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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate the effects of the nitrates toxicity, a study has been carried out on 45 workers of storage and distribution agricultural manures, exposed to nitrate derivatives. Another experimental study has carried out in laboratory on male Albinos wistar rats. These latter were treated with ammonium nitrate (NH(4)NO(3)) introduced by gavage with three increasing concentrations 200, 400 and 600 mg/kg of body weight during three weeks. The biochemical and hematological results on workers showed that no poisoning was announced within this complex, in spite of the observation of kidneys inflammations among about 50% of the population. The chemical treatment of the rats causes a variation in the biochemical and biological parameters: an increase of the hepato-somatic ratio especially in the rats treated by important doses. Moreover, the serum concentration in glucose, cholesterol, creatinin, lactate dehydrogenase and in transaminases (GOT, GPT) was increased significantly compared to the witness in all the treated rats. At the end, the results obtained highlight the detoxifier potential expressed by the reduction in the glutathione level in the deferent organs such as the liver, the kidneys, the spleen, the intestines and the testicles. According to the obtained results, it can be concluded that: (1) living organism can adapt to the lows doses of nitrate for a long time. This is observed in the workers exposed to deferent derivatives of nitrates; (2) high nitrate amounts involve important biological variations even if the exposure time is short. This is proven in the laboratory animals.
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PMID:[Toxicological effects of nitrate: biological study in human and animal]. 1762 19

Lead (Pb(2+)) is a well-known highly toxic element. The mechanisms of the Pb(2+) toxicity are not well understood for nitrogen metabolism of higher plants. In this paper, we studied the effects of various concentrations of PbCl(2) on the nitrogen metabolism of growing spinach. The experimental results showed that Pb(2+) treatments significantly decreased the nitrate nitrogen (NO(-)(3)-N) absorption and inhibited the activities of nitrate reductase, glutamate dehydrogenase, glutamine synthase, and glutamic-pyruvic transaminase of spinach, and inhibited the synthesis of organic nitrogen compounds such as protein and chlorophyll. However, Pb(2+) treatments increased the accumulation of ammonium nitrogen NH(+)(4)-N)in spinach cell. It implied that Pb(2+) could inhibit inorganic nitrogen to be translated into organic nitrogen in spinach, thus led to the reduction in spinach growth.
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PMID:Influences of lead (II) chloride on the nitrogen metabolism of spinach. 1795 1

Synergistic therapeutic potential of ferritin (5mg/kg, i.p.) and propolis (honeybee hive product; 200mg/kg, p.o.) was analyzed to encounter the beryllium induced biochemical and ultra morphological alterations. Female albino rats were exposed to beryllium nitrate (1mg/kg, i.p.) daily for 28 days followed by treatment of above mentioned therapeutic agents either individually or in combination for five consecutive days. Exposure to beryllium increased its concentration in serum, liver and kidney and significantly altered the activities of CYP2E1 and CYP1A2 enzymes, microsomal lipid peroxidation and microsomal proteins. Activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transpeptidase, bilirubin, protein, creatinine and urea in serum as well as hemoglobin and blood glucose level; activity of acid phosphatase, alkaline phosphatase, adenosine triphosphatase, glucose-6-phosphatase and succinic dehydrogenase, total triglycerides, total cholesterol, total protein contents, glycogen contents, lipid peroxidation and glutathione level in liver and kidney were significantly altered after beryllium administration. Beryllium exposure severely altered ultramorphology of liver and kidney that proved its toxic consequences at cellular level. Ferritin in combination with propolis dramatically reversed the alterations of these variables towards control in a synergistic manner concluding its beneficial effects over monotherapy in attenuating beryllium induced systemic toxicity.
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PMID:Synergistic effects of ferritin and propolis in modulation of beryllium induced toxicogenic alterations. 1862 18

The involvement of oxidative and nitrosative mediators in liver injury caused by heat stress remains unclear. This study aimed to elucidate the role of endothelial nitric oxide synthase (eNOS), and inducible NOS (iNOS)-derived NO and nitrotyrosine in the whole-body hyperthermia (WBH)-induced liver injury. Rats were anesthetized with intraperitoneal pentobarbital, and were exposed to a heating lamp for 60 min to raise the core temperature to 42.5 degrees C. The rats were maintained at the hyperthermic state for an additional 50 min. Blood urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, lactic dehydrogenase, creatine phosphokinase, amylase, lipase, nitrate/nitrite, methyl guanidine, and proinflammatory cytokines (tumor necrosis factoralpha, interleukin-1beta and interleukin-10) were measured before and 14 h after hyperthermia. Immunohistochemical staining was employed to detect the eNOS, iNOS and nitrotyrosine levels. Western blotting was used to examine the expression of heatshock protein 70 (HSP 70). Histopathological examination of the liver tissue was performed. WBH caused liver injury accompanied with significant increases in biochemical factors, nitrate/nitrite, methyl guanidine, and proinflammatory cytokines. In addition, WBH enhanced the eNOS, iNOS, nitrotyrosine and HSP 70 levels. WBH caused hepatic injury. The pathogenetic mechanism is likely mediated through the NOS-derived NO, free radical, proinflammatory cytokines and nitrotyrosine. The enhanced expression of HSP 70 may play a protective role.
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PMID:Oxidative and nitrosative mediators in hepatic injury caused by whole body hyperthermia in rats. 1866 11

The influences of 50 and 100muM Ni on growth, tissue Ni accumulation, concentrations of nitrate, ammonium, glutamate, and proline as well as the activities of nitrate reductase (NR), nitrite reductase (NiR), glutamine synthetase (GS), glutamate synthase (GOGAT), glutamate dehydrogenase (GDH), alanine aminotransferase (AlaAT), and aspartate aminotransferase (AspAT) were examined in the shoots of wheat seedlings cv. Zyta. Exposure of the seedlings to Ni resulted in a rapid accumulation of this metal in the shoots, which was accompanied by significant reduction in fresh weight of these organs. Tissue nitrate content decreased in response to Ni stress, while ammonium concentration increased substantially. Glutamate concentration was slightly lowered up to the 4th day of the metal exposure. In contrast, proline content increased significantly, starting from the first day after Ni treatment. NR activity showed a decline of up to 40% below the control level after Ni application; however, its activation state remained unaltered. Heavy metal treatment also resulted in a marked decrease in NiR activity, which after 7d of exposure to 100muM Ni was almost 80% lower than in the control. GS activity in wheat shoots was not influenced by Ni application. Contrary to Fd-GOGAT exhibiting reduced activity in the shoots of Ni-treated wheat seedlings, NADH-GOGAT activity was considerably enhanced, exceeding the control value even by 165%. After 7d of exposure to Ni, both NADH-GDH and NAD-GDH activities in wheat shoots were markedly induced; however, NAD-GDH activity showed a significant decrease at the early stage of the experiment. Both AlaAT and AspAT glutamate-producing activities were considerably stimulated by Ni treatment. Our results suggest that induction of NADH-GOGAT, NADH-GDH, AlaAT, and AspAT activities may compensate for the reduced Fd-GOGAT activity and serve as an alternative means of glutamate synthesis in wheat shoots under Ni stress.
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PMID:Nickel-induced changes in nitrogen metabolism in wheat shoots. 1918 88

It has been reported that increased nitric oxide (NO) production by the hepatocytes during chronic inflammatory processes, plays an important role in the pathogenesis of chronic hepatitis B. The aim of this study was to investigate the relationship between serum levels of NOx (nitrite + nitrate) with the viral load and alanine aminotransferase (ALT) levels in chronic hepatitis B (CHB) patients. A total of 93 CHB patients (67 male, 26 female; mean age: 47.3 +/- 10.9 years) and 53 healthy control subjects (17 male, 36 female; mean age: 58.6 +/- 2.1 years) followed-up during 2006-2007 period were included to the study. Hepatitis B virus (HBV) serologic markers, viral load and ALT levels were studied by chemiluminescence method (Ortho-Clinical Diagnostics, USA), by real-time polimerase chain reaction (PCR) (ABI PRISM 7700, Applied Biosystem, CA), and by Aeroset System (Abbott Laboratories, USA), respectively. NOx levels were determined by a method which was based on the reduction of nitrate to nitrite by cadmium. Mean levels of ALT and HBV-DNA of the patients were found as 98.7 +/- 138.4 IU/I and 1.6 x 10(9) +/- 4.0 x 10(9) copies/ml, respectively. In the evaluation of mean levels of NOx in patient and control groups, the difference was found statistically significant (30.6 +/- 21.7 micromol/l and 23.7 +/- 5.2 micromol/l, respectively; p< 0.05). In view of the relationship between the parameters, a positive correlation was detected between viral load and ALT levels (r= 0.768; p< 0.001), besides the significant correlations between NOx and viral load, and NOx and ALT (r= 0.346, p= 0.001 and r= 0.314, p= 0.002, respectively). As a result, although the NOx levels in chronic hepatitis patients were found higher than those in the control group, and significant correlations were detected between NO, viral load and ALT, the exact role of NO in the disease pathogenesis and outcome needs to be studied further at cellular level.
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PMID:[Investigation of the relationship between serum nitric oxide levels, HBV-DNA and ALT levels in chronic hepatitis B patients]. 1933 84

GYY4137 (morpholin-4-ium-4-methoxyphenyl(morpholino) phosphinodithioate) is a slow-releasing hydrogen sulfide (H(2)S) donor. Administration of GYY4137 (50 mg/kg, iv) to anesthetized rats 10 min after lipopolysaccharide (LPS; 4 mg/kg, iv) decreased the slowly developing hypotension. GYY4137 inhibited LPS-induced TNF-alpha production in rat blood and reduced the LPS-evoked rise in NF-kappaB activation, inducible nitric oxide synthase/cyclooxygenase-2 expression, and generation of PGE(2) and nitrate/nitrite in RAW 264.7 macrophages. GYY4137 (50 mg/kg, ip) administered to conscious rats 1 or 2 h after (but not 1 h before) LPS decreased the subsequent (4 h) rise in plasma proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6), nitrite/nitrate, C-reactive protein, and L-selectin. GYY4137 administration also decreased the LPS-evoked increase in lung myeloperoxidase activity, increased plasma concentration of the anti-inflammatory cytokine IL-10, and decreased tissue damage as determined histologically and by measurement of plasma creatinine and alanine aminotransferase activity. Time-expired GYY4137 (50 mg/kg, ip) did not affect the LPS-induced rise in plasma TNF-alpha or lung myeloperoxidase activity. GYY4137 also decreased the LPS-mediated upregulation of liver transcription factors (NF-kappaB and STAT-3). These results suggest an anti-inflammatory effect of GYY4137. The possibility that GYY4137 and other slow-releasing H(2)S donors exert anti-inflammatory activity in other models of inflammation and in humans warrants further study.
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PMID:GYY4137, a novel hydrogen sulfide-releasing molecule, protects against endotoxic shock in the rat. 1937 98

For Dutch sandy regions, linear regression models have been developed that predict nitrate concentrations in the upper groundwater on the basis of residual nitrate contents in the soil in autumn. The objective of our study was to validate these regression models for one particular sandy region dominated by dairy farming. No data from this area were used for calibrating the regression models. The model was validated by additional probability sampling. This sample was used to estimate errors in 1) the predicted areal fractions where the EU standard of 50 mg l(-1) is exceeded for farms with low N surpluses (ALT) and farms with higher N surpluses (REF); 2) predicted cumulative frequency distributions of nitrate concentration for both groups of farms. Both the errors in the predicted areal fractions as well as the errors in the predicted cumulative frequency distributions indicate that the regression models are invalid for the sandy soils of this study area.
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PMID:Validation of regression models for nitrate concentrations in the upper groundwater in sandy soils. 1967 82

Opisthorchis viverrini (OV) infection is endemic in northeastern Thailand. We have previously reported that OV infection induces oxidative and nitrative DNA damage via chronic inflammation, which contributes to the disease and cholangiocarcinogenesis. Here, we examined the effect of curcumin, an antioxidant, on pathogenesis in OV-infected hamsters. DNA lesions were detected by double immunofluorescence and the hepatic expression of oxidant-generating and antioxidant genes was assessed by quantitative RT-PCR analysis. Dietary 1.0% curcumin significantly decreased OV-induced accumulation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), an oxidative DNA lesion, and 8-nitroguanine, a nitrative DNA lesion, in the nucleus of bile duct epithelial and inflammatory cells. Expression of oxidant-generating genes (inducible nitric oxide synthase; iNOS, its nuclear transcriptional factor, NF-kappaB, and cyclooxygenase-2), and plasma levels of nitrate, malondialdehyde, and alanine aminotransferase, were also decreased in curcumin-treated group. In contrast, curcumin increased the mRNA expression of antioxidant enzymes (Mn-superoxide dismutase and catalase), and ferric-reducing anti-oxidant power in the plasma. In conclusion, curcumin reduced oxidative and nitrative DNA damage by suppression of oxidant-generating genes and enhancement of antioxidant genes, leading to inhibition of oxidative and nitrative stress. Therefore, curcumin may be used as a chemopreventive agent to reduce the severity of OV-associated diseases and the risk of cholangiocarcinoma (CCA).
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PMID:Curcumin reduces oxidative and nitrative DNA damage through balancing of oxidant-antioxidant status in hamsters infected with Opisthorchis viverrini. 1975 8

This study investigated the effect of astaxanthin (ASX; 3,3-dihydroxybeta, beta-carotene-4,4-dione), a water-dispersible synthetic carotenoid, on liver ischemia-reperfusion (IR) injury. Astaxanthin (5 mg/kg/day) or olive oil was administered to rats via intragastric intubation for 14 consecutive days before the induction of hepatic IR. On the 15th day, blood vessels supplying the median and left lateral hepatic lobes were occluded with an arterial clamp for 60 min, followed by 60 min reperfusion. At the end of the experimental period, blood samples were obtained from the right ventricule to determine plasma alanine aminotransferase (ALT) and xanthine oxidase (XO) activities and animals were sacrificed to obtain samples of nonischemic and postischemic liver tissue. The effects of ASX on IR injury were evaluated by assessing hepatic ultrastructure via transmission electron microscopy and by histopathological scoring. Hepatic conversion of xanthine dehygrogenase (XDH) to XO, total GSH and protein carbonyl levels were also measured as markers of oxidative stress. Expression of NOS2 was determined by immunohistochemistry and Western blot analysis while nitrate/nitrite levels were measured via spectral analysis. Total histopathological scoring of cellular damage was significantly decreased in hepatic IR injury following ASX treatment. Electron microscopy of postischemic tissue demonstrated parenchymal cell damage, swelling of mitochondria, disarrangement of rough endoplasmatic reticulum which was also partially reduced by ASX treatment. Astaxanthine treatment significantly decreased hepatic conversion of XDH to XO and tissue protein carbonyl levels following IR injury. The current results suggest that the mechanisms of action by which ASX reduces IR damage may include antioxidant protection against oxidative injury.
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PMID:Effect of astaxanthin on hepatocellular injury following ischemia/reperfusion. 1990 May


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