title: Accelerated thymus involution in magnesium-deficient rats is related to enhanced apoptosis and sensitivity to oxidative stress.
abstract: Experimental Mg deficiency leads to alterations in the immune response. Reduction of thymus weight and histological changes were previously observed in Mg-deficient rats after several weeks on a deficient diet, suggesting that functions of this immune organ may be affected by Mg deficiency. More recently, changes in the immune system during early Mg deficiency were shown. Thus, in the present study we examined modifications in the thymus during the early stages of Mg deficiency in weanling rats. From our results, it appears that Mg deficiency accelerates thymus involution. The assessment of apoptosis (enumeration of apoptotic cells on the basis of morphological criteria and intranucleosomal degradation of genomic DNA) showed greater values in thymuses from Mg-deficient rats as compared with controls. This was observed very early, since a significant difference was shown on the second day of deficiency, before reduced weight of thymus, which was recorded in the later period. These results indicate the relationship of accelerated thymus involution with an active process of cell death. Mg deficiency led to histological changes in the thymus. In the early stage of deficiency (second day) the presence of inflammatory cells was shown, suggesting that the inflammatory process was already occurring in the tissue studied. Later (eighth day) an increased proportion of epithelial reticular cells in the cortex was shown, indicating a remodelling process occurring in this period. Enhanced susceptibility to peroxidation also occurred very early during Mg deficiency. It may be hypothesized that disturbances in Mg status of short duration could have cellular effects with various deleterious consequences.
authors.affiliation: Centre de Recherche en Nutrition Humaine d'Auvergne, Unité Maladies Métaboliques et Micronutriments, INRA, St-Genès-Champanelle, France.
authors.forename: C
authors.initials: C
authors.lastname: Malpuech-Brugère
authors.forename: W
authors.initials: W
authors.lastname: Nowacki
authors.forename: E
authors.initials: E
authors.lastname: Gueux
authors.forename: J
authors.initials: J
authors.lastname: Kuryszko
authors.forename: E
authors.initials: E
authors.lastname: Rock
authors.forename: Y
authors.initials: Y
authors.lastname: Rayssiguier
authors.forename: A
authors.initials: A
authors.lastname: Mazur
mesh_terms: D000818:Animals; D017209:Apoptosis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D018956:CD5 Antigens / Q000032:analysis; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D007958:Leukocyte Count; D008214:Lymphocytes / Q000276:immunology / Q000473:pathology; D008275:Magnesium Deficiency / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009929:Organ Size; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D012156:Reticulocytes / Q000473:pathology; D013950:Thymus Gland / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology; D013997:Time Factors
chemical_list: D018956:CD5 Antigens