Department of Experimental Oncology, Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, 12 R. Weigl Street, 53-114 Wroclaw, Poland, Centre de Recherches en Nutrition Humaine d’Auvergne, Unité Maladies Métaboliques et Micronutriments, INRA, Theix, 63122 St-Genes-Champanelle, France, Department of Pathological Anatomy, Pathophysiology, Microbiology and Forensic Veterinary Medicine, Agricultural Academy, 31, Norwid Street, 50-375 Wroclaw, Poland
It has been well documented that experimental hypomagnesemia in rodents evokes, as an early consequence, an inflammatory response. This also leads to the activation of cells producing reactive species of oxygen and, as a result, to the oxidative damage of tissues. Several studies have shown that lungs might be a specific target of Mg deficiency. Here, we report that 3 weeks of Mg deficiency in mice resulted in inflammatory processes in the lungs, including interstitial and perivascular pneumonia, manifested by the infiltration of leukocytes, plasmocytes and histiocytes, as well as the phenomenon of disseminated intravascular coagulation (DIC). These phenomena were accompanied by changes in gene expression assessed by cDNA array. In this study we identified 26 genes significantly changed by Mg deficiency, mostly involved in the anti-oxidative response, regulation of cell cycle and growth, apoptosis as well as cell-cell and cell-matrix interactions. We conclude that these changes are related to the phenomena of inflammatory and oxidative processes and consecutive remodeling occurring in the tissues as a result of Mg deficiency. This may have implications for at least several lung pathologies, including allergies, asthma, SIDS (Sudden Infant Death Syndrome) or facilitate formation of lung metastases.