Kohda C, Nishimura K, Gemba M
Nihon Yakurigaku Zasshi. 1979 Jan;75(1):91-8.
Rats were provided a normal laboratory diet or a low Ca.vitamin D-deficient diet. After the administration of 1 alpha-hydroxycholecalciferol, mitochondria, microsomes and slices were prepared from kidney cortex of both control and treated rats. When 1 alpha-hydroxycholecalciferol was given to normal and low Ca.vitamin D-deficient rats, Ca accumulation in mitochondria was stimulated during 30 minutes and the high calcium content was maintained at the subsequent incubation. There was a significant decrease of mitochondrial Ca2+-ATPase and Mg2+-ATPase activities with low Ca.vitamin D depletion, but both enzyme activities were restored by 1 alpha-hydroxycholecalciferol treatment of the depleted rats. Ca2+-ATPase and Mg2+-ATPase activities of microsomes were not altered with the administration of 1 alha-hydroxycholecalciferol. In contrast to results of mitochondrial Ca transport, changes in Ca influx and efflux of slices were not significant in response to the treatment of low Ca.vitamin D-deficient rats with 1 alpha-hydroxycholecalciferol. The results of the present study suggest that 1 alpha-hydroxycholecalciferol plays a role in the process of Ca accumulation and ATP hydrolysis of mitochondria in kidney cortex.
给大鼠提供正常实验室饮食或低钙、维生素D缺乏饮食。给予1α-羟基胆钙化醇后,从对照大鼠和处理大鼠的肾皮质制备线粒体、微粒体和切片。当给正常和低钙、维生素D缺乏大鼠给予1α-羟基胆钙化醇时,线粒体中的钙积累在30分钟内受到刺激,并且在随后的孵育过程中高钙含量得以维持。低钙、维生素D缺乏会导致线粒体Ca2+-ATP酶和Mg2+-ATP酶活性显著降低,但对缺乏该物质的大鼠进行1α-羟基胆钙化醇处理后,两种酶的活性均得以恢复。给予1α-羟基胆钙化醇后,微粒体的Ca2+-ATP酶和Mg2+-ATP酶活性未发生改变。与线粒体钙转运结果相反,用1α-羟基胆钙化醇处理低钙、维生素D缺乏大鼠后,切片的钙流入和流出变化不显著。本研究结果表明,1α-羟基胆钙化醇在肾皮质线粒体的钙积累和ATP水解过程中发挥作用。