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Vol. 289, Issue 3, 1301-1305, June 1999

Transport of Ochratoxin A by Renal Multispecific Organic Anion Transporter 1

Minoru Tsuda , Takashi Sekine, Michio Takeda, Seok Ho Cha, Yoshikatsu Kanai, Miyako Kimura and Hitoshi Endou

Department of Pharmacology and Toxicology, Kyorin University School of Medicine, Mitaka, Tokyo, Japan (M.T., T.S., M.T., S.H.C., Y.K., H.E.); and Department of Toxicology, Kyoritsu College of Pharmacy, Minato-ku, Tokyo, Japan (M.K.)

In the present study, we investigated the transport of ochratoxin A (OTA) by kidney-specific organic anion transporter 1 (OAT1). When expressed in Xenopus laevis oocytes, OAT1 mediated sodium-independent uptake of OTA (Km = 2.1 µM). Piroxicam, which has been shown to prevent the nephrotoxicity of OTA, inhibited OAT1-mediated uptake of OTA. By contrast, another protective compound, aspartame, did not. Using a cell line derived from the mouse kidney terminal proximal tubule (S3) transfected with OAT1 cDNA, we investigated the transport of OTA and also its effect on cell proliferation and cell viability. S3 cells expressing OAT1 mediated the saturable transport of OTA (Km = 0.57 µM). Cell proliferation was suppressed in S3 cells expressing OAT1 when exposed to 2 and 10 µM OTA. This suppression was rescued by the coaddition of 1 mM p-aminohippurate in the media. The present study indicates that OTA is transported by OAT1 and that the accumulation of OTA via OAT1 in proximal tubular cells is the primary event in the development of OTA nephrotoxicity.

0022-3565/99/2893-1301$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1999 by The American Society for Pharmacology and Experimental Therapeutics


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