Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.109 (AST)
 6,066 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antioxidant activity of [N, N'-Bis (salicylidene) ethane-1, 2-diaminato] oxovanadium (IV) complex (VO-salen complex) was evaluated using different in vitro evaluating systems including superoxide anion (O(2)(-)) and hydrogen peroxide (H(2)O(2)) scavenging activities. In addition, the inhibitory effects of this compound on protein oxidation and inhibition of Fe(2+)/ascorbate-induced lipid peroxidation were studied using rat liver homogenate. In vitro results revealed that the VO-salen complex has strong inhibitory effects on protein oxidation and lipid peroxidation of the liver homogenate along with a concentration-dependent quenching of H(2)O(2) and O(2)(-) radicals. In an in vivo approach, hepatoprotective potential of the VO-salen complex against liver damages induced by CCl(4) treatment was also investigated. After intraperitoneal injection of CCl(4) to rats, various biochemical changes associated with liver injury and/or oxidative stress were measured. The results showed that the sera levels of ALT, AST, ALP and the content of hepatic thiobarbituric acid reactive substances (TBARS) were all increased and the glutathione (GSH) content and the hepatic superoxide dismutase (SOD) and catalase (CAT) activities were decreased in CCl(4)-treated rats. However, simultaneous treatment of rats with VO-salen (0.6 mg/kg) and CCl(4) significantly attenuated the sera levels of ALT, AST, ALP and the hepatic TBARS content. In addition, by VO-salen therapy, the hepatic SOD and CAT activities and the GSH content were all restored back almost to their normal levels. The liver damages were also significantly ameliorated as compared to the CCl(4)-treated rats. Based on these results, the VO-salen complex might be considered as an effective antioxidant and hepatoprotective agent suitable for further biological evaluation.
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PMID:Radical scavenging abilities and hepatoprotective effect of [N, N'-Bis (salicylidene) ethane-1, 2-diaminato] oxovanadium (IV) complex in CCl4-treated rats. 1964 Jun 93

Lambda-cyhalothrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of lambda-cyhalothrin (LTC) to induce oxidative stress, changes in biochemical parameters and enzyme activities in the kidney of male rats and its possible attenuation by Vitamin C (vit C). Renal function, histopathology, tissue malondialdehyde (MDA), protein carbonyl (PCO) levels, antioxidant enzyme activities and reduced glutathione (GSH) levels were evaluated. Exposure of rats to lambda-cyhalothrin, during 3 weeks, caused a significant increase in kidney MDA and protein carbonyl levels (p<0.01) as compared to controls. Co-administration of vitamin C was effective in reducing MDA and PCO levels. The kidney of LTC-treated rats exhibited severe vacuolations, cells infiltration and widened tubular lumen. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) were significantly decreased due to lambda-cyhalothrin exposure. Co-administration of vitamin C ameliorated the increase in enzymatic activities of aminotransferases (AST and ALT), lactate dehydrogenase (LDH), creatinine and urea levels and improved the antioxidant status. These data indicated the protective role of ascorbic acid against lambda-cyhalothrin-induced nephrotoxicity and suggested a significant contribution of its antioxidant property to these beneficial effects.
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PMID:Toxic effects of lambda-cyhalothrin, a synthetic pyrethroid pesticide, on the rat kidney: Involvement of oxidative stress and protective role of ascorbic acid. 1973 94

Gibberellic acid (GA(3)), a plant growth regulator, was largely used in agriculture of many countries including Tunisia. However, its potential hazardous effects on human health were relatively unexplored. The purpose of this study was to investigate the effects of GA(3) on hepatic function in female rats and their pups. Animals were given daily 200 ppm GA(3) in drinking water from the 14th day of pregnancy until day 14 after delivery. It was found that GA(3) induced liver damages as evidenced by the elevation of plasma aminotransferases (ALT, AST), lactate dehydrogenase activities, bilirubin and albumin levels. Hepatotoxicity was objectified by the significant increase of malondialdehyde (MDA) level and a decrease of antioxidant enzyme activities such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione content in liver of suckling pups and their mothers. Impairment of hepatic function corresponded histologically. We have observed blood vessels congestion and leucocytes infiltration, which were more pronounced in hepatocytes of dams than those of suckling pups. Results of this current study suggest that exposure rats to GA(3) induces hepatotoxicity and histopathological changes in liver of female rats and their progeny.
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PMID:Hepatotoxicity induced by gibberellic acid in adult rats and their progeny. 1981 99

The antioxidant effect of CoQ(10) on N-nitrosodiethylamine (NDEA)-induced oxidative stress was investigated in mice. Food intake and body weight were similar in both CoQ(10) and control groups during the 3-week experimental period. NDEA significantly increased the activities of typical marker enzymes of liver function (AST, ALT and ALP) both in control and CoQ(10) groups. However, the increase of plasma aminotransferase activity was significantly reduced in the CoQ(10) group. Lipid peroxidation in various tissues, such as heart, lung, liver, kidney, spleen and plasma, was significantly increased by NDEA, but this increase was significantly reduced by 100 mg/kg of CoQ(10). Superoxide dismutase activity increased significantly upon NDEA-induced oxidative stress in both the control and CoQ(10) groups with the effect being less in the CoQ(10) group. Catalase activity decreased significantly in both the control and CoQ(10) groups treated with NDEA, again with the effect being less in the CoQ(10) group. The lesser effect on superoxide dismutase and catalase in the NDEA-treated CoQ(10) group is indicative of the protective effect CoQ(10). Thus, CoQ(10) can offer useful protection against NDEA-induced oxidative stress.
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PMID:Antioxidant Effect of CoQ(10) on N-nitrosodiethylamine-induced Oxidative Stress in Mice. 1988 17

To investigate the effects of atorvastatin and cinnamon on serum lipid profile, oxidative stress, antioxidant capacity, hepatic enzymes activities, nitric oxide (NO) as well as homocysteine (Hcy) in hypercholesterolemic rats, 48 male albino rats, weighing 130-190 gm were divided into 2 groups, normal group fed on basal rat chow diet (n=12) and high cholesterol group (HCD) were fed on 1% cholesterol-enriched diet for 15 day (n=36). Hypercholesterolemic rats were divided into 3 subgroups (n=12 for each) fed the same diet and treated with atorvastatine (HCD+Atorvastatin) or cinnamon extract (HCD+cinnamon) or none treated (HCD) for 3&6 weeks. Serum triglycerides (TG), Total cholesterol (TC), low density lipoprotein (LDL), high density lipoprotein (HDL), ALT, AST, NO, Hcy, hepatic reduced glutathione (GSH), Malondialdehyde (MDA) and antioxidant enzymes, Superoxide dismutase (SOD) and catalase activity were measured. Results showed that HCD increased significantly TG, TC, LDL-C, ALT, AST, Hcy and hepatic MDA, while lowered significantly antioxidant enzyme activities and NO levels. Atorvastatin therapy significantly increased HDL-C, NO and antioxidant activity while decreased LDL-C, MDA and Hcy concentrations. Serum TG, TC, LDL-C, ALT, AST and hepatic MDA levels were significantly lowered meanwhile, serum HDL, NO values and hepatic antioxidant activities were significantly, higher in cinnamon-treated than untreated group. These results indicate that lipid abnormalities, oxidative injury and hyperhomocystienemia were induced by HCD and this study recommend that administration of atorvastatine or cinnamon provided protection against the lipemic-oxidative disorder and act as hypocholesterolemic, hepatoprotective agent and improve cardiovascular function through modulation of oxidative stress, NO and Hcy.
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PMID:Oxidative markers, nitric oxide and homocysteine alteration in hypercholesterolimic rats: role of atorvastatine and cinnamon. 1991 18

Acetaminophen is one of the most popular analgesic and antipyretic drugs and its overdose, which can cause severe damage to liver and kidneys, is one of the most common reasons of emergency admissions. In this study we investigated the effects of curcumin, derived from plant Curcuma longa, on acetaminophen toxicity, and the possibility of combining therapy of curcumin and N-acetyl cysteine (NAC) to treat this toxicity. The experiments were conducted on 72 male Sprague-Dawley rats randomly divided into 12 groups. Control group was left without treatment, and the other groups were treated with different combinations of acetaminophen, curcumin and NAC. 15min after intraperitoneal injection, the blood level of curcumin was measured using HPLC. Blood levels of AST (aspartate aminotransferase), ALT (alanine aminotransferase), blood urea nitrogen and creatinine were determined 18 and 42h after acetaminophen injection. One week later, the left kidney and the caudate lobe of the liver were harvested to assay glutathione peroxidase, catalase and malondialdehyde. The right kidney and the remaining lobes of the liver were used for histopathology. Analysis of organ function and oxidation parameters showed that curcumin significantly reduced toxic effects of acetaminophen on the liver and kidneys in a dose-dependent manner and significantly potentiated the protective effects of NAC. These findings were confirmed by histopathology. It is concluded that curcumin can protect the liver and kidney from the damage caused by acetaminophen overdose. Moreover, curcumin has the potential to be used in a combination therapy with NAC, significantly decreasing the therapeutic dose of NAC and therefore its side-effects.
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PMID:Curcumin protects rats against acetaminophen-induced hepatorenal damages and shows synergistic activity with N-acetyl cysteine. 1991 35

We evaluated whether repeated arsenic preexposure can increase acetaminophen-induced hepatic oxidative stress. Rats were exposed to arsenic (25 ppm; rat equivalent concentration of maximum groundwater contamination level) via drinking water for 28 days. Next day, they were given single oral administration of acetaminophen (420 or 1000 mg/kg b.w.). Hepatotoxicity was evaluated by assessing serum biomarkers, cytochrome-P450 (CYP) content, CYP3A4- and CYP2E1-dependent enzymes, lipid peroxidation and antioxidants. Arsenic or acetaminophen increased serum ALT and AST activities and depleted CYP. Arsenic decreased, but acetaminophen increased CYP-dependent enzyme activities. These agents independently increased lipid peroxidation and decreased antioxidants. Arsenic did not alter the effects of acetaminophen on serum biomarkers, caused further CYP depletion and decreased acetaminophen-mediated induction of drug-metabolizing enzymes. Arsenic enhanced the lower dose of acetaminophen-mediated lipid peroxidation and glutathione depletion with no further alterations in enzymatic antioxidants. However, arsenic attenuated the higher dose-mediated lipid peroxidation and glutathione depletion with improvement in glutathione peroxidase and glutathione reductase activities, further decrease in catalase and no alterations in superoxide dismutase and glutathione-S-transferase activities. Results show that arsenic preexposure increased the susceptibility of rats to hepatic oxidative stress induced by the lower dose of acetaminophen, but reduced the oxidative stress induced by the higher dose.
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PMID:Influence of repeated preexposure to arsenic on acetaminophen-induced oxidative stress in liver of male rats. 1993 28

In the present study, we have addressed the ability of curcumin to suppress MTX-induced liver damage. Hepatotoxicity was induced by injection of a single dose of MTX (20mg/kg I.P.). MTX challenge induced liver damage that was well characterized histopathologically and biochemically. MTX increased relative liver/body weight ratio. Histologically, MTX produced fatty changes in hepatocytes and sinusoidal lining cells, mild necrosis and inflammation. Biochemically, the test battery entailed elevated activities of serum ALT and AST. Liver activities of superoxide dismutase (SOD), catalase (CAT) and level of reduced glutathione (GSH), were notably reduced, while lipid peroxidation, expressed as malondialdhyde (MDA) level was significantly increased. Administration of curcumin (100mg/kg, I.P.) once daily for 5 consecutive days after MTX challenge mitigated the injurious effects of MTX and ameliorated all the altered biochemical parameters. These results showed that administration of curcumin decreases MTX-induced liver damage probably via regulation of oxidant/anti-oxidant balance. In conclusion, the present study indicates that curcumin may be of therapeutic benefit against MTX-cytotoxicity.
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PMID:Curcumin attenuates methotraxate-induced hepatic oxidative damage in rats. 2002 70

This study was designed to evaluate the protective effect of kolaviron (KV), a biflavonoid from Garcinia kola seeds, against gamma-radiation (5 Gy)-induced oxidative stress in brain of Wistar rats. Vitamin C (VC) served as standard antioxidant. Forty-four rats were divided into 4 groups of 11 animals each. One group was un-irradiated (normal), two groups were treated with KV and VC (250 mg/kg) for 6 weeks prior to and 8 weeks after irradiation, and fourth group was only irradiated. Rats were sacrificed 1 and 8 weeks after irradiation. Cellular alterations were monitored using changes in the levels of malondialdehyde (MDA)-an index of lipid peroxidation, superoxide dismutase (SOD), glutathione-S-transferase (GST), reduced glutathione (GSH), catalase (CAT), alanine and aspartate aminotransferases (ALT and AST), urea and creatinine. MDA levels increased significantly (p<0.05) by 90% and 151% after 1 and 8 weeks of irradiation. Furthermore, levels of GSH and antioxidant enzymes were significantly (p<0.05) decreased in gamma-irradiated animals. GSH and GST decreased by 61% and 43% after 1 week, and by 75% and 74%, after 8 weeks of exposure, respectively. gamma-Irradiation decreased SOD and CAT levels by 53% and 68%, respectively, and caused significant (p<0.05) increases in serum ALT, AST and urea after 8 weeks of exposure. Treatment with KV and VC significantly decreased the levels of MDA, ALT, AST and urea. The antioxidant indices were significantly ameliorated in KV-treated animals. These data suggest that kolaviron may protect against gamma-radiation-induced oxidative stress in brain of exposed rats.
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PMID:Protective effect of kolaviron, a biflavonoid from Garcinia kola seeds, in brain of Wistar albino rats exposed to gamma-radiation. 2011 50

Astaxanthine (3,3'-dihydroxy-beta,beta'-caroten-4,4'-dione) (AST), a red-colored carotenoid pigment, possesses extremely powerful antioxidative activity. However, its drawbacks reside in poor solubility in aqueous system, resulting in extremely low bioavailability. To ameliorate such defects, we prepared AST encapsulated within liposomes (AST-L) and tested with Hep3B and HepG2 cell lines. AST-L had size 251+/-23 nm with AST content 89.0+/-8.6 mg/g. AST-L apparently showed improved stability and transportability. The overall transport time was 7.55 h and 6.00 h for free AST and AST-L, respectively. AST-L more effectively activated antioxidant enzymes like superoxide dismutase, catalase and glutathione S-transferase than free AST. Hep3B consumed AST more rapidly than HepG2 cell lines. Moreover, AST-L when combined with gamma radiation (10 Gy) therapy potentially triggered subG(1) arrest in Hep3B and HepG2 cell lines in a dose-responsive manner (p<0.05). To conclude, the poor bioavailability of AST can be improved by liposomal encapsulation, which can be a good adjuvant remedy in gamma radiotherapy.
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PMID:Improved membrane transport of astaxanthine by liposomal encapsulation. 2022 58


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