BILE CANALICULAR MEMBRANE PATHOLOGY IN CYTOCHALASIN-B-INDUCED CHOLESTASIS

  • 1 January 1977
    • journal article
    • research article
    • Vol. 37  (4) , 350-356
Abstract
The mechanism of cytochalasin B-induced intrahepatic cholestasis was examined using electron cytochemical techniques. Since the earliest lesions were apparently in hepatic canaliculi, markers were used for 3 canalicular membrane components, i.e., ruthenium red for the glycoprotein-rich surface coat, the Mg2+-ATPase reaction as an example of a membrane-bound protein, and uranyl acetate en bloc and ruthenium red staining for the canalicular membrane-associated microfilaments. In rat liver infused in vivo with cytochalasin B reduction in bile flow correlated with bile canalicular dilation, loss of the ruthenium red-positive surface coat from the canalicular membrane and loss of demonstrable Mg2+-APTase activity. Structural alterations in microfilaments with widening of the ectoplasmic zone were noted. In isolated rat liver cells in vitro identical changes were found. Bile canaliculi isolated from the in vivo cytochalasin B-infused rat liver lacked their normal investment of microfilaments. Detachment of the filaments from the bile canalicular membrane may be involved in the mechanism of cytochalasin B-induced cholestasis.

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