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

---

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

New biologically active compounds (BAC) created on the basis of nicotinic acid possess hepatoprotective action. The preparations were introduced preventively in doses of 10 mg/kg during 14 days. Litonit and nicogamol increased survival of experimental animals by 36.8% and nicotinic acid by 26.8%. ALT, AST, GGT activity in the blood serum was reduced. The activity of the main antioxidant enzymes (SOD and catalase) grew in the rat liver tissue in parallel with inhibition of DK and MDA activity. Morphological picture of the rat liver, most evident after application of litonit improved. Hepatoprotective action of these BAC are attributed to their membrano stabilizing effects.
...
PMID:[Mechanisms of hepatoprotective action of new nicotinic acid derivatives in experimental CCL4-induced liver injury]. 142 11

The saponins (ASI, SK) used in this study was extracted from the root of Astragalus membranaceous Bge and Astragalus sieversianus Pull. ASI and SK were found to protect liver from chemical injury induced by CCl4, D-galactosamine and acetaminophen in mice. The two saponins were shown to impede the elevation of SGPT level, decrease the MDA content and increase the GSH concentration in mouse liver. Obvious improvement of histological changes were also observed. The protective action of ASI and SK against the hepatotoxicity was also shown in experiments using primary cultured rat hepatocytes. The average value of GPT in the medium treated with different concentration of ASI and SK (0.00075-0.18 mmol/L) was lower than that in control. Analyzing through multiple linear correlation, we showed that the lowering of SGPT was negatively related to the increase of GSH, positively related to the decrease of MDA in mice given CCl4 or acetaminophen in combination with ASI or SK. These results indicate that the hepato-protective effects of ASI and SK may be due to their anti-oxidation activities, since the content of liver protein in mice given ASI or SK was more than that in the controls. Moreover, the level of hepatic microsomal cytochrome P-450 in all mice given the two saponins were significantly increased, the liver metabolism and immunoregulating action produced by ASI and SK may be also involved in their hepato-protective effects.
...
PMID:[Effects of astragalus (ASI, SK) on experimental liver injury]. 144 65

Forty-three male mongrel dogs (12.5 +/- 2.5 kg) were divided into normal control (n = 7), immediate infusion (n = 8), non-infusion (n = 13) and delayed infusion (n = 15) groups. A 50% TBSA third degree surface burn was produced by igniting 3% napalm for 30 seconds on the shaved back. Cardiac, pulmonary, hepatic, renal and gastrointestinal functions were monitored following the thermal injury. The findings of these studies showed that mean arterial pressure, cardiac index, left ventricular work, right ventricular work, ADP/O ratio and ATP were all significantly decreased (P less than 0.05). However pulmonary artery wedge pressure, pulmonary vascular resistance, systemic vascular resistance, P(A-a)O2, Beef, Cr, UN, ALT, LDH, TB, DB, and MDA were markedly increased (P less than 0.05). Severe shock occurred soon after burns. Thirteen dogs died within 12 hours in the non-infusion group. All the dogs were resuscitated when immediate infusion of lactic acid Ringers solution was given according to Parkland formula, and all of them tide over shock stage smoothly without obvious changes in visceral functions. However, dogs were not resuscitated when infusion was delayed 6 hours postburn. The changes in visceral were even more severe in this group than those in non-infusion group. These results demonstrated that delayed resuscitation was an important factor of MOF in the early postburn stage. The marked increase in MDA in the myocardiac, lung, liver, renal and gastrointestinal tissues indicated that lipoperoxidation by free oxygen radicals was closely related with visceral damages.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Experimental study on early multiple organ failure after severe burns]. 159 85

The action of schizandrin B (Sin B) was observed in freshly isolated hepatocytes damaged by FeSO4/cysteine and CCl4. Two types of free radicals, .OH and .CCl3, generated from FeSO4/cysteine and CCl4, respectively, induced lipid peroxidation in hepatocytes. It was found that the speed of lipid peroxidation (MDA production) and the degree of alteration in hepatocyte morphology were closely related to the type of free radicals. MDA production and membrane protrusion of hepatocytes injuries by FeSO4/cysteine were faster and more severe than those observed with CCl4. Sin B was shown to decrease the production of MDA and the release of GPT and LDH, and to increase hepatocyte viability as well as maintaining the integrity of the hepatocyte membrane surface. These actions of Sin B were stronger than vitamin E at the same concentration. It was observed that no inhibitory effect of phenobarbital, a typical inducer of cytochrome P-450, as Sin B induced liver cytochrome P-450, on MDA production in hepatocytes damaged by FeSO4/cysteine. The results suggest that Sin B possesses antioxidant activity.
...
PMID:[Action of schizandrin B, an antioxidant, on lipid peroxidation in primary cultured hepatocytes]. 262 22

A study was conducted to elucidate the possible role of singlet oxygen in pathogenesis of D-galactosamine-induced liver injury. Tissue and plasma levels of singlet oxygen were determined with chemiluminescence analysis. Following results were obtained: 1) Chemiluminescence as well as malondialdehyde, which is regarded as one of terminal products of lipid peroxidation, significantly increased in the liver and plasma of rats treated with D-galactosamine. 2) Elevation of plasma GPT and total bilirubin was also observed in rats with D-galactosamine-induced liver injury. Histological examination of the liver revealed submassive hepatic necrosis. 3) Administration of vitamin E, a radical scavenger of singlet oxygen, significantly inhibited the increases of chemiluminescence and MDA in the liver and plasma as well as the elevations of GPT and total bilirubin in the plasma. Histological changes of the liver were also found to improve significantly by vitamin E administration. In conclusion, singlet oxygen seems to be definitely involved, at least in part, in pathogenesis of liver damage induced by D-galactosamine. In addition, inhibition of the liver injury is possible, to some extent, by administration of vitamin E, one of the potent radical scavengers of singlet oxygen.
...
PMID:[Role of singlet oxygen in pathogenesis of liver injury in rats treated with D-galactosamine]. 279 56

Sixty gnotobiotic rats with 5 strains of bacteria in intestine were randomized to 4 groups: (1) Sham injury group (controls, n = 6). (2) Early fluid resuscitation (EFR) group (n = 24), receiving fluid resuscitation (Parkland formula) immediately after scald (40% TBSA, third degree). (3) Delayed fluid resuscitation (DFR) group (n = 24) receiving resuscitation 6 hours later after scald. (4) Treatment group (n = 12) receiving DFR and the therapy of VitC and VitE. At 8, 24, 48 and 72 hours after injury, the animals (n = 6, at each point) were sacrificed and the content of oxygen free radicals (OFR), SOD,GSHPx and MDA in the heart, liver, kidney and lung were determined. Morphological Changes of organs, PaO2, PaCO2 and the content of serum CPK, LDH, GPT, GOT, BUN and Cr were also examined. Both EFR and DFR groups demonstrated elevated content of OFR and MDA and reduced content of SOD and GSHPx in their organs. Morphological and serological changes were also observed. All these changes were more obvious in DFR group than in EFR group. After the treatment of VitC and VitE, the changes were ameliorated. Our results suggested that DFR induced the production of OFR, resulting in lipid peroxidation and that OFR injury might be one of the main factors in the pathogenesis of multiple organ injury after DFR.
...
PMID:[Multiple organ injury after delayed fluid resuscitation in severely scalded rats: role of oxygen free radicals]. 764 95

In order to assess the liver protective activity and the antioxidant properties of a new silybin complex (IdB1016), we carried out a short-term pilot study on 20 patients with chronic active hepatitis (CAH), randomly assigned to 240 mg of silybin b.i.d. (10 patients, 4 m/6 f, mean age: 50 years) or placebo (10 patients, 2 m/8 f, mean age: 55 years). Blood samples were collected before and after 7 days of treatment for liver function tests (LFTs), malonaldehyde (MDA) as an index of lipid peroxidation, and copper (Cu) and zinc (Zn), two trace elements involved in protecting cells against free radical-mediated lipid peroxidation. In the treated group, there was a statistically significant reduction of mean (+/- SEM) serum concentrations of aspartate aminotransferase (AST) from 88.0 (+/- 13.3) to 65.9 (+/- 7.5) u/l, (p < 0.01), of alanine aminotransferase (ALT) from 115.9 (+/- 12.9) to 82.5 (+/- 10.6) u/l (p < 0.01), of gamma-glutamyltranspeptidase (gamma-GT) from 51.4 (+/- 9.3) to 41.3 (+/- 4.2) u/l (p < 0.02) and of total bilirubin (TB) from 0.76 (+/- 0.08) to 0.53 (+/- 0.04) mg/dl (p < 0.05). Alkaline phosphatase (AP) fell slightly from 143.4 (+/- 6.4) to 137.5 (+/- 7.8) u/l. There were no significant changes in MDA, Cu or Zn serum concentrations. These results show that IdB1016 may improve LFTs related to hepatocellular necrosis and/or increases membrane permeability in patients affected by CAH.
...
PMID:A pilot study on the liver protective effect of silybin-phosphatidylcholine complex (IdB1016) in chronic active hepatitis. 822 95

The protective action of Glycyrrhiza flavonoids (GF), the major components in the radix of Glycyrrhiza, on carbon tetrachloride-induced hepatotoxicity was investigated. The carbon tetrachloride-induced increases of serum glutamic-pyruvic transaminase and lactate dehydrogenase were significantly inhibited by GF dose-dependently. Carbon tetrachloride-induced necrosis in mice were ameliorated by GF pretreatment. Concomitantly, the carbon tetrachloride-induced elevation of MDA in the liver was lowered by GF. GF neither reduced the activities of the two enzymes in normal mouse sera nor directly inhibited the activities of the two enzymes in the serum. These findings suggest that the anti-lipid peroxidation effect of GF was contributed to its protective action against carbon tetrachloride-induced hepatotoxicity.
...
PMID:[The protective action of glycyrrhiza flavonoids against carbon tetrachloride hepatotoxicity in mice]. 828 64

Methylene dianiline (DDM) is a chemical intermediate in the production of isocyanates and other industrial chemicals, and it is hepatotoxic in humans. The acute hepatotoxicity of orally administered DDM was characterized in rats. Rats receiving DDM (25-225 mg/kg, per os) demonstrated a dose-dependent elevation in serum alanine aminotransferase activity, g-glutamyltransferase activity, and serum bilirubin concentration. DDM also caused a decrease in bile flow and an elevation in liver weight. Significant changes in these markers of liver injury occurred between 8 and 12 hr after a single, oral administration of DDM. Histologically, DDM caused multifocal, necrotizing hepatitis with neutrophil infiltration. Changes in the portal regions consisted of bile ductular necrosis, portal edema, neutrophil infiltration, mild fibrin exudation, and segmental necrotizing vasculitis. The role of cytochrome P450 monooxygenase (MO)-mediated metabolism in DDM hepatotoxicity was evaluated using the MO inhibitors, aminobenzotriazole and SKF-525A and the MO inducers phenobarbital and beta-naphthoflavone. Aminobenzotriazole provided protection from DDM-induced hepatotoxicity, whereas SKF-525A had no effect. The effect of phenobarbital pretreatment depended on the dose of DDM administered. At a dose of DDM that produced a maximal hepatotoxic response, phenobarbital did not influence hepatotoxicity. However, phenobarbital pretreatment provided protection against the hepatotoxic effects of a lower dose of DDM. beta-naphthoflavone pretreatment had a more modest effect on DDM-induced hepatic insult. These results demonstrate that DDM causes acute hepatotoxicity in the rat that is dose and time dependent. Results using inducers and inhibitors of MO suggest that DDM requires bioactivation to exert toxicity; however, the relationship between metabolism and toxicity may be complex.
...
PMID:Characterization of acute 4,4'-methylene dianiline hepatotoxicity in the rat. 835 98

Hibiscus protocatechuic acid (PCA), a simple phenolic compound isolated from Hibiscus sabdariffa L., was studied for its protective effects against oxidative damage induced by tert-butylhydroperoxide (t-BHP) in a primary culture of rat hepatocytes. It had been reported that exposure of isolated hepatocytes to t-BHP results in leakage of lactate dehydrogenase (LDH) and alanine transaminase (ALT), peroxidation of cellular lipids, and depolarization of mitochondria. The present investigations showed that PCA at concentrations of 0.05 mg/ml and 0.10 mg/ml significantly decreased the leakage of LDH (P < 0.01) and ALT (P < 0.05 and P < 0.01) and the formation of malondialdehyde (MDA; P < 0.05 and P < 0.01) induced by 30-min treatment with t-BHP (1.5 mM) in primary cultured rat hepatocytes. PCA also attenuated t-BHP (0.10 mM) induced mitochondrial depolarization as determined by a retention test of rhodamine 123 and DNA repair synthesis as evidenced by unscheduled DNA synthesis (UDS). In addition, PCA exhibited an effective ability to quench 1,1-diphenyl-2-picrylhydrazyl radicals (DPPH). In conclusion, PCA demonstrated protective effects against cytotoxicity and genotoxicity of hepatocytes induced by t-BHP. One of mechanisms of PCA's protective effect may be associated with its property of scavenging free radicals.
...
PMID:Hibiscus protocatechuic acid protects against oxidative damage induced by tert-butylhydroperoxide in rat primary hepatocytes. 876 Mar 95


1 2 3 4 5 6 7 8 9 10 Next >>

---