical Production in Thymus of Magnesium-Deficient Rats: Implications to Enhanced Thymus Involution and Immunity

Abstract

Magnesium plays an important role in the maintenance of host regulatory mechanisms in inflammation and immunity. It is well known that dietary magnesium deficiency in rodents, and especially in rats, causes inflammation (for review[l,2]). This inflammatory reaction is characterized by peripheral vasodilatation, splenomegaly and leukocytosis. Elevated levels of proinflammatory cytokines and acute phase proteins have also been observed during magnesium deficiency [1,2]. On the other hand several observations on the modifications in the immune response during this deficiency have been reported [3]. Since T lymphocytes play a key role in the immune response in the present study we examined modifications occurred in the thymic gland during experimental magnesium deficiency. The thymus presents marked variations in its structure depending on the age and the condition of the organism as a whole. This organ is largest in embryos and gradually and continuously involutes throughout life. However, this process of normal or age involution may be complicated by the rapid changes of “accidental involution”[4]. Since the pioneering work of Selye (1936) it is known that following noxious stimuli, stress results in thymic involution and lymphopenia.