DEYRUP I J
J Gen Physiol. 1957 Sep 20;41(1):49-61. doi: 10.1085/jgp.41.1.49.
Rat kidney cortical slices, during incubation in vitro, lose previously accumulated radiosulfur when exposed to conditions (e.g. addition to the medium of metabolic inhibitors) which normally depress the uptake of S(35). The extent of this loss is not affected significantly by the presence of phlorhizin, an agent which enhances markedly radiosulfate accumulation. On the other hand, when tissues are chilled to 1 degrees C., loss is slight or negligible even in the presence of metabolic inhibitors. These data, and observations on the effect of pre-incubation of kidney slices in S(35)-free media before the addition of radiosulfate, have been interpreted as evidence that S(35) accumulation in vitro may be resolved into at least two processes, namely (a) entrance of the isotope-labelled anion into the cells, by diffusion and/or active transport, and (b) complexing of S(35) (in ionic or other form) with an intracellular component. The postulated complex is stabilized, perhaps through inactivation of a specific enzyme, by chilling the tissue to 1 degrees C. Possible relationships are discussed among the observations noted above, sulfur metabolism in general, and aspects of the known in vivo transport mechanism for sulfate ion; i.e., renal tubular reabsorption.
大鼠肾皮质切片在体外孵育期间,当暴露于通常会抑制³⁵S摄取的条件(例如向培养基中添加代谢抑制剂)时,会失去先前积累的放射性硫。根皮苷(一种能显著增强放射性硫酸盐积累的物质)的存在对这种损失的程度没有显著影响。另一方面,当组织冷却至1℃时,即使存在代谢抑制剂,损失也很小或可忽略不计。这些数据,以及关于在添加放射性硫酸盐之前将肾切片在无³⁵S培养基中预孵育的效果的观察结果,已被解释为体外³⁵S积累可能至少可分为两个过程的证据,即:(a) 同位素标记的阴离子通过扩散和/或主动转运进入细胞,以及 (b) ³⁵S(以离子或其他形式)与细胞内成分结合。通过将组织冷却至1℃,推测的复合物可能通过使特定酶失活而得以稳定。本文讨论了上述观察结果、一般硫代谢以及已知的硫酸根离子体内转运机制(即肾小管重吸收)各方面之间可能的关系。