Sergeev I N, Kim R H, Arkhapchev Iu P, Kodentsova V M, Alekseeva I A
Vopr Med Khim. 1987 Nov-Dec;33(6):96-103.
Effect of vitamin B2 deficiency on metabolism, reception and biochemical functions of vitamin D was studied in young rats. Deficiency in vitamin B2 was shown to cause a moderate hypocalcemia as well as a decrease in the active transport of calcium in small intestine and in concentration of 25-OH D in blood serum, lowered formation of 24,25 (OH)2D3 in kidney slices and decreasing content of nuclear receptors for 1,25 (OH)2D3 (fre and bound in vivo) in small intestine mucose. After administration of cholecalciferol into the animals deficient in vitamins D and B2 within 24 hrs or 6 days before death restoration of the calcium metabolism parameters was retarded as a result of less distinct stimulation of I-hydroxylase and of low activity of 24-hydroxylase 25-OH D3 in kidney as well as due to a moderate increase in content of bound receptors of 1,25 (OH)2D3 in small intestine mucose and, apparently, because of reduced production of the proteins dependent on vitamin D in the tissue (Ca2+-ATPase and alkaline phosphatase). The data obtained suggest the possible importance in rickets of vitamin B2 deficiency mediated via its influence on metabolism and reception of vitamin D.
在幼鼠中研究了维生素B2缺乏对维生素D代谢、受体及生化功能的影响。结果表明,维生素B2缺乏会导致中度低钙血症,以及小肠中钙的主动转运减少、血清中25-OH D浓度降低、肾切片中24,25 (OH)2D3生成减少、小肠黏膜中1,25 (OH)2D3核受体(体内游离和结合形式)含量降低。在维生素D和B2缺乏的动物死亡前24小时或6天给予胆钙化醇后,由于对I-羟化酶的刺激不明显、肾中24-羟化酶25-OH D3活性低,以及小肠黏膜中1,25 (OH)2D3结合受体含量适度增加,且显然是由于组织中依赖维生素D的蛋白质(Ca2+-ATP酶和碱性磷酸酶)产生减少,钙代谢参数的恢复受到阻碍。所获得的数据表明,维生素B2缺乏通过影响维生素D的代谢和受体可能在佝偻病中具有重要作用。