Sergeev I N, Arkhapchev Y P, Spirichev V B
Institute of Nutrition, Academy of Medical Sciences of the USSR, Moscow.
J Nutr. 1990 Oct;120(10):1185-90. doi: 10.1093/jn/120.10.1185.
Ascorbic acid deficiency in guinea pigs fed a vitamin D-replete diet caused a moderate reduction of Ca level in serum and bone; 25-hydroxy-cholecalciferol or 25-hydroxyergocalciferol (25-OHD) serum concentration tended to decline; renal 25-hydroxycholecalciferol-1-hydroxylase (1-OHase) activity decreased 50%; and 25-hydroxycholecalciferol-24-hydroxylase activity increased 1.6-fold. Chromatin 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] receptor concentration in the intestinal mucosa decreased 20-30%, and the percentage of occupied receptors decreased from 12-15% to 6-8%. Receptor affinity for 1,25-(OH)2D3 did not change (Kd = 0.24-0.26 nmol/L, Kd2 = 0.06-0.10 nmol/L), but the cooperativity coefficient decreased from 1.7 to 1.4. Vitamin C deficiency potentiated effects of vitamin D deprivation and impaired a restorative action of vitamin D. It was accompanied by a marked delay in the elevation of 25-OHD concentration in serum as well as decreased 1-OHase activity in kidneys and a lower concentration of occupied 1,25-(OH)2D3 receptors in the intestinal mucosa. The data demonstrate a critical role for ascorbic acid in vitamin D metabolism and binding.
给豚鼠喂食富含维生素D的饮食时，维生素C缺乏导致血清和骨骼中的钙水平适度降低；血清25-羟基胆钙化醇或25-羟基麦角钙化醇（25-OHD）浓度有下降趋势；肾脏25-羟基胆钙化醇-1-羟化酶（1-OHase）活性降低50%；25-羟基胆钙化醇-24-羟化酶活性增加1.6倍。肠道黏膜中染色质1,25-二羟基胆钙化醇[1,25-(OH)2D3]受体浓度降低20%-30%，被占据受体的百分比从12%-15%降至6%-8%。受体对1,25-(OH)2D3的亲和力未改变（解离常数Kd = 0.24-0.26 nmol/L，Kd2 = 0.06-0.10 nmol/L），但协同系数从1.7降至1.4。维生素C缺乏增强了维生素D缺乏的影响，并损害了维生素D的恢复作用。它伴随着血清中25-OHD浓度升高的明显延迟，以及肾脏中1-OHase活性降低和肠道黏膜中被占据的1,25-(OH)2D3受体浓度降低。这些数据证明了维生素C在维生素D代谢和结合中的关键作用。
