Mechanism of bifonazole-induced [Ca2+]i increases in MDCK renal tubular cells.

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Cho KJ, Su W, Chen WC, Law YP, Fang HC, Liu CP, Cheng JS, Lee KC, Lo YK, Chang HT, Huang JK, Jan CR

Mechanism of bifonazole-induced [Ca2+]i increases in MDCK renal tubular cells.

Chin J Physiol. 2001 Sep 30;44(3):97-101.

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11767287 [ View in PubMed
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Abstract

The effect of the antifungal drug bifonazole on Ca2+ homeostasis in Madin Darby canine kidney (MDCK) cells was investigated. Cell suspensions were loaded with the Ca2+-sensitive dye fura-2, and the fluorescence changes were measured with a spectrofluorophotometer. At concentrations between 10-80 microM bifonazole increased cytosolic free Ca2+ levels ([Ca2+]i) in a concentration-dependent manner. The Ca2+ signals were partly inhibited by removing extracellular Ca2+. Bifonazole (40 microM) released Ca2+ from the store sensitive to 1 microM thapsigargin, an endopolasmic reticulum Ca2+ pump inhibitor. Bifonazole (40 microM) per se induced capacitative Ca2+ entry while reduced 1 microM thapsigargin-induced capacitative Ca2+ entry. Inositol 1,4,5-trisphosphate may be involved in bifonazole-induced Ca2+ release because inhibiting phospholipase C with 2 microM U73122 partly reduced the bifonazole response. Together, bifonazole increased [Ca2+]i in renal tubular cells by inducing intracellular Ca2+ release and extracellular Ca2+ influx.

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