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The mycotoxin ochratoxin A deranges pH homeostasis in Madin-Darby canine kidney cells

M Gekle1, R Vogt, H Oberleithner

  • 1Department of Physiology, University of Würzburg, Germany.

Insights

Ochratoxin A (OTA) blocks anion channels in kidney cells, increasing intracellular chloride and altering pH. This toxin disrupts cell homeostasis, impacting kidney cell function and morphology.

Area of Science:

  • Nephrology
  • Cell Physiology
  • Toxicology

Background:

  • Ochratoxin A (OTA) is a nephrotoxin known to affect kidney cells.
  • OTA exposure mimics alkaline stress in Madin-Darby canine kidney (MDCK) cells.
  • The precise effects of OTA on intracellular pH (pHi), chloride (Cl-i), and cell volume remain to be fully elucidated.

Purpose of the Study:

  • To investigate the impact of Ochratoxin A on intracellular pH, chloride levels, and cell volume in MDCK cells.
  • To determine if OTA affects MDCK cells under normal and alkaline conditions.
  • To understand the role of anion conductance in OTA-induced cellular changes.

Main Methods:

  • Utilized video-imaging and microelectrode techniques to monitor MDCK cells.
  • Applied Ochratoxin A (1 µmol/L) to cells under normal (pH 7.4) and alkaline (pH 7.7) conditions.
  • Assessed changes in intracellular pH (pHi), intracellular chloride (Cl-i), and cell volume.

Main Results:

  • OTA increased Cl-i by 2.6 mmol/L at normal pH and by 8.6 mmol/L at alkaline pH.
  • OTA elevated pHi by 0.11 units under alkaline conditions.
  • The Cl-/HCO3- exchange inhibitor DNDS abolished OTA-induced changes, and OTA did not alter cell volume.

Conclusions:

  • Ochratoxin A blocks plasma membrane anion conductance, increasing intracellular chloride without affecting cell volume.
  • OTA disrupts the driving force of Cl-/HCO3- exchange, leading to increased pHi during alkaline stress.
  • OTA interferes with pHi and Cl-i homeostasis, causing morphological and functional alterations in kidney cells.

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