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:3.5.4.4 (adenosine deaminase)
5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The enzyme activities of cultured early erythroid progenitor cells (burst-forming unit erythroid, BFU-E) were measured and were compared with the activities of mature erythrocytes. The enzyme activity of acetylcholinesterase was not detectable in the erythroblasts. The ratios of phosphofructokinase and glutathione peroxidase were low due to low enzyme activities in both the erythroblasts and erythrocytes. The ratios of triose phosphate isomerase, phosphoglycerate kinase, and adenylate kinase were low due to high enzyme activities in both the erythroblasts and erythrocytes. The ratios of hexokinase, glucose phosphate isomerase, monophosphoglyceromutase, pyruvate kinase, and adenosine deaminase were high due to high enzyme activities in the erythroblasts. The isozyme of erythroblast hexokinase was of the prototype isozyme I, while pyruvate kinase was predominantly of the prototype M2, with two hybrid isozymes to the anodal side by electrophoresis. These facts suggest that there is a greatly different metabolic pattern during the maturation of the erythroid cells.
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PMID:Enzyme activities of cultured erythroblasts. 403 55

Activities of adenosine deaminase, 5'-nucleotidase, xanthine oxidase, superoxide dismutase, glutathione peroxidase and catalase enzymes were measured in cancerous and non-cancerous adjacent colorectal tissues from 10 patients. Activities of DNA turn-over enzymes (ADA, 5'NT and XO) were found increased and those of free-radical metabolizing enzymes (SOD, GSH-Px and CAT) decreased in cancerous tissues compared with those of non-cancerous adjacent ones. Malondialdehyde (MDA) concentrations in cancerous tissues were also found higher than those of non-cancerous tissues, which indicated accelerated lipid peroxidation in the cancerous tissues. In the correlation analysis, disordered enzymatical relations were observed between the enzymes of both metabolic pathways. Results suggest that activities of purine metabolizing enzymes increase to cope with accelerated purine metabolism in cancerous tissues and, enzymatic antioxidant defense potential of cancerous tissues decreases due to carcinogenic processes in the tissues. Reduced antioxidant defense system makes the cancerous tissue more vulnerable to toxic effects of some free-radical species.
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PMID:Activities of the enzymes participating in purine and free-radical metabolism in cancerous human colorectal tissues. 992 74

Activities of adenosine deaminase (ADA), 5'nucleotidase (5'NT), xanthine oxidase (XO), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) and levels of thiobarbituric acid reagent substances (TBARS) were measured in 10 cancerous and 10 noncancerous human prostate tissues. Decreased activities of DNA turnover enzymes (ADA and 5'NT), increased activities of GSH-Px and CAT, and unchanged activities of SOD and XO were observed in cancerous prostate tissues compared with those of noncancerous ones. TBARS levels were found to be higher in cancerous tissues than noncancerous ones. In correlation analysis, mostly positive correlations were established between enzyme activities of the cancerous tissues, whereas no meaningful correlations were found between enzyme activities of the noncancerous tissues except for a positive correlation between XO and SOD. The results indicate that the activities of DNA turnover enzymes were reduced, which was possibly an attempt to lower the rate of purine catabolism, and the activities of GSH-Px and CAT enzymes were increased, probably in response to increased free radical stress occurring in cancerous prostate tissues. Increased concentrations of TBARS suggested oxidant stress and thus accelerated peroxidative reactions in the cancerous tissues, even though antioxidant defense mechanisms were activated. These findings suggest that enzymatic antioxidant systems of cancerous prostate tissues cannot sufficiently eliminate oxidant factors and prevent cellular peroxidative reactions occurring during the carcinogenic process.
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PMID:Activities of DNA turnover and free radical metabolizing enzymes in cancerous human prostate tissue. 1037 Mar 68

To investigate the features of erythrocyte metabolism in extremely immature infants, we assayed 21 enzyme activities and glutathione level in cord erythrocytes from 28 extremely low-birth-weight infants (ELBWI; defined as birth weight <1,000 g). The results were compared with those from normal adults and non-neonatal reticulocyte-rich controls. Statistical analysis revealed that activities of six enzymes (glucosephosphate isomerase, phosphoglycerate kinase, monophosphoglycerate mutase, enolase, glucose-6-phosphate dehydrogenase (G6PD), and glutathione reductase) were significantly higher, and those of eight other enzymes (phosphofructokinase, 6-phosphogluconate dehydrogenase (6PGD), glutathione peroxidase, adenylate kinase, adenosine deaminase, acetylcholinesterase, NADH methemoglobin reductase, and catalase) were lower in ELBWI taking their marked reticulocytosis into consideration. The 6PGD/G6PD ratio, which is consistently unchanged under various physiological and pathological conditions, was markedly reduced in ELBWI. Our results support the previous reports that neonatal erythrocytes have a unique metabolic pattern which is different from that of adult erythrocytes, and also suggest that the 6PGD/G6PD ratio might be an index for the developmental immaturity of fetal erythrocytes. This is the first report describing the pattern of erythrocyte enzyme activities in ELBWI.
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PMID:Erythrocyte enzyme activities in cord blood of extremely low-birth-weight infants. 1050 2

The aim of this experimental study was to investigate whether nebivolol has protective effects against neuronal damage induced by spinal cord ischemia/reperfusion (I/R). Twenty-one rabbits were divided into three groups: group I (control, no I/R), group II (only I/R) and group III (I/R+nebivolol). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the aortic bifurcation. Seventy-two hours postoperatively, the motor function of the lower limbs was evaluated in each animal. The animals were sacrificed at 72 h, and histopathological and biochemical analyses were carried out in the lumbar spinal cords. The motor deficit scores in nebivolol group were different from I/R group at 72 h (3.25+/-0.70 vs. 1.75+/-1.28, p=0.01). I/R produced a significant increase in the superoxide dismutase (SOD), xanthine oxidase (XO), adenosine deaminase (ADA) and myeloperoxidase (MPO) activities in spinal cord tissue when compared with control group. Nebivolol treatment prevented the increase of all those enzymes activities produced by I/R. A significant decrease in spinal cord glutathione peroxidase (GSH-Px) level was seen in I/R group and nebivolol treatment prevented the decrement in the spinal cord tissue GSH-Px contents. On the other hand, I/R produced a significant increase in the spinal cord tissue malondialdehyde (MDA) and nitric oxide (NO) contents, this was prevented by nebivolol treatment. In conclusion, this study demonstrates a considerable neuroprotective effect of nebivolol on neurological, biochemical and histopathological status during periods of spinal cord I/R in rabbits.
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PMID:The protective effect of nebivolol on ischemia/reperfusion injury in rabbit spinal cord. 1561 Sep 28

The antioxidant effect of cytaphate (0,0-dimethyl-N-cytisinyl phosphate) has been studied in outbred white rats with alloxan-induced insulin-dependent diabetes mellitus. The content of malonic dialdehyde, diene conjugates, ketodienes, middle-weight molecules, primary and secondary products of lipid peroxidation (LPO), and Schiff bases and the activity of catalase, glutathione peroxidase, and adenosine deaminase in erytrocytes have been evaluated. The state of oxidative protein modification, the content of malonic dialdehyde and diene conjugates, and the superoxide-anion production in the blood plasma have been determined. In the blood of animals with model diabetes, the LPO and oxidative protein modification processes were intensified and the level of superoxide anion production was increased. The administration of cytaphate led to a decrease of the LPO intensity and oxidative protein modification and to normalization of the level of superoxide anion production and the activity of enzymes involved in the antioxidant protection system.
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PMID:[The influence of cytaphate on the status of oxidative metabolism in rats with diabetic nephropathy]. 1627 12

Cisplatin is one of the most active cytotoxic agents in the treatment of cancer. High doses of cisplatin have also been known to produce hepatotoxicity. Several studies suggest that supplementation with an antioxidant can influence cisplatin-induced hepatotoxicity. The present study was designed to determine the effects of cisplatin on the liver oxidant/antioxidant system, and the possible protective effects of caffeic acid phenethyl ester (CAPE) on liver toxicity induced by cisplatin. Twenty-four adult female Wistar albino rats were divided into four groups of six rats each: control, cisplatin, CAPE, and cisplatin+CAPE. Cisplatin and CAPE were injected intraperitoneally. Liver tissue was removed to study the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), myeloperoxidase (MPO), xanthine oxidase (XO), adenosine deaminase (ADA), and the levels of malondialdehyde and nitric oxide (NO). The activities of SOD and GSH-Px increased in the cisplatin+CAPE and CAPE groups compared with the cisplatin group. CAT activity was higher in the cisplatin +CAPE group than the other three groups. XO activity was lower in the cisplatin group than the control group. MPO activity was also increased in the cisplatin group compared to the control and CAPE groups. It can be concluded that CAPE may prevent cisplatin-induced oxidative changes in liver by strengthening the antioxidant defence system by reducing reactive oxygen species and increasing antioxidant enzyme activities.
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PMID:Protective effect of caffeic acid phenethyl ester (CAPE) administration on cisplatin-induced oxidative damage to liver in rat. 1643 19

The aims of this study are to investigate the contribution effect of oxidative stress in MK-801-induced experimental psychosis model, and to show that prevention of oxidative stress may improve prognosis. Because oxidative damage has been suggested in the neuropathophysiology of schizophrenia, the possible protecting agents against lipid peroxidation are potential target for the studies in this field. For this purpose, Wistar Albino rats were divided into three groups: the first group was used as control, MK-801 was given to the rats in the second group and MK-801+omega-3 essential fatty acids (EFA) was given to the third group. MK-801 was given intraperitoneally at the dose of 0.5mg/(kgday) once a day for 5 days in experimental psychosis group. In the second group, 0.8g/(kgday), omega-3 FA (eicosapentaenoic acid, 18%, docosahexaenoic acid, 12%) was given to the rats while exposed MK-801. In control group, saline was given intraperitoneally at the same time. After 7 days, rats were killed by decapitation. Prefrontal brain area was removed for histological and biochemical analyses. As a result, malondialdehyde (MDA), as an indicator of lipid peroxidation, protein carbonyl (PC), as an indicator of protein oxidation, nitric oxide (NO) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities as antioxidant enzymes, and xanthine oxidase (XO) and adenosine deaminase (AD) activities as an indicator of DNA oxidation was found to be increased significantly in prefrontal cortex (PFC) of MK-801 group (P<0.0001) compared to control group. In omega-3 FA treated rats, prefrontal tissue MDA, PC and NO levels as well as SOD, GSH-Px, XO, and AD enzyme activities were significantly decreased when compared to MK-801 groups (P<0.0001) whereas catalase (CAT) enzyme activity was not changed. Moreover, in the light of microscopic examination of MK-801 groups, a great number of apoptotic cells were observed. omega-3 FA supplementation decreased the apoptotic cell count in PFC. The results of this study revealed that oxidative stress and apoptotic changes in PFC may play an important role in the pathogenesis of MK-801-induced neuronal toxicity. This experimental study also provides some evidences for the protective effects of omega-3 FA on MK-801-induced changes in PFC of rats.
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PMID:The protective effects of omega-3 fatty acids against MK-801-induced neurotoxicity in prefrontal cortex of rat. 1697 Oct 21

Excess of intracellular reactive oxygen species results in an environment that may modulate gene expression, or damage cellular molecules. These events are assumed to contribute to the process of carcinogenesis. In the present study, we measured the extent of lipid peroxidation and antioxidative status in colonic tumors and normal colonic mucosa obtained from 25 patients with colorectal carcinoma. Levels of lipid peroxides (PD) and of thiobarbituric acid reactive substances (TBARS) were significantly increased, by 54 and 59%, respectively, in tissue specimens obtained from the colonic tumor as compared with normal colonic mucosa (PD, 2.78+/-0.31 versus 1.81+/-0.29 nmol/mg tissue, TBARS, 0.86+/-0.1 versus 0.54+/-0.08 nmol/mg tissue). Activities of the antioxidant enzymes catalase and glutathione peroxidase (GPx) were also higher (by 67 and 29%, respectively) than in normal mucosa, probably in response to the increased free radical stress occurring in cancerous tissues. Myeloperoxidase (MPO) and adenosine deaminase (ADA) are markers of activated leukocytes and are related to the production of oxygen free radicals by these cells. Their activities were significantly elevated in the neoplastic tissue as compared to the normal tissue (MPO, 7.4+/-1.5 versus 4.1+/-0.95 U/mg tissue, ADA, 4.17+/-0.65 versus 2.99+/-0.80 U/g tissue), suggesting a possible involvement of activated leukocytes in the enhanced oxidative stress in the cancerous tissue. Our results demonstrate an enhanced oxidative stress in the neoplastic tissue. Leukocyte activation was also higher in the carcinogenic tissue, indicating a possible contribution of these cells to a further oxidative stress-derived tissue injury. These observations add to previous studies and may encourage therapeutic trials with antioxidants as a means of preventing colorectal cancer and preventing further tissue injury in the neoplastic tissue and its surroundings.
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PMID:Enhanced oxidative stress and leucocyte activation in neoplastic tissues of the colon. 1719 21

MK-801 was shown to be one of the most neurotoxic non-competitive NMDA receptor antagonists. It is known that repeated injection of MK-801 was proposed in an animal model in psychosis. The aims of this study are to investigate the contributing effect of oxidative stress in MK-801-induced experimental psychosis model, and to show that prevention of oxidative stress may improve prognosis. Furthermore, there is evidence that oxygen free radicals play an important role in the pathophysiology of schizophrenia. In this study, Wistar Albino rats were divided into three groups: 1st group: Control, 2nd group: MK-801, 3rd group: MK-801+CAPE (Caffeic acid phenethyl ester) group. MK-801 was given intraperitoneally at the dose of 0.5 mg/kg/day for 5 days. CAPE was given to the treatment group while exposed to MK-801. In control group, saline was given intraperitoneally at the same time. After 7 days, rats were killed by decapitation. Prefrontal cortex (PFC) of rats was removed for biochemical and histological analyses. As a result, malondialdehyde (MDA), protein carbonyl (PC), nitric oxide (NO) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and xanthine oxidase (XO) and adenosine deaminase (AD) enzyme activities were found to be increased significantly in prefrontal cortex (PFC) of MK-801 group (p<0.0001) compared to control group. In CAPE treated rats, prefrontal tissue MDA, PC, NO levels and, GSH-Px, XO, AD enzyme activities were significantly decreased when compared to MK-801 groups (p<0.0001) whereas catalase (CAT) enzyme activity was not changed. Moreover, in the light of microscopic examination of MK-801 groups, a great number of apoptotic cells were observed. CAPE treatment decreased the apoptotic cell count in PFC. The results of this study showed that MK-801-induced neurotoxicity caused oxidative stress in PFC of rats. This experimental study may also provide some evidences for the new treatment strategies with antioxidants in schizophrenia.
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PMID:Oxidative stress in prefrontal cortex of rat exposed to MK-801 and protective effects of CAPE. 1737 54


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