Experimental Magnesium Depletion **†
نویسنده
چکیده
I have both coveted and feared this opportunity to deliver the John P. Peters Lecture. Coveted it since, as a student of his, I wish to do him honor; and feared it since, as a student of his, I know I will not satisfy his requirements for excellence. Dr. Peters eschewed long introductions to scientific presentations and referred disparagingly to the early paragraphs as mere "throatclearing." In appropriate respect, then, to his standards, let me say simply that I feel at once both deeply honored and humble to have been selected to deliver this lecture this year. The work I wish to present this afternoon has to do with some observations in experimental magnesium depletion, and in this discussion I would like to describe some of the structural and chemical alterations that were noted, offer a partial interpretation for some of these, and then describe some studies which have been directed toward a definition of the role of magnesium in the activation of an enzyme system which may be intimately linked with some of the observations noted in the magnesium deficiency state. Let me acknowledge initially that these studies were accomplished in collaboration with Dr. Robert Whang and Dr. James Richardson. In addition, we are indebted to Dr. Jean Oliver for his help; and finally, the studies on the magnesium activation of erythrocyte ghost ATPase were done in the laboratory of, and with the collaboration of, Dr. D. C. Tosteson of the Department of Physiology and Pharmacology at Duke Medical Center. The initial studies had the simple goal of a description of the alterations one might note in experimental magnesium deficiency in the rat. The experimental design1 consisted of pair-feeding rats by groups a diet free of sodium, potassium, chloride, phosphorus, and magnesium. In addition, each animal
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ورودعنوان ژورنال:
- The Yale Journal of Biology and Medicine
دوره 36 شماره
صفحات -
تاریخ انتشار 1964