Abstract
Injections of 2-deoxy- d-galactose induce acute liver injury in guinea pigs. Ultrastructural changes is hepatocytes include a hypertrophy of the smooth and a reduction of the rough endoplasmic reticulum, fatty infiltration, and nucleolar fragmentation. Kupffer cells are enlarged and increased in number. The activities of sorbitol dehydrogenase, glutamate dehydrogenase, glutamate oxaloacetate transaminase, and the bilirubin concentration are greatly increased in plasma. The early metabolic events caused by 2-deoxy- d-galactose have been studied in freeze-clamped livers after administration of a single dose. Formation and accumulation of nonphysiologic UDP-2-deoxy-hexoses function as a trapping mechanism for uridine phosphate. Specific, enzymatic measurements reveal the rapid induction of UTP deficiency, associated with a depletion of UDP-glucose and UDP-galactose pools. Administration of the same dose per kilogram of body weight decreases the hepatic UTP content to 25% of normal for more than 7 hr in guinea pigs, and to 25–30% of normal for less than 2 hr in rats. The mechanisms compensating UTP deficiency are much more active in rat as compared to guinea pig liver. This difference accounts for the previously reported finding, that pure 2-deoxy- d-galactose does not provoke signs of liver injury in the rat. All of the ultrastructural and biochemical lesions induced by 2-deoxy- d-galactose have also been observed after administration of d-galactosamine, although both galactose analogs do not share any common metabolites. However, 2-deoxy- d-galactose is less efficient and therefore does not cause extensive hepatocellular necrosis.
Published Version
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