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Research ArticleArticle

Exposure to Ochratoxin A Impairs Organic Anion Transport in Proximal-Tubule-Derived Opossum Kidney Cells

Christoph Sauvant, Stefan Silbernagl and Michael Gekle
Journal of Pharmacology and Experimental Therapeutics October 1998, 287 (1) 13-20;
Christoph Sauvant
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Stefan Silbernagl
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Michael Gekle
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Abstract

Ochratoxin A (OTA) is a widespread mycotoxin, which is nephrotoxic and carcinogenic. Because a decline in net-secretion ofpara-aminohippuric acid (PAH) was observed after chronic OTA exposition in vivo, we investigated the effect of OTA on proximal-tubule-derived opossum kidney (OK) cells. OTA up to 10−5 mol/liter had no acute effect on PAH transport when bovine serum albumin (BSA) was present. By contrast, 72-hr incubation of OK cells led to a decrease of PAH transport with half-maximal inhibition at 6 · 10−7 mol/liter for transepithelial secretion and 6 · 10−8 mol/liter for basolateral uptake of PAH. Incubation of OK cells with 10−6 mol/liter OTA for 72 hr reduced the affinity of PAH uptake, and decreased the maximum secretion rate to one-fifth of control values. Apical uptake of amino acids and basolateral uptake of glutarate were not affected. In addition, no signs of general toxic action could be observed. Specific basolateral binding affinity of PAH was reduced to 50% of control. Furthermore, incubation with OTA led to a decrease of PAH efflux across the apical membrane, although efflux across the basolateral membrane and the amount remaining in the cells increased as compared to control. By contrast to control cells, uptake of PAH in OTA-treated cells was not stimulated after preloading with glutarate. Our data show, that 1) long-term incubation with free OTA in the nanomolar range reduces the activity of the organic anion transporter, 2) without influencing general cell function. 3) OTA seems to act preferentially on organic anion transport, by affecting the exchange of organic anions and dicarboxylates. 4) Thereby, OTA reduces its own secretion. 5) The excretion of other xenobiotics and drugs may be also impaired, whereby OTA can exert an indirect toxic action.

Footnotes

  • Send reprint requests to: Dr. Christoph Sauvant, Physiologisches Institut, Universität Würzburg, Röntgenring 9, 97070 Würzburg, Germany.

  • ↵1 This work was supported by the Deutsche Forschungsgemeinschaft, DFG Grant Si 170/7-2 and Ge 905/3-3.

  • Abbreviations:
    α-KG
    α-ketoglutarate
    BEN
    Balkan endemic nephropathy
    BSA
    bovine serum albumin
    CIN
    chronic interstitial nephropathy
    FCS
    fetal calf serum
    OAT
    organic anion transporter
    OCT
    organic cation transporter
    OK cells
    opossum kidney cells
    OTA
    ochratoxin A
    PAH
    para-aminohippuric acid
    PKC
    protein kinase C
    TEA
    tetraethylammonium
    LDH
    lactate dehydrogenase
    • Received December 19, 1997.
    • Accepted May 15, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 287, Issue 1
1 Oct 1998
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Research ArticleArticle

Exposure to Ochratoxin A Impairs Organic Anion Transport in Proximal-Tubule-Derived Opossum Kidney Cells

Christoph Sauvant, Stefan Silbernagl and Michael Gekle
Journal of Pharmacology and Experimental Therapeutics October 1, 1998, 287 (1) 13-20;

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Research ArticleArticle

Exposure to Ochratoxin A Impairs Organic Anion Transport in Proximal-Tubule-Derived Opossum Kidney Cells

Christoph Sauvant, Stefan Silbernagl and Michael Gekle
Journal of Pharmacology and Experimental Therapeutics October 1, 1998, 287 (1) 13-20;
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