Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various in vitro-inhibitors were added with 3H-benzo(a)pyrene (BP) into the perfusion fluids in isolated rat lung perfusions to see whether their effects are dependent on the integrity of tissue. 3H-BP and its metabolites were measured by thin-layer chromatography and radiometry from both samples of perfusion medium and homogenates of lung tissue. The total covalent binding to lung tissue was used as a measure of the formation of reactive metabolites. In methylcholanthrene-induced rat lung, the metabolism of BP was inhibited by alpha-naphthoflavone, an inhibitor of monooxygenase, and less with diethylmaleate, a depletor of glutathione, with salicylamide, an inhibitor of conjugases, and, astonishingly, with D-saccharo-1,4-lactone, an inhibitor of beta-glucuronidase. With trichloropropene oxide, which inhibits epoxide hydratase, the metabolism was either decreased or unchanged. Nicotine had no effect on BP-metabolism. Nicotine and diethylmaleate increased statistically significantly and alpha-naphthoflavone and salicylamide decreased the covalent binding of radioactivity to lung tissue. In most cases, the changes in BP metabolism observed during perfusion can be explained on the basis of effects of modifiers on the enzyme systems.
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PMID:Effects of various in vitro--inhibitors of benzo(a)pyrene metabolism in isolated rat lung perfusion. 47 52

Recently, the detection of urinary glucuronide conjugates of nicotine and its two major metabolites, trans-3'-hydroxycotinine and cotinine, showed that glucuronidation is an important pathway of nicotine metabolism in humans. (S)-(-)-Nicotine-N(+)-1-beta-glucuronide (quaternary N-glucuronide with linkage through the pyridino-nitrogen of nicotine) was shown to be an important nicotine metabolite of humans in vivo. The present study was undertaken to develop an animal model for this process, in order to ascertain the factors influencing quaternary N-glucuronide formation. (S)-(-)-Nicotine-N(+)-1-beta-glucuronide was formed in vitro when [2'-14C]-nicotine was incubated with Triton X-100 activated marmoset hepatic microsomes in the presence of uridine diphosphoglucuronic acid; it was not formed when activated microsomal preparations of rabbit, guinea-pig, or rat were used as enzyme source. The glucuronide was characterised by comparison with authentic synthetic (S)-(-)-nicotine-N(+)-1-beta-glucuronide using HPLC. The rate of formation of the glucuronide was almost linear during up to four hours of incubation, but still only accounted for a maximum of 6.0% of the available substrate at the end of five hours incubation. The synthetic and biosynthetic (S)-(-)-nicotine-N(+)-1-beta-glucuronides were hydrolysed by beta-glucuronidase and alkali, but were resistant to acid hydrolysis. The results support the concept that the marmoset may be a good animal species to mimic man in studies of nicotine metabolism during exposure to tobacco smoke. In vitro studies using (+/-)-trans-3'-hydroxycotinine or (S)-(-)-cotinine (as potential substrate) and [14C]-uridine diphospho-glucuronic acid (as cofactor) failed to produce any new radiolabelled glucuronide when the above microsomal preparations were used.
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PMID:Evidence for the biosynthesis of A glucuronide conjugate of (S)-(-)-nicotine, but not (S)-(-)-cotinine or (+/-)-trans-3'-hydroxycotinine by marmoset hepatic microsomes. 1071 38

Nicotine alkaloids are synthesized in the root of Nicotiana species, and their synthesis increases after insect attack, wounding and jasmonate treatment of the leaf. Putrescine N-methyltransferase (PMT) catalyzes the first committed step in nicotine biosynthesis. The expression patterns of the three Nicotiana sylvestris PMT genes (NsPMT1, NsPMT2, and NsPMT3) are reported in this study. Transcripts of the NsPMT genes were detected only in the root, and were up-regulated by methyl jasmonate treatment. When the 5'-flanking regions of NsPMT1, NsPMT2, and NsPMT3 were fused independently to beta-glucuronidase reporter gene and introduced into N. sylvestris by Agrobacterium-mediated transformation, all introduced transgenes were expressed in the cortex, endodermis, and xylem in the root, as well as upregulated by methyl jasmonate treatment. These qualitatively similar patterns of expression for the NsPMT genes are achieved with only 0.25 kb of their conserved 5'-flanking regions, which contained no known jasmonate-responsive elements.
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PMID:Jasmonate induction of putrescine N-methyltransferase genes in the root of Nicotiana sylvestris. 1096 39

Mitogen-activated protein kinase (MAPK) cascades play a pivotal role in environmental responses and developmental processes in plants. Previous researches mainly focus on the MAPKs in groups A and B, and little is known on group C. In this study, we isolated and characterized GhMPK7, which is a novel gene from cotton belonging to the group C MAPK. RNA blot analysis indicated that GhMPK7 transcript was induced by pathogen infection and multiple defense-related signal molecules. Transgenic Nicotina benthamiana overexpressing GhMPK7 displayed significant resistance to fungus Colletotrichum nicotianae and virus PVY, and the transcript levels of SA pathway genes were more rapidly and strongly induced. Furthermore, the transgenic N. benthamiana showed reduced ROS-mediated injuries by upregulating expression of oxidative stress-related genes. Interestingly, the transgenic plants germinated earlier and grew faster in comparison to wild-type plants. beta-glucuronidase activity driven by the GhMPK7 promoter was detected in the apical meristem at the vegetative stage, and it was enhanced by treatments with signal molecules and phytohormones. These results suggest that GhMPK7 might play an important role in SA-regulated broad-spectrum resistance to pathogen infection, and that it is also involved in regulation of plant growth and development.
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PMID:GhMPK7, a novel multiple stress-responsive cotton group C MAPK gene, has a role in broad spectrum disease resistance and plant development. 2060 49