Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.1.21 (thymidine kinase)
7,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male rat liver undergoes a process of demasculinization during hepatic regeneration following partial hepatectomy. The possibility that antiandrogens might potentiate this demasculinization process and in so doing augment the hepatic regenerative response was investigated. Adult male Wistar rats were treated with the antiandrogen flutamide (2 mg/rat/day or 5 mg/rat/day subcutaneously) or vehicle for three days prior to and daily after a 70% partial hepatectomy. At various times after hepatectomy, the liver remnants were removed and weighed. Rates of DNA and polyamine synthesis were assessed by measuring thymidine kinase and ornithine decarboxylase activities, respectively. Hepatic estrogen receptor status and the activity of alcohol dehydrogenase, an androgen-sensitive protein, were measured. Prior to surgery, the administration of 5 mg/day flutamide reduced the hepatic cytosolic androgen receptor activity by 98% and hepatic cytosolic estrogen receptor content by 92% compared to that present in vehicle-treated controls. After hepatectomy, however, all differences in sex hormone receptor activity between the treatment groups were abolished. The rate of liver growth after partial hepatectomy in the three groups was identical. Moreover, hepatectomy-induced increases in ornithine decarboxylase activity and thymidine kinase activity were comparable. These data demonstrate that, although flutamide administration initially alters the sex hormone receptor status of the liver, these affects have no effect on the hepatic regenerative response following a partial hepatectomy.
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PMID:Effect of antiandrogen flutamide on measures of hepatic regeneration in rats. 259 58

Aging of IMR-90 human diploid fibroblasts in culture is accompanied by specific changes of polyamine metabolism including: (a) a fivefold decrease of serum-induced activity of ornithine decarboxylase (ODC1 EC 4.1.1.17); (b) a six to tenfold increase of polyamine catabolism; and (c) a reduction of putrescine uptake. These changes apparently led to a significant reduction of putrescine accumulation in senescent cells following serum stimulation. Since the induction of ODC is a mid-G1 event, the change of polyamine metabolism may be related to changes of expression of other cell-cycle-dependent genes during cellular aging. In addition to ODC gene, we have examined the expression of two early G1 genes, c-erbB and c-myc, and one late G1/S gene thymidine kinase, at mRNA levels, in both young and old IMR-90 cells. We have also compared the enzyme activities of two late G1/S genes, thymidine kinase and thymidylate synthetase, in young and old cells following serum stimulation. We did not observe significant changes of c-erbB, c-myc, and ODC mRNA levels during cellular senescence. However, we found that serum-induced mRNA level of thymidine kinase gene in old IMR-90 cells was significantly reduced compared to that in the young cells. Results also demonstrate that aging of IMR-90 cells was accompanied by significant decrease of both thymidine kinase and thymidylate synthetase activities. In view of the recognized importance of polyamines in growth regulation, it is possible that alteration of polyamine metabolism may contribute to the impairment of expression of some key G1/S genes and such impairment may contribute to the ultimate loss of dividing potential in senescent cells.
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PMID:Polyamine metabolism and cell-cycle-dependent gene expression in IMR-90 human diploid fibroblasts during senescence in culture. 263 84

Hepatic thymidine kinase (TK) and ornithine decarboxylase (ODC) activities were used to quantify the regenerative response to injury with galactosamine. After massive damage with 1000 mg/kg galactosamine, TK activity (DNA synthesis) peaked between 62 and 120 hours. This peak of activity was depressed as much as 91% by six subcoma doses of dimethyl disulfide (DMDS) given between 24 hours and 64 hours after galactosamine administration. Similar doses of octanoic acid (OA) had no effect, and doses of NH4Cl had no effect except at 120 hours. The first peak of ODC activity (initiation of cell growth) at 45 hours was depressed about 60% by six subcoma doses of NH4Cl or DMDS injected between 27 hours and 42 hours. OA again had no effect. After 400 mg/kg galactosamine, a narrow but high peak of TK activity occurred at 62 hours. This peak of activity was depressed more than 50% by six subcoma doses of NH4Cl, OA, or DMDS given between 24 hours and 54 hours. The first peak of ODC activity at 36 hours was similarly reduced by more than 50% by similar doses of each of the toxins given between 24 hours and 34 hours. The overt neurologic effects of the toxins were dissipated within 1 hour of each injection. The depressive effect of NH4Cl and OA on TK and ODC activities during regeneration after massive centrolobular injury with acetaminophen was more consistently present and more extensive than that seen after injury with galactosamine.
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PMID:Effect of hepatic failure toxins on regenerative enzymes in the liver after injury with galactosamine in the rat. 270 58

In chick embryo retina during development, DNA synthesis and the activities of DNA polymerase, thymidine kinase, thymidylate synthetase, and ornithine decarboxylase (ODC) declined in parallel from day 7 to 12. The administration in ovo of hydrocortisone reduced significantly, particularly at 8-10 days of incubation, both DNA synthesis and the four enzyme activities tested. The effect was dose dependent, reaching the maximum with 50-100 nmol of hydrocortisone, 8-16 h after treatment. The highest inhibition was found for ODC activity (70%), followed by thymidine kinase activity (62%) and DNA synthesis (45%), whereas activities of DNA polymerase and thymidylate synthetase were reduced only by 30%. The inhibitory effect was exerted by all the glucocorticoids tested, with dexamethasone and hydrocortisone being the most efficacious. The results support the view that glucocorticoids reduce the proliferative events in chick embryo retina, particularly at 8-10 days of embryonic life.
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PMID:Biochemical aspects of chick embryo retina development: the effects of glucocorticoids. 270 12

The mucosa within 2 cm of cancers of the large bowel (transitional mucosa) shows histologic and histochemical changes which may indicate premalignant change. In this study, the authors used specimens from resected colonic tissue to compare morphometric, proliferative, and enzyme markers in transitional mucosa with those in cancer tissue and with those in uninvolved mucosa at least 10 cm from the cancer. Proliferative activity was assessed using the Ki 67 monoclonal antibody technique whereas a variety of methods were used to determine enzyme activities in mucosal homogenates. When compared to uninvolved mucosa, crypts in transitional mucosa contained greater number of cells, were significantly deeper and wider and were more likely to be branched. However, crypts in transitional mucosa had a significantly lower labelling index using the Ki 67 technique and there was no evidence of a shift in the proliferative zone towards the bowel lumen. The activities of ornithine decarboxylase, thymidine kinase, alkaline phosphatase, and lactate dehydrogenase were similar in transitional and uninvolved mucosa. Cancer tissue showed significantly higher levels of activity for ornithine decarboxylase and lactate dehydrogenase. Transitional mucosa showed morphometric changes but there were no proliferative or enzyme markers to suggest a higher than expected risk for malignant change.
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PMID:An assessment of proliferative and enzyme activity in transitional mucosa adjacent to colonic cancer. 275 83

Persistent slight or modest increments in blood ammonia level resulting from continuous intravenous infusion of NH4+ depressed hepatic thymidine kinase (TK) activity (DNA synthesis) by 30% after two-lobe (70%) hepatectomy, by 32% after subtotal (90%) hepatectomy, by 80% after massive injury with 1400 mg/kg acetaminophen, and by 92% after massive injury with 1000 mg/kg galactosamine. Ornithine decarboxylase activity (reflecting initiation of regeneration) was similarly depressed by 65% after 70% hepatectomy, by 58% after acetaminophen, and by 87% after galactosamine. It was not depressed after 90% hepatectomy. Intermittent marked but transient increments in blood ammonia level resulted in similar but slightly smaller enzyme reductions after the injuries with the toxins, and a reduction of 92% in TK activity after 70% hepatectomy. Thus, after toxic injury, both regenerative enzymes were substantially depressed by excess ammonia, whether present transiently in large amounts or persistently in small amounts. After partial hepatectomy, TK activity was similarly depressed by the large transient amounts of ammonia but was less affected by the persistent smaller amounts.
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PMID:Regenerative enzyme activity of the liver after partial hepatectomy or toxic injury depressed by continuous NH4+ infusion. 280 96

During permissive infection, human cytomegalovirus (HCMV) increases the activities of certain cellular enzymes. In this report, we show that induction of these cellular genes occurs at the level of RNA. The abundance of several additional growth-regulated cellular transcripts in HCMV-infected human foreskin fibroblasts (HFF) was also compared to that in serum-stimulated HFF cells. HCMV infection of HFF cells resulted in increased abundance of ornithine decarboxylase, thymidine kinase, heat-shock protein 70 (hsp70), and brain creatine kinase transcripts. In contrast to serum treatment, infection with HCMV did not result in dramatic increases in c-myc, beta-actin, or metallothionein IIA RNA. The induction of hsp70 RNA occurred during the earliest stage of HCMV infection of HFF cells, preceding its induction in serum-stimulated HFF cells by several hours. Thus, a role for the earliest events in HCMV infection in the induction of hsp70 RNA is suggested.
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PMID:Selective induction of chromosomal gene expression by human cytomegalovirus. 284 46

A number of metabolic changes within the liver occur concurrent with hepatic regeneration. These processes suggest that the administration of an antiestrogen might alter the rate of hepatic regeneration. To examine this question, male Wistar rats were treated with tamoxifen (0.1 mg/rat/day or 1.0 mg/rat/day) or vehicle for three days prior to and after partial hepatectomy, and the anatomic and biochemical process of hepatic regeneration was assessed. Tamoxifen administration caused a dose-dependent decrease in the hepatic cytosolic estrogen receptor activity and, conversely, a dose-dependent increase in cytosolic androgen receptor activity. Despite these changes in baseline hepatic sex steroid receptor status, all receptor activities were comparable between the three groups within 24 hr of partial hepatectomy. Moreover, no differences in any of the parameters assessing hepatic regeneration following partial hepatectomy were evident: liver-body ratio, ornithine decarboxylase activity, and thymidine kinase activity. This lack of effect of tamoxifen treatment on hepatic regeneration suggests either that estrogens do not play a role in the modulation of liver growth after partial hepatectomy or that, once initiated, the regenerative process per se determines a series of events that regulate hepatocellular sex hormone receptor status independent of extrahepatic stimuli.
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PMID:Effect of tamoxifen on hepatic regeneration in male rats. 291 Jun 79

In order to estimate the effects of protein and amino acids on regenerating liver, the induction of enzymes involved in synthesis of DNA was studied in rats fed protein free diet. In the regenerating livers of rats of the protein free diet, increase of liver weight and DNA content were stopped 48 hours after hepatectomy, and induction of DNA synthesizing enzymes such as dCMP deaminase, ribonucleotide reductase, and thymidine kinase were depressed and shortened. On the other hand, induction of protein or RNA synthesizing enzymes such as polyamine, ornithine decarboxylase, and tyrosine aminotransferase were not depressed by protein deprivation. The results indicate that protein deprivation inhibits the DNA synthesizing enzymes specifically, and regenerating liver cells can not enter S phase of cell cycle. When rats were maintained solely by total parenteral nutrition after hepatectomy, amino acids were essential for induction of DNA synthesizing enzymes. In particular, induction of these enzymes were regulated by 7 amino acids include Val, Leu, Ile, Met, Trp, Phe, and Thr, and most of these plasma amino acid levels were depressed after hepatectomy. By administration of amino acids for 12 hours just after hepatectomy, the DNA synthesizing enzymes were almost normally induced. This suggests that amino acids administration just after hepatectomy is effective to induce the DNA synthesizing enzymes for hepatic regeneration.
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PMID:[The effects of protein and amino acids on DNA synthesis in regenerating liver]. 308 37

To evaluate the roles of ornithine decarboxylase (ODC) and polyamines in the regulation of epithelial repair, rabbit mid-small intestine after transient ischaemic villus injury in the presence and absence of DL-difluoromethylornithine (DFMO), an irreversible inhibitor of ODC was studied. Rabbits received 2% (w/v) DFMO in drinking water for two days before undergoing a sham laparotomy, or a 90 minute mesenteric vascular occlusion of 20 cm of mid-intestine. DFMO fed and control rabbits were studied four, 24, 72, or 120 hours after this ischaemic intestinal injury. In controls, ischaemic injury caused shortened villi at four hours (p less than 0.01), diminished mucosal sucrase and alkaline phosphatase activities at 24 hours (p less than 0.05), but raised ODC (p less than 0.001) and thymidine kinase (p less than 0.01) activities at four hours with recovery by 72 hours. DFMO treatment significantly reduced ODC activity at all stages of the experiment and significantly inhibited the rise in activity observed after injury (p less than 0.01). Mucosal concentrations of the polyamines, spermidine and spermine, were similar in the sham operated groups; four hours and 24 hours after ischaemia, they increased in the DFMO animals (p less than 0.01) but fell (p less than 0.05) in those that did not receive DFMO. After ischaemic injury, DFMO treatment inhibited ODC but failed to influence recovery of villus structure or enzyme activities in the small intestine. We conclude that ODC and the polyamines, spermidine and spermine, are not key regulators of small intestinal repair after transient ischaemia.
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PMID:Failure of ornithine decarboxylase inhibition to alter small intestinal epithelial repair after transient segmental ischaemia. 313 52


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