Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.7 (DNA polymerase)
 17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obstructive jaundice, produced by ligating the common bile duct, induced a transient DNA replication followed by cell proliferation in rat liver. At 48 h after the operation, DNA polymerase alpha activity started to increase and reached its maximum level (more than twice the control) at day 4. At day 7, the enzyme level had decreased to the control level. Pulse-labeling experiment using radioactive thymidine showed that the rate of DNA synthesis increased approximately 2.5-fold in the same pattern as that of DNA polymerase alpha. The mitotic index in hepatocytes also increased 10-fold at day 4 and then decreased. The proliferation of liver cells induced by obstructive jaundice mimics the regeneration of partially hepatectomized liver, although the response was slightly delayed and the proliferation was transient.
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PMID:Induction of DNA replication and cell growth in rat liver by obstructive jaundice. 190 Aug 21

Hepatitis B virus-like particles including: small spheres and filaments 15--25 nm in diameter together with a 35--40 nm Dane particle-like virion have been identified in sera of patients with non-A, non-B hepatitis. In a coded serological study, such particles were detected transiently in 3/4 acute, and persistently in 7/8 chronic cases of non-A, non-B hepatitis with non-A, non-B antigenemia. Only 2/12 similar cases without non-A, non-B antigens (Ag) in serum had detectable particles but neither patients with drugs, or type A hepatitis, nor cases of obstructive jaundice. The particles did not express hepatitis B surface (HBs) or non-A, non-B Ag at their surface but were associated, in three patients, with significant endogenous DNA polymerase activity. Furthermore, particles similar to hepatitis B cores (BHc) and also associated with DNA polymerase activity were demonstrated by sucrose gradient ultracentrifugation of a liver homogenate obtained from a patient who had died of non-A, non-B hepatitis. The non-A, non-B hepatitis virion described here appears, therefore, as a hepatitis B-like virus. The exact kinship between these two agents is currently being investigated.
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PMID:Non-a, non-b hepatitis: identification of hepatitis-B-like virus particles in serum and liver. 677 42

Portal vein branch occlusion induces atrophy of occluded hepatic lobes, concomitantly associated with the complementary hypertrophy of unoccluded lobes. In this context, selective embolization of the portal vein branch supplying the area to be resected has been performed prior to extended hepatectomy to reduce the risk of postoperative liver failure. However, carcinoma of the hepatic hilus is often associated with obstructive jaundice. At present it is still obscure whether cholestatic hepatocytes can also respond well to the proliferation stimuli caused by the portal vein branch embolization. To clarify this point, we made a rat model of portal vein branch ligation in combination with cholestasis. As an indicator of proliferation, we determined the activity of DNA polymerase alpha and the mitotic index. The results demonstrate that, even in the cholestatic liver, the expression of DNA polymerase alpha in unoccluded lobes was induced by contralateral portal vein branch ligation. The maximal degree of DNA polymerase alpha induction in the cholestatic liver was similar to that in the noncholestatic liver, i.e., fivefold above that in the resting liver. The level of DNA polymerase alpha activity correlated well with the mitotic index in the same tissue. Furthermore, the cell proliferation after the portal vein branch occlusion is not suppressed by the preceding external biliary drainage, which had been shown to suppress the liver regeneration after partial hepatectomy. From these results, it is concluded that portal vein branch ligation induces liver cell proliferation in unoccluded lobes, irrespective of the presence of cholestasis.
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PMID:Portal vein branch occlusion induces cell proliferation of cholestatic rat liver. 859 23

Translocation of bacteria and endotoxin has long been documented in obstructive jaundice, and altered intestinal barrier function is considered to be one of the important mechanisms for this phenomenon. Proliferating cell nuclear antigen (PCNA), also known as cyclin, is an auxiliary protein of DNA polymerase-delta, and the level of synthesis correlates directly with rates of cellular proliferation and DNA synthesis. This study was designed with the aim of evaluating the effect of obstructive jaundice on PCNA expression in small bowel epithelium. Male Sprague-Dawley rats were randomized to four groups. Group A (n = 10, control group) underwent a sham operation. Group B (n = 9, obstructive jaundice group for 1 week) underwent common bile duct ligation. Group C (n = 8, obstructive jaundice group for 2 weeks) underwent common bile duct ligation. Group D (n = 8, obstructive jaundice group for 2 weeks) underwent common bile duct ligation with oral glutamine intake. After periods of 7 days and 2 weeks, segments of small bowel were harvested from groups A & B and groups C & D, respectively. Nuclear immunohistochemical expression of PCNA in small bowel was evaluated. The PCNA-labeling index [(PCNA-positive cells/500 cells) x 100] was quantified. Comparisons among the four groups were performed. The PCNA-labeling index in small bowel of group B was significantly higher than that of group A (29.0% vs 21.2%, p = 0.001). After 2 weeks of common bile duct ligation, the PCNA-labeling index in small bowel of group C was significantly lower than that of group A (19.4% vs 21.2%, p = 0.045). With oral glutamine intake daily, the PCNA-labeling index in small bowel of Group D was restored and was significantly higher than that of group A (24.5% vs 21.2%, p = 0.002). Obstructive jaundice for 1 week upgraded PCNA expression in rat small intestine. PCNA expression in rat small intestine later became depressed after obstructive jaundice for 2 weeks. Oral glutamine intake daily could effectively restore the PCNA expression in small bowel of rats subjected to obstructive jaundice for 2 weeks.
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PMID:Obstructive jaundice alters proliferating cell nuclear antigen expression in rat small intestine. 1595 52