Spanos E, Barrett D I, Chong K T, MacIntyre I
Biochem J. 1978 Jul 15;174(1):231-6. doi: 10.1042/bj1740231.
Primary cultures of chick kidney cells convert 25-hydroxycholecalciferol into more-polar metabolites. Cells from vitamin D-deficient chicks have high 25-hydroxycholecalciferol 1 alpha-hydroxylase (1 alpha-hydroxylase) activity, but no 25-hydroxycholecalciferol 24-hydroxylase (24-hydroxylase) activity. Physiological concentrations of 1,25-dihydroxycholeclaciferol suppress 1 alpha-hydroxylase and induce 24-hydroxylase activity. The inhibition of 1 alpha-hydroxylase preceded the induction of 24-hydroxylase. In contrast, oestradiol-17 beta had no effect on the activity of either hydroxylase under a variety of experimental conditions. These results clearly demonstrate that 1,25-dihydroxycholecalciferol, but not oestrogen, acts directly on the kidney cells to regulate the metabolism of 25-hydroxycholecalciferol.
鸡肾细胞原代培养物可将25-羟胆钙化醇转化为极性更强的代谢产物。来自维生素D缺乏雏鸡的细胞具有较高的25-羟胆钙化醇1α-羟化酶(1α-羟化酶)活性,但没有25-羟胆钙化醇24-羟化酶(24-羟化酶)活性。生理浓度的1,25-二羟胆钙化醇可抑制1α-羟化酶并诱导24-羟化酶活性。1α-羟化酶的抑制先于24-羟化酶的诱导。相比之下,在各种实验条件下,雌二醇-17β对这两种羟化酶的活性均无影响。这些结果清楚地表明,直接作用于肾细胞以调节25-羟胆钙化醇代谢的是1,25-二羟胆钙化醇,而非雌激素。