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:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of acetaldehyde administration for 4 weeks on antioxidant protection systems was investigated in liver of rats. Liver SOD activity was decreased from control value 542.4 U/g of tissue to 411.2 U/g of tissue in experimental group (24% decrease). GSH-Px activity was practically unchanged and liver CAT activity was significantly decreased (35%). Sulfhydryl compounds in liver non-proteins following ACH treatment were decreased from 4.22 mumol/g of tissue in control group to 2.86 mumol/g of tissue (23%). Furthermore acetaldehyde treatment caused significant increase in MDA level in liver (78% increase).
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PMID:The diminution of liver glutathione content and changes in activities of antioxidant enzymes in long-term acetaldehyde poisoning. 128 37

Some of the phenothiazines and dibenz[b,f]azepines exert an antiproliferative effect on HEp-2 and rat prolactinoma cells. The same compounds also have effects on different membrane-bound biochemical events, such as H2O2 formation and the peroxide-generated chemiluminescence of polymorphonuclear leukocytes. The superoxide dismutase inhibition by 7,8-dioxochlorpromazine and 6,9-dioxochlorpromazine have some relation to the growth inhibitory action on the growth of HEP-2 and prolactinoma cells in vitro. The antiproliferative effects of phenothiazines were synergized with resistance modifiers like verapamil, omeprazole and tubulozole-C, due to increased drug-influx or decreased drug-efflux and due to possible action on the cytoskeleton.
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PMID:In vitro antiproliferative effects of tricyclic psychopharmaceutical agents and synergism with some resistance modifiers. 156 77

In isoprenaline-induced myocardial infarction in rabbits, the circulating neutrophils (neu) were in an activated state. tanshinone (tan, ig) suppressed the neu functions (acid-phosphatase release, adhesiveness, and phagocytosis) dose-dependently and reduced myocardial necrosis concomitantly. There was a positive correlation between neu functions and myocardial necrosis. In addition, tan caused an obvious decrease in content of lipoperoxide malondialdehyde in serum and myocardium, an increase in superoxide dismutase activity, an inhibition of leukocytic infiltration, and a production of prostaglandin E2 in myocardium. These effects were also related closely to the suppression of neu functions. Anti-inflammatory drug dexamethasone was used as control and had similar effects on Neu functions and myocardial infarction. It is suggested that the prophylactic effects of tan on myocardial infarction may result from the inhibition of circulating neu functions.
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PMID:[Relationship between inhibitory action of tanshinone on neutrophil function and its prophylactic effects on myocardial infarction]. 178 Dec 93

The dioxathiadiaza-heteropentalenes, HEP-I (4,4-dimethyl-1,7-dioxa-2,6-diaza- 7 alpha lambda 4-thia-3H,5H-benzo[cd]pentalene), HEP-II (1,7-dioxa-2, 6-diaza-4, 7 alpha lambda 4-dithia-3H, 5H-benzo[cd]pentalene), HEP-III (1,7-dioxa-2,6-diaza-4, 7 alpha lambda 4-dithia-3H, 5H-benzo[cd]pentalene-4-oxide), and HEP-IV (1,7-dioxa-2,6-diaza-4,7 alpha lambda 4-dithia-3H, 5H-benzo[cd]pentalene-4,4-dioxide), inhibited growth of Escherichia coli in a simple glucose-salt medium, with their toxicities following the order of HEP-IV greater than HEP-III greater than HEP-II greater than HEP-I. These toxicities could be suppressed by yeast extract added to the glucose-salt medium. Yeast extract also facilitated maximal induction of superoxide dismutase (SOD) and catalase. The redox potentials of HEP-I-HEP-IV and the rates of oxygen uptake dependent on heteropentalenes in cyanide-resistant respiration of E. coli were correlated with the induction of SOD and catalase. Thus, the higher the redox potential of the compounds, the more potent they were for induction of enzyme production. Under anaerobic conditions, HEP-IV did not inhibit E. coli growth. These results indicate that HEP-I-HEP-IV can be reduced within the cell of E. coli and then reoxidized by molecular oxygen, generating O2- and H2O2. The toxicities of the heteropentalenes depend largely upon superoxide and/or hydrogen peroxide toxicity, and SOD and catalase provide a defense against the potential cytotoxicity of these species.
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PMID:Dioxathiadiaza-heteropentalenes mediate superoxide and hydrogen peroxide production in Escherichia coli. 253 60

An interest to the study of superoxide dismutase (SOD) is growing as it has become known that this enzyme may be used as a medical preparation and in the biochemical research. The aim of the work presented is to investigate the influence of temperature and UV radiation on the structural-functional properties of SOD. Copper- and zinc-containing SOD from bovine erythrocytes with the light of a DRT-400 lamp (dose of irradiation 1.5 x 10(3) J/m2) through an UFS-1 light filter (240-390 nm). The influence of temperature (20-85 degrees C) on the functional properties of native and UV modified SOD has been studied. The process of thermodenaturation of the enzyme proceeds at least two consecutive stages. SOD is stable within the temperature interval 20-70 degrees C. Kinetics of thermodenaturation of protein has been studied. It was established that UV light increases enzyme thermostability. Changes found in the kinetic characteristics of the UV-irradiated SOD are apparently due to its conformational rearrangements.
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PMID:[Kinetic regularities of thermal inactivation of superoxide dismutase]. 855 68

To test the hypothesis that oxygen radicals play an important role in the nonvagal component of the noncholinergic bronchoconstriction in vivo, 37 guinea pigs weighing 329 +/- 8 g were randomly divided into five groups: group 1, vagotomy; group 2, vagotomy + CAT (catalase); group 3, vagotomy + SOD (superoxide dismutase); group 4, vagotomy + PBN (alpha-phenyl-N-tert-butyl nitrone); and group 5, capsaicin pretreatment. CAT, SOD, and PBN are antioxidants. Each animal was anesthetized, paralyzed, artificially ventilated, and pretreated with atropine and phenoxybenzamine. Immediately after acute capsaicin challenge, animals in group 1 exhibited decreases in maximal expiratory flow, dynamic respiratory compliance, and total lung capacity, as well as an increase in functional residual capacity, indicating noncholinergic airway constriction. The bronchoconstriction was significantly ameliorated by SOD and PBN, and it was almost abolished by capsaicin pretreatment. Thirty minutes after acute capsaicin challenge, there was a significant decrease in airway NEP activity and an increase in lung substance P level in group 1 but not in other groups. These results indicate that nonvagal component of noncholinergic bronchoconstriction is partially modulated by oxygen radicals.
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PMID:Oxygen radicals in the nonvagal component of noncholinergic airway constriction. 889 67

We investigated the efficacy in reducing myocardial preservation and reperfusion (P/R) injury of direct hydroxyl radical scavenging by nicaraven as compared with scavenging of both superoxide radicals and hydrogen peroxides by superoxide dismutase (SOD) and catalase (CAT), respectively. Isolated rat hearts were mounted on a Langendorff (L) apparatus to estimate the baseline aortic flow (AF), coronary flow (CF), cardiac output (CO), systolic pressure (SP), aortic mean pressure (MP), rate pressure product, and LV dp/dt. They were divided into 3 groups: group 1, 12 hr storage in HTK solution; group 2, 12 hr storage in HTK solution containing 2.5x10(5) U/L SOD and 2x10(5) U/L mg/L CAT; and Group 3, 12 hr storage in HTK solution containing 10(-3) M nicaraven. SOD, CAT, and nicaraven were administered intraperitoneally before harvesting. Hearts were stored in each preservation solution at 4, and then reperfused. Postpreservative function and concentrations of leaked enzymes were measured. The hearts were switched back to the L-mode and paced at 330 beats/min. CF following perfusion with Krebs-Henseleit bicarbonate buffer (KHB) solution containing 10(-6) M 5-hydroxytryptamine (5-HT) or 10(-5) M nitroglycerin (NTG) then evaluated. The myocardial water content also was measured. The recovery of CF, CO, SP, MP, and LV dp/dt was significantly greater in group 3 than in group 1. The recovery of CF was superior to that in group 2 (P<0.05). There were no significant differences in the recovery of cardiac function between groups 1 and 2. 5-HT caused a decrease in CF in each group, however, CF in group 3 was higher than that in group 1 (P<0.05). NTG caused no significant differences among the groups. There were no significant differences in leaked enzymes and myocardial water content among the three groups. These results suggest that nicaraven protects against myocardial P/R injury through its hydroxyl radical scavenging activity, and that therapy with oxygen-free radical scavengers should be directed toward inactivation of hydroxyl radicals rather than superoxide radicals and/or hydrogen peroxides.
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PMID:The role of a hydroxyl radical scavenger (nicaraven) in recovery of cardiac function following preservation and reperfusion. 890 Mar 8

Osteoclast development from hematopoietic bone marrow precursors is associated with the expression of various enzymes, receptors, adhesion molecules, and other specialized components. Among these is a novel 150 kD superoxide dismutase-related membrane glycoprotein, originally identified by its reaction with the anti-osteoclast monoclonal antibody 121F. This antigen is uniquely restricted to osteoclasts in bone, universally present on osteoclasts from multiple species, induced during osteoclast differentiation in vitro and in ovo, and required at high levels for avian osteoclastic bone pit resorption. Expression of a comparable human antigen was investigated using human leukemic FLG 29.1 cells capable of differentiating towards an osteoclast-like phenotype. Phorbol ester, 1,25 (OH)2 vitamin D3, and osteoblast-derived soluble factors elicited dose and time-dependent inductions of this antigen as measured by enzyme-linked immunosorbent assay (ELISA) and immunocytochemical staining, coincident with their display of multiple other osteoclastic features. Synergistic interactions of these modulators led to further elevations in the ultimate expression levels of this antigen, although not to the full extent associated with in vivo-formed avian osteoclasts. The potent antiresorptive hormone 17beta-estradiol, but not its inactive alpha isomer, partially suppressed the phorbol ester-induced elevation of the 121F antibody-reactive antigen in FLG 29.1 cells as it does in avian osteoclast-like cells. Characterization of the human antigen isolated from FLG 29.1 cells by 121F immunoaffinity purification demonstrated that this regulated membrane component was synthesized by these human cells, more abundant following their differentiation into osteoclast-like cells, and similar biochemically and immunologically to the 150 kD integral membrane glycoprotein previously described from avian osteoclasts. Therefore, this report is the first documentation that human osteoclast-like FLG 29.1 cells express, in a developmentally regulated fashion, a homolog of the specific 150 kD avian osteoclast surface antigen that is related to superoxide dismutase, a protective free radical scavenging enzyme and is essential for osteoclastic bone resorption.
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PMID:A human homolog of the 150 kD avian osteoclast membrane antigen related to superoxide dismutase and essential for bone resorption is induced by developmental agents and opposed by estrogen in FLG 29.1 cells. 905 69

Exposure to silica has been associated with progressive pulmonary inflammation and fibrosis. While the fibroblasts play an important role in the pathogenesis of silicosis, the direct interaction between silica and fibroblasts is poorly understood. We observed that silica particles stimulated intracellular ROS generation in Rat2 fibroblast, evidenced by DCFH oxidation. Silica-induced DCFH oxidation was inhibited by catalase and DPI, a flavoenzyme inhibitor. Additionally, the time course of elevation of the intracellular ROS was paralleled by the increases of MEK and ERK phosphorylation. Silica-induced ERK phosphorylation was also effectively attenuated by catalase and DPI. However, SOD enhanced the silica-induced ERK phosphorylation, indicating a role for H(2)O(2) in ERK activation. Furthermore, ERK and MEK phosphorylation are reproduced by H(2)O(2) treatment. Taken together, these results demonstrate that silica stimulates ROS production via flavoenzyme-dependent mechanism in Rat2 fibroblasts and the H(2)O(2), in turn, serves as a signal transduction element in activating MEK-ERK pathway.
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PMID:Silica-induced generation of reactive oxygen species in Rat2 fibroblast: role in activation of mitogen-activated protein kinase. 1047 90

We have now found that the most potent, Cpd 5 [2-(2-mercaptoethanol)-3-methyl-1, 4-napthoquinone], inhibits growth of doxorubicin-resistant and doxorubicin-sensitive breast cancer cells (MCF 7r and MCF 7w) in culture. Growth inhibition by Cpd 5 was antagonized by the thiol antioxidants glutathione and cysteine, but not by catalase or superoxide dismutase, suggesting that growth inhibition is probably via conjugation of cellular thiols. In support of this, we found that Cpd 5 inhibited the activity of thiol containing cellular protein tyrosine phosphatase (PTP) enzyme, with consequent induction of various tyrosine phosphoproteins, but not serine or tyrosine phosphoproteins. The tyrosine phosphorylation was also inhibited by exogenous glutathione or cysteine and could be enhanced by depletion of cellular glutathione by BSO. This effect of Cpd 5 on protein tyrosine phosphorylation was highly selective, however. Tyrosine phosphorylation of EGF-R, Erb-B2, and ERK1/2 was increased, but not that of Insulin-R or JNK. ERK1/2 tyrosine phosphorylation and growth inhibition increased with increasing concentrations of Cpd 5. Furthermore, suppression of Cpd 5-mediated ERK1/2 phosphorylation by an ERK-kinase inhibitor antagonized growth inhibition. These results suggest a strong correlation between ERK1/2 phosphorylation by Cpd 5 and growth inhibition. This novel K-vitamin analog thus inhibits MCF 7 cell growth and induces selective protein tyrosine phosphorylation.
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PMID:Growth inhibition and protein tyrosine phosphorylation in MCF 7 breast cancer cells by a novel K vitamin. 1105 8


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