iPr2P-F (di-isopropyl phosphorofluoridate) administration to rats produces a liver-dependent specific elevation of plasma β-glucuronidase activity. The response is unaffected by puromycin pretreatment. By using subcellular-fractionation techniques, the rise in plasma β-glucuronidase activity was correlated temporally with a fall in liver microsomal β-glucuronidase activity. After iPr2P-F treatment, liver microsomal membranes are depleted of β-glucuronidase but slowly return to normal over 1 week. On the other hand, liver lysosomal β-glucuronidase activity is high at early time points (less than 60min) after iPr2P-F administration but decreases to below control values; this lasts for a few days. The response to iPr2P-F was demonstrated in isolated hepatocytes prepared from iPr2P-F-treated rats. In such preparations, microsomal β-glucuronidase is lost rapidly, followed by a specific decrease in hepatocyte lysosomal β-glucuronidase. The results suggest that a pool of microsomal β-glucuronidase serves as precursor to plasma β-glucuronidase in iPr2P-F-treated rats, and further, that microsomal β-glucuronidase may serve as precursor to lysosomal β-glucuronidase.

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