Cold resistance of the brain during hibernation. Temperature sensitivity of the partial reactions of the Na+, K+-ATPase. |
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Authors: | S S Goldman R W Albers |
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Affiliation: | Department of Biochemistry, School of Dentistry, Tokyo Medical and Dental University, Yushima, Bunkyo-ku, Tokyo, Japan;The First Department of Medicine and Student Health Center, University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan;Research Laboratories, Teikoku Hormone Manufacturing Company, Kawasaki, Japan |
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Abstract: | The regulatory effect of calcium added in vitro on 25-hydroxycholecalciferol metabolism was studied in kidney mitochondria and in renal tubules from vitamin D-deficient chicks. The addition of calcium (0.05 – 0.2 mm) to mitochondrial suspensions prepared with calcium-chelating agents caused a marked and dose-related stimulation of 1-hydroxylation. A sharp decline in the activity was induced by higher concentrations of calcium (0.3 – 0.7 mm). A similar but less striking biphasic effect of calcium on 1-hydroxylation was observed in mitochondria prepared in the absence of calcium chelating agents. The effect of calcium was not a consequence of accelerated mitochondrial translocation of either exogenous NADP or Mg2+ but was related to mitochondrial calcium content. The addition of inhibitors of the calcium uptake, i.e., LaCl3 or ruthenium red, or a calcium ionophore (A 23187) significantly inhibited the calcium-induced stimulation of the 1-hydroxylation reaction. Similar calcium effects were also observed in renal tubules isolated from intact, but not from parathyroidectomized, vitamin D-deficient chicks. These data strongly suggest that mitochondrial calcium plays an important role in the regulation of 1-hydroxylase activity in kidney. |
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Keywords: | To whom all correspondence should be addressed. |
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