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:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The high sensitivity of reverse transcriptase-polymerase chain reaction for detecting low copy number mRNA transcripts has been standardized to analyze the mRNA profiles of catalase, glutathione peroxidase, CuZn-superoxide dismutase and aldose reductase, with respect to the housekeeping gene cyclophilin, in rat lenses cultured in hyperglycemic (50mM glucose) or oxidative (100 microM H2O2) media for 24, 40 and 60 hr. In response to hyperglycemia mRNA expression of catalase appeared to be inhibited at 24 hr but attained normal levels by 40 hr. On the other hand, mRNA levels of catalase were higher than normal between 40 and 60 hr in the presence of H2O2. Glutathione peroxidase mRNA abundance although enhanced in response to both hyperglycemia as well as H2O2-induced stress, displayed opposite trends with time-an increase from 24-60 hr due to hyperglycemia and a decrease to normal by 60 hr in the presence of H2O2. In contrast, CuZn-superoxide dismutase was inhibited at 50 mM glucose achieving baseline levels by 60 hr, while H2O2 elicited an induction at 24 hr which waned to basal levels by 60 hr. Interestingly, aldose reductase was unaffected by hyperglycemia but showed an appreciable increase with time upon exposure of the lens to H2O2. The role of these enzymes in cataractogenesis with regard to their respective mRNA levels is discussed.
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PMID:Semi-quantitation of mRNA by polymerase chain reaction. Levels of oxidative defense enzymes and aldose reductase in rat lenses cultured in hyperglycemic or oxidative medium. 873 24

Antioxidant enzymes from S. mansoni, cytosolic Cu-Zn superoxide dismutase (CT-SOD), signal-peptide-containing SOD (SP-SOD), glutathione peroxidase (GPX), and glutathione transferase (GST) were compared for their relative levels of transcript expression throughout development in a semiquantitative reverse transcriptase-polymerase chain reaction assay. All of the antioxidant enzymes exhibited a similar pattern of developmental regulation. Adult worms have the highest level of specific mRNA compared with larval stages. GST shows the highest level of expression, being approximately 10-fold more abundant than CT-SOD and SP-SOD and 100-fold more abundant than GPX. This order of expression was nearly consistent for all the developmental stages studied. To localize the antioxidant enzymes, immunofluorescence staining was performed on 3-hr schistosomula and adult worms. GPX, SP-SOD, and CT-SOD were all found to be associated with the adult tegument and gut epithelium. SP-SOD was also associated with organelle and cell membranes of parenchymal cells and interestingly with the spines of adult worms. Schistosomula, on the other hand, showed little immunofluorescence. These studies further demonstrate the developmental regulation of antioxidant enzymes and localize them to the host-parasite interface, supporting the notion that they have a role in allowing adult worms to evade immune attack.
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PMID:Schistosoma mansoni: the developmental regulation and immunolocalization of antioxidant enzymes. 914 42

The genomes of both bacteria and eukaryotic organisms are known to encode selenoproteins, using the UGA codon for seleno-cysteine (SeC), and a complex cotranslational mechanism for SeC incorporation into polypeptide chains, involving RNA stem-loop structures. These common features and similar codon usage strongly suggest that this is an ancient evolutionary development. However, the possibility that some viruses might also encode selenoproteins remained unexplored until recently. Based on an analysis of the genomic structure of the human immunodeficiency virus HIV-1, we demonstrated that several regions overlapping known HIV genes have the potential to encode selenoproteins (Taylor et al. [31], J. Med. Chem. 37, 2637-2654 [1994]). This is provocative in the light of overwhelming evidence of a role for oxidative stress in AIDS pathogenesis, and the fact that a number of viral diseases have been linked to selenium (Se) deficiency, either in humans or by in vitro and animal studies. These include HIV-AIDS, hepatitis B linked to liver disease and cancer, Coxsackie virus B3, Keshan disease, and the mouse mammary tumor virus (MMTV), against which Se is a potent chemoprotective agent. There are also established biochemical mechanisms whereby extreme Se deficiency can induce a proclotting or hemorrhagic effect, suggesting that hemorrhagic fever viruses should also be examined for potential virally encoded selenoproteins. In addition to the RNA stem-loop structures required for SeC insertion at UGA codons, genomic structural features that may be required for selenoprotein synthesis can also include ribosomal frameshift sites and RNA pseudoknots if the potential selenoprotein module overlaps with another gene, which may prove to be the rule rather than the exception in viruses. One such pseudoknot that we predicted in HIV-1 has now been verified experimentally; a similar structure can be demonstrated in precisely the same location in the reverse transcriptase coding region of hepatitis B virus. Significant new findings reported here include the existence of highly distinctive glutathione peroxidase (GSH-Px)-related sequences in Coxsackie B viruses, new theoretical data related to a previously proposed potential selenoprotein gene overlapping the HIV protease coding region, and further evidence in support of a novel frameshift site in the HIV nef gene associated with a well-conserved UGA codon in the 1-reading frame.
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PMID:Genomic structures of viral agents in relation to the biosynthesis of selenoproteins. 915 12

Alzheimer's disease (AD) has been hypothesized to be associated with oxidative stress. In this study, the expression of key oxidative stress-handling genes was studied in hippocampus, inferior parietal lobule, and cerebellum of 10 AD subjects and 10 control subjects using reverse transcriptase-polymerase chain reaction (RT-PCR). The content of Mn-, Cu,Zn-superoxide dismutases (Mn- and Cu,Zn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GSSG-R) mRNAs, and the "marker genes" (beta-actin and cyclophilin) mRNAs was determined. This study suggests that gene responses to oxidative stress can be significantly modulated by the general decrease of transcription in the AD brain. To determine if the particular oxidative stress handling gene transcription was induced or suppressed in AD, the "oxidative stress-handling gene/beta-actin" ratios were quantified and compared with control values in all brain regions studied. The Mn-SOD mRNA/beta-actin mRNA ratio was unchanged in all regions of the AD brain studied, but an increase of the Cu,Zn-SOD mRNA/beta-actin mRNA ratio was observed in the AD inferior parietal lobule. The levels of peroxidation handling (CAT, GSHPx, and GSSG-R) mRNAs normalized to beta-actin mRNA level were elevated in hippocampus and inferior parietal lobule, but not in cerebellum of AD patients, which may reflect the protective gene response to the increased peroxidation in the brain regions showing severe AD pathology. The results of this study suggest that region-specific differences of the magnitude of ROS-mediated injury rather than primary deficits of oxidative stress handling gene transcription are likely to contribute to the variable intensity of neurodegeneration in different areas of AD brain.
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PMID:The expression of key oxidative stress-handling genes in different brain regions in Alzheimer's disease. 1009 42

Because programmed cell death (PCD) is an important mode of pericyte dropout in human diabetic retinopathy, whether increased oxidative stress in cells with diminished antioxidant defenses plays a causative role in the PCD process in diabetic pericytes has been studied. Ten diabetic and eight non-diabetic eye-bank eyes from 5 diabetic and 4 non-diabetic patients were included in this study. From individual neural retinas pericytes were isolated by a newly developed immunomagnetic technique. Total mRNA of the purified pericytes was isolated for quantitative reverse transcriptase (RT)-PCR assay. mRNA levels of a death protease (CPP32), the major enzyme that initiates the proteolytic cascade leading to cell death, were determined in association with the expression of antioxidative enzymes including glutathione peroxidase (GSH-Px), glutathione reductase, CuZn superoxide dismutase (SOD), MnSOD and catalase genes in pericytes. In comparison with pericytes from non-diabetic retinas, pericytes from diabetic retinas highly expressed CPP32 genes (4 +/- 0.6 fold increase, p < 0.01, n = 9). In diabetic pericytes, up-regulation of glutathione peroxidase (GSH-Px) (8.2 +/- 0.9 fold increase, p < 0.01, n = 9) and down-regulation of glutathione reductase (Gr) (4.1 +/- 0.4 fold decrease, p < 0.05, n = 9) and CuZnSOD (2.1 +/- 0.7 fold decrease, p < 0.05, n = 9) were observed. mRNA levels of MnSOD and catalase of diabetic pericytes did not differ significantly from those of non-diabetic pericytes. Overexpression of a member of interleukin-1 beta-converting enzyme (ICE) family, CPP32, indicated that the pericytes from diabetic retinas are in a "pre-PCD" state. This is the first evidence that the ICE family of death proteases is involved in pericyte dropout in diabetes. In these pre-PCD cells, the expression of antioxidant enzyme genes also was changed. Up-regulation of GSH-Px indicates a compensation mechanism to meet the demand of excessive glutathione in reduced form. Decreased levels of both glutathione reductase and CuZnSOD, despite the oxidative stress in the diabetic condition, suggest the breakdown of the antioxidant defense in pericytes. Most importantly, the altered gene profile of scavenging enzymes under diabetic conditions, correlating with overexpression of the cell death protease gene, together suggest increased oxidative stress as an etiological agent of pericyte dropout in diabetic retinopathy.
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PMID:Altered mRNA levels of antioxidant enzymes in pre-apoptotic pericytes from human diabetic retinas. 1009 40

The aim of this work was to study the induction and secretion of interleukin 8 (IL-8) and some oxidative stress parameters after ethanol (EtOH), acetaldehyde (Ac) or lipopolysaccharide (LPS) treatment on HepG2 cells. Cells were treated with 50 mM EtOH, 175 &mgr;M Ac or 1 &mgr;g/ml of LPS. IL-8 induction and secretion were determined in the presence of the toxics, and the effect of antioxidants N-acetyl-L-cysteine and 1,1,3,3-tetramethyl-2-thiourea was evaluated. Further, the effect of adding polyclonal anti-human tumor necrosis factor alpha (TNF-alpha) and H(2)O(2) was studied, and catalase, superoxide dismutase and glutathione peroxidase activities were determined. Lipid peroxidation increased significantly only in Ac-treated cells. All toxics failed to decrease significantly the intracellular levels of reduced GSH. Catalase activity was diminished in all treatments, while other enzyme activities did not present changes. No change in peroxide production was found with any treatment. IL-8 secretion increased in Ac (41%) and in LPS (38%)-treated cells. Antioxidant and anti-TNF-alpha treatments decreased IL-8 secretion. H(2)O(2) (0.25 mM)-treated cells increased IL-8 secretion. IL-8 reverse transcriptase-polymerase chain reaction results correlated with secretion values. Our results show that Ac and LPS treatment produced an increased IL-8 induction and secretion. Oxidative stress and TNF-alpha are mediators in IL-8 response. This observation suggests that in the in vivo liver, the mechanism of ethanol-induced IL-8 production requires ethanol metabolism, and hepatocytes do not require the interaction among different populations of liver cells to respond.
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PMID:Interleukin 8 response and oxidative stress in HepG2 cells treated with ethanol, acetaldehyde or lipopolysaccharide. 1280 41

We recently showed that zerumbone, a sesquiterpene found in subtropical ginger, suppresses colonic tumor marker formation in rats and induces apoptosis in colon cancer cell lines. In our present study, the anti-tumor initiating and promoting activities of zerumbone in mouse skin were evaluated using a conventional 2-stage carcinogenesis model. A single topical pretreatment to mouse skin (2 micromol) 24 hr before application of dimethylbenz[a]anthracene (0.2 micromol) markedly suppressed tumor incidence by 60% and the number of tumors by 80% per mouse. Repeated pretreatment (16 nmol) twice weekly during the post-initiation phase reduced the number of 12-O-tetradecanoylphorbol-13-acetate (TPA, 1.6 nmol)-induced tumors by 83% as well as their diameter by 57%. Multiple reverse transcriptase (RT) PCR experiments revealed that zerumbone (2 micromol) enhanced the mRNA expression level of manganese superoxide dismutase, glutathione peroxidase-1, glutathione S-transferase-P1 and NAD(P)H quinone oxidoreductase in the epidermis, but not that of cytochrome p450 1A1 or 1B1. Further, it diminished TPA-induced cyclooxygenase-2 protein expression and phosphorylation of extracellular signal-regulated kinase 1/2, while pretreatment(s), in either the priming or activation stage or both, reduced double TPA application-induced hydrogen peroxide formation and edema induction by 29% to 86%, respectively. Histologic examination revealed that pretreatment(s) with zerumbone suppressed leukocyte infiltration and reduced proliferating cell nuclear antigen-labeling indices. Together, our results indicate that zerumbone is a promising agent for the prevention of both tumor initiating and promoting processes, through induction of anti-oxidative and phase II drug metabolizing enzymes as well as attenuation of proinflammatory signaling pathways.
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PMID:Zerumbone, a sesquiterpene in subtropical ginger, suppresses skin tumor initiation and promotion stages in ICR mice. 1512 79

Our previous study reported that oxysterol cholestane-3beta,5 alpha, 6 beta-triol (Triol) induced vascular smooth muscle cells (VSMCs) apoptosis, which was inhibited by selenium pretreatment. To further investigate the mechanisms of the inhibition, the glutathione peroxidase (GPx) activity, the total antioxidant capacity (T-AOC), the total superoxide dismutase (SOD) activity, and the level of lipid peroxidation (the content of malondialdehyde, MDA) of VSMCs were measured, and fluidity of cell membrane, reactive oxygen species (ROS) level, the reduction of mitochondrial membrane potential (Delta psi(m)), and the intracellular Ca(2+) in single cell were detected using several fluorescence indicators. Meanwhile, the mRNA levels of c-myc, bcl-2, GPx, and thioredoxin reductase (TR) were measured by reverse transcriptase polymerase chain reaction (RT-PCR) analysis. The results showed that the decrease of GPx activity, T-AOC, SOD activity, the fluidity of cell membrane, the Delta psi(m), and the mRNA expression of c-myc, bcl-2, GPx, and TR of VSMCs and the increase of MDA, ROS generation, and intracellular Ca(2+), significantly induced by Triol (10 microM, 24h) were inhibited to a different extent, respectively, when cells were pretreated with sodium selenite (50 nM, 12 or 24h) before exposure to Triol. These effects were time dependent and enhanced with prolongation of the time of pretreatment. In conclusion, the results in the present work showed that the mechanism of selenium inhibition of cell apoptosis induced by oxysterols in rat VSMCs was related with the antioxidation of selenoproteins.
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PMID:Mechanisms of selenium inhibition of cell apoptosis induced by oxysterols in rat vascular smooth muscle cells. 1603 82

In the present study, we investigated the expression of protease-activated receptors (PARs), receptors for thrombin, in substantia nigra pars compacta (SNpc) of Parkinson disease (PD) brains and cultures of human neurons, astrocytes, oligodendrocytes, and microglia as determined by immunocytochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR). Expression of PAR-1 was demonstrated only in glial fibrillary acidic protein-positive astrocytes in SNpc, and the number of astrocytes expressing PAR-1 increased in SNpc of PD as compared with nonneurologic control brain. Immunoreactivity for thrombin and prothrombin was stronger in astrocytes and the vessel walls in SNpc of PD brains. PAR-1 was expressed in human astrocytes and neurons, but not in oligodendrocytes or microglia as determined by RT-PCR. We investigated thrombin-mediated activation of human astrocytes. Thrombin treatment activates human astrocytes and induces morphologic change and a marked increase in proliferation of astrocytes. Increased expression of glial cell line-derived growth factor and glutathione peroxidase (GPx) but no change in the expression of nerve growth factor and inflammatory cytokines/chemokine (IL-1beta, IL-6, IL-8, MCP-1) was found in thrombin/PAR-activated astrocytes. Next, we studied the neuroprotective effect exerted by thrombin-activated astrocytes in human cerebral neuron x human neuroblastoma hybrid neurons. Although thrombin showed neurotoxicity against human hybrid neurons in a dose-dependent manner, the conditioned media derived from thrombin-pretreated astrocyte cultures promoted the survival of human hybrid neurons. The protective effect was completely inhibited with a GPx inhibitor, mercaptosuccinic acid, indicating that GPx released from thrombin/PAR-activated astrocytes is responsible for neuroprotection of hybrid neurons against thrombin cytotoxicity. The present study suggests that the increased expression of PAR-1 in astrocytes in SNpc of PD brain is the restorative move taken by the brain to provide neuroprotection against neuronal degeneration and cell death of dopaminergic neurons caused by noxious insults during the progression of PD pathology.
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PMID:Upregulation of protease-activated receptor-1 in astrocytes in Parkinson disease: astrocyte-mediated neuroprotection through increased levels of glutathione peroxidase. 1641 Jul 50

Reactive oxygen species (ROS) are formed by all aerobic organisms, and are involved in the numerous physiological and pathophysiological processes. Opioid peptides belong to a class of bioactive compounds of great interest because of their opiate-like activity. We determined the influence of methionine-enkephalin (MENK) on age-associated oxidant/antioxidant status in liver of CBA mice. Lipid peroxidation (LPO), total superoxide dismutase (tSOD), catalase (CAT), and glutathione peroxidase (Gpx) activities of 1, 4, 10 and 18 months old male and female control and MENK treated (10 mg/kg bw) CBA mice were determined. MENK showed gender-related effect on both oxidant/antioxidant parameters. It stimulated LPO in males, but suppressed in females. CAT and Gpx activities were lowered upon MENK exposure in males, but in females the activities were modulated by MENK. The relative mRNA levels for the antioxidant enzymes CuZnSOD, MnSOD, CAT and Gpx-1 were determined by reverse transcriptase polymerase chain reaction (RT-PCR) in groups where differences in activities between control and treated samples were observed. Changes of mRNA level in MENK treated groups showed that transcriptional regulation is both gender- and age-related. Comparison of enzyme activities and mRNA levels in control and MENK treated groups showed that, in some cases parallel changes occurred, while in other cases nonparallel changes were found. These results suggest that transcriptional changes are in accordance with enzyme activities in some cases, while in other cases posttranscriptional regulation of antioxidant enzymes may exist.
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PMID:Methionine-enkephalin modulated regulation of oxidant/antioxidant status in liver of CBA mice. 1651 20


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