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Long-term Effect of Suboptimal Dietary Magnesium on Magnesium and Calcium Contents of Organs, on Cold Tolerance and on Lifespan, and its Pathological Consequences in Rats¹

Division of Biological Sciences, National Research Council of Canada, Ottawa, Canada K1A 0R6

Sprague-Dawley male rats selected at 5 weeks of age were kept at 28° or 6° for 69, 240, or 517 days and were fed a semipurified diet containing either a normal (52 mg/100 g) or a suboptimal amount of magnesium (Mg) (10 mg/100 g). Within the first 69 days, typical signs of Mg deficiency were evident in 28° and 6° acclimated rats fed a suboptimal level of Mg. These included skin sores in 50% of the rats, a significant reduction in growth, a severe reduction in Mg content of all organs except heart, brown fat, thymus and duodenum, a severe calcification in the kidney, and after severe cold stress (4 hours at -20°) more calcified necrotic lesions in heart than in controls fed the normal Mg diet. During this time, the rats had apparently become adapted to the low Mg diet for, between 69 and 517 days, skin sores disappeared. There were no further reductions in growth, and Mg content in any of the organs; calcification of the kidney did not increase; and after severe cold stress, there were no differences in the number of heart lesions compared to controls. In spite of this adaptation, however, the homeostatic potential, measured in terms of cold tolerance at -20°, gradually decreased with the duration of the Mg deficiency. The reduction of Mg content in different tissues was not any greater at 6° than at 28°, but the consequences were more severe at 6°. Calcium content increased in heart, aorta and brown fat; there was more damage to the heart after severe cold stress, and longevity was reduced. Thus, there is a level of Mg deficiency which is characterized by few overt signs of the deficiency, but which over the long-term results in a decline in homeostatic potential.

KEY WORDS: • Magnesium • diet • calcium • cold tolerance • pathology

¹ NRCC No. 16197.

^* To whom proofs should be sent.

² Present address: The University of New England, Department of Physiology, Armidale, N.S.W., Australia.

³ Present address: Civic Hospital, Department of Laboratory Medicine, Ottawa, Canada.

Manuscript received 23 September 1976.