Mouse liver acid phosphatase

Mouse liver acid phosphatase is localized in the Kupffer cells in contrast to the alkaline phosphatase activity which is largely confined to the endothelial linings of the sinusoids. Under the conditions in which the activity of the reticuloendothelial system is enhanced, both enzymic activities are increased (97, 98). 

MacDonald (99) showed that mouse liver acid phosphatase required active sulfhydryl groups for activity and that malonate buffer, pH 5.9, was useful for the assay of this enzyme because it stabilized the enzyme during the period of the assay. 

The centrifugal method of separation employed by Van Lancker and Holtzer (V2) was among the earlier ones in the field, and there was probably considerable cross contamination of the fractions. Nonetheless, the distribution seems more disperse than that obtained by de Duve et al. (DIO) for rat liver with a comparable method. For example, in the case of the mouse pancreas the small mitochondrial fractions, c, d, and e, obtained by centrifugation between 17 X 10 and 263 X 10 gr-min contained 27% of the acid phosphatase and the succeeding microsomal fractions, f and g, obtained by centrifugations between 263 X 10 g-min and 3170 X 10 g-min, contained 24% of the acid phosphatase (V2). For rat liver, comparable fractions, obtained by centrifugation between 33 X 10 to 250 X 10 g-min and 250 X 10 to 3000 X 10 g-min contained 41 and 20%, respectively (DIO). 

TNAP is expressed in human hepatocytes, and bile acids increase its activity [93] and secretion in the bile [94]. TNAP in rat hepatocytes is predominantly localized in the bile canalicular domain of the plasma membrane [95, 96], but can be addressed to the baso-lateral membrane in the presence of high levels of bile acid [97]. In contrast, mouse hepatocytes do not express TNAP [98]. In humans, liver TNAP may be expressed both at the sinusoidal and biliary pole of the hepatocyte. This explains why a significant proportion of TNAP activity in the circulation of healthy individuals originates from the liver. TNAP serum levels are of major clinical relevance as a marker of cholestasis. AP levels increase due to retrograde reflux of biliary alkaline phosphatase, enhanced hepatic synthesis and enzyme release into the serum, and induction of the intestinal alkaline phosphatase form [94, 99, 100]. 

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