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:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of catalase, glutathione peroxidase, superoxide dismutase, O-demethylase, ATPase and succinate dehydrogenase, belonging to two main classes of detoxification enzymes (i.e. hydrolases and oxido-reductases), mostly involved in metabolism and degradation of xenobiotics in insects, were assessed under the influence of kinetin, a plant growth regulator (PGR). The nymphs (48-52 hr old) of Lipaphis erysimi (Kalt.) were permitted to feed on radish plant, Raphanus sativus L. treated with kinetin (400 ppm) for 13, 25 and 37 hr. It was found that the activity of catalase, glutathione peroxidase and superoxide dismutase increased significantly when compared with the control of the same age group, which indicated that these enzymes might be playing a significant role in the metabolism of kinetin in this insect. The activity of O-demethylase showed an increase up to 25 hr of the treatment but it decreased under prolonged treatment whereas the activity of succinate dehydrogenase fluctuated insignificantly. ATPase showed a decrease in the activity with the treatment suggesting kinetin's interference in synthesis of ATPase.
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PMID:Studies on the role of six enzymes in the metabolism of kinetin in mustard aphid, Lipaphis erysimi (Kalt.). 1740 53

Selenium (Se) is an essential element that may bioaccumulate to toxic levels. In fish, the major toxicity symptom is larval teratogenic deformities, but little is known about the effect of Se on other systems such as the physiological stress response and oxidative stress. To test the hypothesis that Se is a chemical stressor that causes toxicity through oxidative stress, juvenile rainbow trout were exposed to waterborne sodium selenite, and physiological stress response and stress-related parameters (plasma cortisol, glucose, T3 and T4, gill Na+/K+-ATPase, the ability of the head kidney to secrete cortisol, and condition factor) and hepatic oxidative stress indicators (reduced glutathione, glutathione peroxidase, and lipid peroxidation) were measured after 96 h (acute exposure to 0-2.67 mg/L Se) and 30 days (sub-chronic exposure to 0-0.16 mg/L). Acute exposure to waterborne sodium selenite significantly increased plasma cortisol levels (control=0.01+/-0.0 ng/mL, and 2.52 mg/L Se=73.5+/-22 ng/mL) and plasma glucose levels (control=0.75+/-0.1 mg/mL, and 3.60 mg/L Se=1.64+/-0.2 mg/mL), but gill Na+/K+-ATPase activities, plasma T3 and T4 levels, and condition factor were unchanged. The 96 h acute selenite exposure decreased hepatic reduced glutathione levels (control=18.4+/-1.5 micromol/mg protein, and 3.60 mg/L Se=12.4+/-1.1 micromol/mg protein). Lipid peroxidation levels (0.03-0.08 U/mg protein) and glutathione peroxidase (3.7-6.0 mU/mg protein) activities significantly varied with treatment. The 30 days sub-chronic exposure increased plasma cortisol, T3, and T4, but there was no effect on plasma glucose levels, gill Na+/K+-ATPase activity, the ability to secrete cortisol, and condition factor. The 30 days sub-chronic exposure to selenite did not alter antioxidant activities or lipid peroxidation levels. These experiments show, for the first time, that exposure to waterborne selenite up to 0.1mg/L, activates the physiological stress response in fish but does not impair cortisol secretion after 30 days. The decrease in reduced glutathione in juvenile rainbow trout subjected to the acute sodium selenite exposure suggests that oxidative stress may play an important role in the effects of Se in fish.
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PMID:Effects of acute and subchronic exposures to waterborne selenite on the physiological stress response and oxidative stress indicators in juvenile rainbow trout. 1756 97

The incorporation of plant-based ingredients, and the possible carry-over of pesticides such as endosulfan, in fish feeds may present new toxicological challenges to aquacultural species. Biological responses of Atlantic salmon (Salmo salar) to a 35-day dietary endosulfan exposure at levels ranging from 4 to 710 microgkg(-1) were assessed using tissue histology and biochemistry. Liver 7-ethoxyresorufin-O-deacetylase (EROD) activity was significantly elevated in the highest exposure group (710 microgkg(-1)) by day 35. Other hepatic indicators of stress impacts and responses (glutathione-S-transferase and glutathione peroxidase activities and hepatic alpha-tocopherol content) remained unchanged. Branchial Na(+), K(+)-ATPase activity was significantly reduced at day 14 in the highest exposure group, but returned to control levels by day 35. Conversely, intestinal Na(+), K(+)-ATPase activity was significantly inhibited at day 35, but again only at the highest exposure level. In contrast to the biochemical results, hepatic and intestinal histology revealed effects of exposure even at the lowest dose tested (4 microgkg(-1)). In the posterior intestine, pathology was characterised by vacuolation and fusion of villi, and in the most severe cases, loss of epithelial integrity in villi tips. In the liver the primary effects were glycogen depletion and lipidosis. These changes were typical of a generalised stress response. While histology endpoints may prove to be the most sensitive indicators of dietary endosulfan exposure, the organismal relevance of these structural changes must be considered in the absence of effects in other biomarkers at dietary levels less than 710 microgkg(-1).
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PMID:Assessing the sensitivity of Atlantic salmon (Salmo salar) to dietary endosulfan exposure using tissue biochemistry and histology. 1767 76

The neuroprotective effects of catalpol, an iridoid glycoside isolated from the fresh Rehmannia roots, on the senescent mice induced by D-galactose were assessed. The mice subcutaneously injected with catalpol (5 or 10 mg/kg, 2 weeks, from fifth week) showed significantly improved learning and memory ability in Morris water maze test compared with d-galactose treated mice (150 mg/kg, 6 weeks). We further investigated the mechanism involved in the neuroprotective effects of catalpol on the mice brain tissue. The results showed that catalpol increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), decreased the malondialdehyde (MDA) level, elevated the activities of Na+ -K+ ATPase and Ca2+ -Mg2+ ATPase on the cerebral cortex and hippocampus of d-galactose treated mouse. All the data suggested that catalpol had the potential to be a useful cognitive impairment treatment, and its beneficial effects may be partly mediated via enhancing endogenous antioxidant enzymatic activities and inhibiting free radical generation.
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PMID:Catalpol ameliorates cognition deficits and attenuates oxidative damage in the brain of senescent mice induced by D-galactose. 1769 78

The present study sought to evaluate the effect of a newly synthesized selenium compound, dicholesteroyl diselenide (DCDS) and diphenyl diselenide (DPDS) on the activities of delta-aminolevulinate dehydratase and Na+/K+-ATPase in the rat brain. The glutathione peroxidase mimetic activity of the two compounds as well as their ability to oxidize mono- and di- thiols were also evaluated. The antioxidant effects were tested by measuring the ability of the compounds to inhibit the formation of thiobarbituric acid reactive species and also their ability to inhibit the formation of protein carbonyls. The results show that DPDS exhibited a higher glutathione peroxidase mimetic activity as well as increased ability to oxidize di-thiols than DCDS. In addition, while DPDS inhibited the formation of thiobarbituric acid reactive species and protein carbonyls, DCDS exhibited a prooxidant effect in all the concentration range (20-167 microM) tested. Also the activities of cerebral delta-aminolevulinate dehydratase and Na+/K+ ATPase were significantly inhibited by DPDS but not by DCDS. In addition, the present results suggested that the inhibition of Na+/K+ ATPase by organodiselenides, possibly involves the modification of the thiol group at the ATP binding site of the enzyme. In conclusion, the results of the present investigation indicated that the non-selenium moiety of the organochalcogens can have a profound effect on their antioxidant activity and also in their reactivity towards SH groups from low-molecular weight molecules and from brain proteins.
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PMID:Comparative studies on dicholesteroyl diselenide and diphenyl diselenide as antioxidant agents and their effect on the activities of Na+/K+ ATPase and delta-aminolevulinic acid dehydratase in the rat brain. 1771 May 41

We investigated if extracellular signal-regulated kinases (ERK) and oxidative stress are involved in the pathogenesis of arterial hypertension induced by chronic leptin administration in the rat. Leptin was administered at a dose of 0.25 mg/kg twice daily s.c. for 4 or 8 days. Blood pressure (BP) was higher in leptin-treated than in control animals from the third day of the experiment. The superoxide dismutase (SOD) mimetic, tempol, normalized BP in leptin-treated rats on days 6, 7 and 8, whereas the ERK inhibitor, PD98059, exerted a hypotensive effect on days 3 through 6. Leptin increased ERK phosphorylation level in renal and aortic tissues more markedly after 4 than after 8 days of treatment. In addition, leptin reduced urinary Na(+) excretion and increased renal Na(+),K(+)-ATPase activity, and these effects were abolished on days 4 and 8 by PD98059 and tempol, respectively. The levels of NO metabolites and cGMP were reduced in animals receiving leptin for 8 days. Markers of oxidative stress (H(2)O(2) and lipid peroxidation products) were elevated to a greater extent after 4 than after 8 days of leptin treatment. In contrast, nitrotyrosine, a marker of protein nitration by peroxynitrite, was higher in animals receiving leptin for 8 days. NADPH oxidase inhibitor, apocynin, prevented leptin's effect on BP, ERK, Na(+),K(+)-ATPase/Na(+) excretion and NO formation at all time points. SOD activity was reduced, whereas glutathione peroxidase (GPx) activity was increased in the group treated with leptin for 8 days. These data indicate that: (1) ERK, activated by oxidative stress, is involved only in the early phase of leptin-induced BP elevation, (2) the later phase of leptin-induced hypertension is characterized by excessive NO inactivation by superoxide, (3) the time-dependent shift from ERK to O(2)(-)-NO dependent mechanism may be associated with reduced SOD/GPx ratio, which favors formation of O(2)(-) instead of H(2)O(2).
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PMID:Role of extracellular signal-regulated kinases (ERK) in leptin-induced hypertension. 1820 59

We have previously evaluated the neuroprotective effect of catalpol on aging mice induced by d-galactose, in which catalpol treatment ameliorated cognition deficits and attenuated oxidative damage in mice brain. To thoroughly elucidate the anti-aging effects of catalpol, the liver and spleen antioxidative systems and energy metabolism in senescent mice induced by d-galactose have been studied. Except control group, mice were subcutaneously injected with d-galactose (150mgkg(-1)body weight) for 6 weeks. Meanwhile, drug group mice were treated with catalpol (2.5, 5, 10mgkg(-1)body weight) and piracetam (300mgkg(-1)body weight) for the last 2 weeks. The activities of endogenous antioxidants and the level of glutathione (GSH) and lipid peroxide in the liver and spleen were assayed. Compared to control group, model group mice had significantly lower spleen index (spleen weight/body weight), lower level of GSH, lower activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), higher level of malondialdehyde (MDA) in the liver and spleen. However, catalpol administration markedly reversed these effects of senescence induced by d-galactose. Simultaneously, catalpol noticeably elevated the decreased activities of lactate dehydrogenase (LDH), glutamine synthetase (GS), Na(+)-K(+)-ATPase, Ca(2+)-Mg(2+)-ATPase and decreased the elevated activity of creatine kinase (CK) in mice liver or spleen. These results implied that the anti-aging effects of catalpol were achieved at least partly by promoting endogenous antioxidant enzyme activities and normalizing energy disturbance. Catalpol may be a potential anti-aging agent and worth testing for further preclinical study aimed for senescence or neurodegenerative diseases such as Alzheimer's and Parkinson's diseases.
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PMID:Further pharmacological evidence of the neuroprotective effect of catalpol from Rehmannia glutinosa. 1828 Dec 3

Inflammation can activate macrophages or monocytes and sequentially release several inflammatory cytokines and reactive oxygen species (ROS). Oxidative stress-induced acute inflammatory response plays an important role in several diseases. This study was designed to investigate the prophylactic effect of the antioxidant lipoic acid (LA) during inflammation-induced mice. Mice were divided in to three groups (n = 8 in each): control, systemic inflammation, and LA treated mice with systemic inflammation. Results show that ROS was significantly higher in lymphocytes, hepatocytes, and astrocytes (P < 0.05) of inflammation induced mice when compared with control but no significant changes were observed in the LA treated group. Increased levels of lipid peroxidation (LPO) and decreased activities of oxidants such as superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione, and ATPase were observed in the inflammation-induced mice, which returned to near normalcy following LA therapy. In vitro study has shown that LA treatment not only suppresses the increased LPO levels but also inhibits the lipid break down resulting from autoxidation. In addition, increased immunoreactivity of the astrocyte marker glial fibrillary acidic protein (GFAP) was observed in the neocortex region of inflammation-induced mice, whereas nuclear factor kappa B p65 (NFkappaB) immunoreactivity was observed in both the neocortex and liver of the same group which were effectively controlled by LA therapy suggesting that LA can efficiently manage systemic inflammation.
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PMID:Efficacy of DL-alpha lipoic acid against systemic inflammation-induced mice: antioxidant defense system. 1840 59

Arsenic is a known global groundwater contaminant. The organochlorine insecticide endosulfan has gained significance as an environmental pollutant due to its widespread use in the control of many food- and non-food-crop-damaging insects. The adverse effects produced by arsenic or endosulfan alone in humans and animals are well documented, but very little is known about the consequences of their coexposure. We evaluated whether their simultaneous exposure can induce oxidative stress and affect antioxidative systems and certain membrane-bound enzymes in erythrocytes of broiler chickens. Day-old chicks were exposed to 3.7 ppm of arsenic via drinking water or 30 ppm of endosulfan-mixed feed or similarly coexposed to these in the same dose levels for 60 days. At term, the impact of their coexposure was assessed by evaluating lipid peroxidation (LPO), activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST), different ATPases and acetylcholinesterase (AChE) in erythrocytes, serum glucose, and levels of glutathione (GSH) and glycosylated hemoglobin (GHb) in blood. LPO was increased with all of the treatments. Catalase was decreased with endosulfan and the coexposure, but not with arsenic, whereas GSH was decreased with arsenic and endosulfan, but not with the coexposure. All of the treatments increased SOD and GPx activities. GST activity was increased only in the coexposed birds. None of the treatments affected the activities of total ATPase and Mg2+-ATPase. Na+-K+-ATPase activity was decreased in the endosulfan-treated and the coexposed birds. All three exposures increased erythrocyte AChE activity. Endosulfan increased the serum glucose level and arsenic and endosulfan increased GHb levels, but these were not altered in the coexposed birds. Erythrocyte protein content was insignificantly decreased with these treatments. Overall, the effects of coexposure were not appreciably different from either of the agents, except on AChE, GSH, and glucose. The results do not reflect any specific type of interaction between these agents in chicken erythrocytes, but they do indicate that the coexposure induces a low level of oxidative stress, which is comparable to that induced by arsenic or endosulfan.
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PMID:Effects of subchronic coexposure to arsenic and endosulfan on the erythrocytes of broiler chickens: a biochemical study. 1844 43

The anti-ulcer properties of astaxanthin fractions such as total carotenoid and astaxanthin esters from Haematococcus pluvialis were evaluated in ethanol-induced gastric ulcers in rats. Since oxygen radical release is a pathogenic factor of ethanol-induced gastric damage, astaxanthin - a free radical scavenger, was investigated as a potential ulcer preventive agent. Astaxanthin fractions - total carotenoid and astaxanthin esters were orally administered to experimental rats at 100, 250 and 500 microg/kg b.w. prior to ulcer induction. Alcian blue binding assay indicates that, total carotenoid and astaxanthin esters at 500 microg/kg b.w could protect gastric mucin approximately 40% and 67% respectively. Pre-treatment with astaxanthin esters, also resulted in significant increase in antioxidant enzyme levels - catalase, superoxide dismutase, and glutathione peroxidase in stomach homogenate. Histopathological examination substantiated the protective effect of astaxanthin in pre-treated rats. The increased antioxidant potencies such as free radical scavenging activity with an IC(50) of approximately 8 microg/ml and reducing power abilities (59 x 10(3) U/g) in vitro, reveal that H. pluvialis astaxanthin may protect gastric mucosal injury by antioxidative mechanism. In addition, approximately 23 fold increased lipoxygenase-inhibitory property, in comparison with standard astaxanthin and significant H(+), K(+)-ATPase-inhibitory activity of astaxanthin esters, in comparison with known proton pump blocking anti-ulcer drug - omeprazole, may envisage the potential gastroprotective effect by regulating the gastric mucosal injury and gastric acid secretion by the gastric cell during ulcer disease.
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PMID:Ulcer preventive and antioxidative properties of astaxanthin from Haematococcus pluvialis. 1860 87


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