作者: Tsuneo Deguchi , Sumio Ohtsuki , Masaki Otagiri , Hitomi Takanaga , Hiroshi Asaba
DOI: 10.1046/J.1523-1755.2002.00318.X
关键词:
摘要: Major role of organic anion transporter 3 in the transport indoxyl sulfate kidney. Background Indoxyl is a uremic toxin that accumulates body because patient's inability to excrete it and induces number symptoms leads chronic renal failure. The functional failure excretion system for causes its accumulation blood. purpose present study was characterize mechanism responsible sulfate. Methods [ H]indoxyl investigated using an vivo tissue-sampling single-injection technique, kidney uptake index (KUI) method. Rat (rOAT3)-expressing Xenopus laevis oocyte used measuring activity. Results Probenecid showed concentration-dependent inhibitory effect on KUI method, inhibited by anions such as para -aminohippuric acid (PAH) benzylpenicillin, weak base cimetidine, toxins, 3-carboxy-4-methyl-5-propyl-2-furanpropanoic (CMPF) hippuric (HA). However, salicylic acid, indomethacin, 3,5,3′-triiodo-L-thyronine indole acetic (IA) had no uptake. rOAT3-expressing oocytes exhibited rOAT3 (K m = 158 μmol/L). Moreover, toxins rOAT3. Conclusions These results suggest sulfate, share Mutual inhibition these via OAT3 may accelerate their and, thereby, progression nephrotoxicity uremia.