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)

In the cacao-growing region in the southern part of the state of Bahia, the organochlorine insecticides, mainly gamma-benzene hexachloride (BHC) and dichlorodiphenyltrichloroethane (DDT), have been used for about 40 years on cacao crops and in public health programs for control of the insect vectors of different diseases, especially malaria. This paper presents the results of tests performed on 127 persons, all males, between the ages of 15 and 52 years, divided into eight groups as follows: three groups consisted of persons occupationally exposed to 1.5% BHC, that is, technical hexachlorocyclohexane (HCH); two groups consisted of individuals who had had occasional contact with the products or worked in areas near those in which they were used; two groups were appliers of DDT, and the last group--the control group--consisted of 50 individuals who had had no history of occupational exposure to insecticides. All the participants underwent testing to determine the parameters of biochemistry, hematology, and organochlorine insecticide residues in the blood. It was found that improper handling of the products and failure to use individual protective equipment, together with longer time of exposure, significantly increased the rates of GOT and GPT in the appliers of DDT and technical HCH, and in the latter the rates of alkaline phosphatase, albumin, and cholesterol were also found to be higher. In view of the high morbidity among pesticide appliers in agriculture and public health campaigns, it is important to institute programs to teach these workers to avoid contamination of their persons and of the environment by developing good hygiene habits, using individual protective equipment, and correctly handling the products. Rural workers and public health authorities must become aware of the importance of protective equipment, periodic health examinations, and reduced environmental pollution in order to lessen occupational risks of field workers and promote improved conditions of life for the rural population at large.
Bol Oficina Sanit Panam 1991 Dec
PMID:[Risk factors related with occupational and environmental exposure to organochlorine insecticides in the state of Bahia, Brazil, 1985]. 183 87

Swiss Webster male mice, 22 +/- 3 g, killed 17-18 h following the concomitant oral administration of acetaminophen (350 mg/kg) and N-acetyl-cysteine (NAC, 100-500 mg/kg, treated) had statistically significant lower plasma transaminases (GOT and GPT) than control mice (acetaminophen + water). Possible mechanisms underlying this protective effect of NAC were examined. NAC (500 mg/kg) reduced [14C]acetaminophen-derived radioactivity in the blood and tissues but increased the percentage of the dose in the gastrointestinal tract. Depletion of hepatic sulphydryl compounds below 75% of the control value was prevented by NAC treatment, whereas urinary excretion of mercapturate and sulfate, metabolites derived from sulphydryls, were proportionally increased and excretion of unchanged drug was decreased by NAC. Absorption of acetaminophen from the small intestine was prevented by NAC and this was attributed to an inhibition in gastric emptying. Since all changes observed following NAC treatment could be attributed to inhibition of gastric emptying, it was considered the major mechanism responsible for affording in mice protection from acetaminophen-induced hepatocellular damage following concomitant oral administration.
...
PMID:N-acetylcysteine-induced inhibition of gastric emptying: a mechanism affording protection to mice from the hepatotoxicity of concomitantly administered acetaminophen. 726 84

1. The roles of cytochrome P450 monooxygenases (P450) and glutathione (GSH) in styrene hepatotoxicity were investigated in mice by pretreating with either phenobarbital (PB; P450 inducer), SKF 525A (P450 inhibitor), N-acetylcysteine (NAC; GSH precursor), or saline (vehicle control) prior to a 6-h exposure to either 500 ppm styrene on air. 2. Styrene caused hepatocellular degeneration or necrosis in all groups; these changes were more extensive and severe in mice pretreated with PB. Styrene significantly increased relative liver weights and serum ALT and SDH levels only in mice pretreated with PB. NAC did not prevent GSH depletion or hepatotoxicity. 3. In the fat of SKF 525A-pretreated mice a slight but statistically significant increase in styrene levels was observed, suggesting that metabolism was decreased; the SO/styrene ratio in the fat of PB-pretreated mice showed a slight, but statistically significant, increase indicating a slight increase in styrene metabolism. Neither SKF 525A nor PB caused changes in microsomal enzyme activity in vitro. 4. These results suggest that styrene may be activated by a pathway not totally dependent upon P450 enzyme activity, or more likely that PB and SKF 525A are not specific for the P450 enzymes involved in activation and detoxification of styrene.
...
PMID:Effects of various pretreatments on the hepatotoxicity of inhaled styrene in the B6C3F1 mouse. 914 79

The aim of the study reported here was to demonstrate that dengue hemorrhagic fever occurs in Puerto Rico, that it is underreported, and that this underreporting is due partly to underdiagnosis in hospitals. Surveillance for severe dengue identified 986 hospitalizations for suspected dengue in 1990-1991. At the time, on the basis of available clinical and laboratory data, the surveillance system routinely identified 20 DHF cases, including three with dengue shock syndrome (DSS). Our subsequent review of these 986 patients' hospital records identified 102 whose records supported a clinical diagnosis of DHF (88) or DSS (14). Of the 102, there were 57 with positive virologic or serologic results for dengue and that met the World Health Organization criteria for DHF (fever, hemorrhagic manifestations, thrombocytopenia, and excessive capillary permeability). This group of 57 patients had a mean age of 38 years, contained a preponderance of males (34, 59.3%), included eight cases of DSS, and involved two (3.5%) fatalities (in females 16 and 55 years old). Hemorrhagic manifestations were mild; hemoconcentration, hypoalbuminemia, and elevated aspartate and alanine aminotransferase (AST and ALT) levels were frequently encountered. The median duration of hospitalization was five days. The clinical description of these laboratory-positive DHF cases in Puerto Rico is consistent with previous descriptions of DHF in the medical literature; but the patients' age distribution is similar to the pattern typically found in the Americas (where all age groups tend to be affected), as opposed to Southeast Asia (where mostly younger children are affected). The number of DHF cases identified by our study was nearly three times that reported through the established surveillance system. Our findings indicate that recognition and reporting of DHF by local clinicians needs to be improved.
Rev Panam Salud Publica 1997 May
PMID:Clinical manifestations of dengue hemorrhagic fever in Puerto Rico, 1990-1991. Puerto Rico Association of Epidemiologists. 918 59

Carbaryl, a carbamate pesticide, (LC50 15.08 mg/l for 96 hr, i.e. lethal concentration with 50% mortality) induced perturbations in the levels of certain biochemical components including the activities of some enzymes in the blood and liver of the fresh-water catfish, Clarias batrachus exposed to sublethal concentrations (1, 2 and 4 mg/l) of the pesticide for 96 hr and 15 days. The pesticide caused a decrease in the levels of total protein and glucose with a concomitant increase in the levels of inorganic phosphate and lactic acid in fish serum. However, very little change was recorded in the serum cholesterol level. The treatment of the fish with carbaryl led to a marked increase in the activities of transaminases (GOT and GPT), phosphatases (acid and alkaline) and lactate dehydrogenase in the fish serum, the magnitude of the effect being dependent on the pesticide concentration and duration of exposure. The increase in lactic acid concentration with subsequent decrease in glucose concentration indicates an enhanced rate of glycolysis due to pesticide stress. Furthermore, the significant decrease in the activity of fish liver succinate dehydrogenase suggests that anaerobic metabolism was favored over aerobic oxidation of glucose through Kreb's cycle in order to mitigate the energy crisis for survival. The rise in the activities of transaminases and acid phosphatase due to pesticide intoxication suggest enhanced protein catabolism and probable hepatocellular damage in the organism.
...
PMID:Effect of carbaryl on some biochemical constituents of the blood and liver of Clarias batrachus, a fresh-water teleost. 1047 30

Administration of acetaminophen (ACP, 400 mg/kg, i.p.) to fasted, male Swiss-Webster mice caused a rapid 90% decrease in total hepatic glutathione (GSH) and a 58% decrease in mitochondrial GSH by 2 h post ACP. This was followed by a time-dependent decrease (72%) in hepatic AdoMet synthetase activity and rise in plasma ALT levels (>10000 U/l) at 24 h post ACP treatment. AdoMet synthetase activity was maintained at 82, 78 and 60% of controls, respectively, by the cysteine prodrugs PTCA, CySSME and NAC. Total hepatic and mitochondrial GSH levels were also protected from severe ACP-induced depletion by CySSME and MTCA. These results suggest that the maintenance of GSH homeostasis by cysteine prodrugs can protect mouse hepatic AdoMet synthetase, a sulfhydryl enzyme whose integrity is dependent on GSH, as well as the liver itself from the consequences of oxidative stress elicited by toxic metabolites of xenobiotics.
...
PMID:Acetaminophen-induced suppression of hepatic AdoMet synthetase activity is attenuated by prodrugs of L-cysteine. 1208 14

Azathioprine (AZA) is an important drug used in the therapy of autoimmune system disorders. It induces hepatotoxicity that restricts its use. The rationale behind this study was the proven efficacy of N-acetylcysteine (NAC; a replenisher of sulfhydryls) and reports on the antioxidant potential of aminoguanidine (AG; an iNOS inhibitor), that might be useful to protect against the toxic implications of AZA. AG (100 mg/kg; i.p.) or NAC (100 mg/kg; i.p.) were administered to the Wistar male rats for 7 days and after that AZA (15 mg/kg, i.p.) was given as a single dose. This caused an increase in the activity of hepatic aminotransferases (AST and ALT) in the serum 24 h after AZA treatment. AZA (7.5 or 15 mg/kg, i.p.) also caused an increase in rat liver lipid peroxides and a lowering of reduced glutathione (GSH) contents. In the other part of experiment, protective effects of AG and NAC were observed on AZA induced hepatotoxicity. NAC significantly protected against the toxic effects produced by AZA. Pretreatment with NAC prevented any change in the activities of both the aminotransferases after AZA. This pretreatment also resulted in a significant decline in the contents of lipid peroxides and a significant elevation in GSH level was evident after AZA treatment. In the group with AG pretreatment the activities of AST and ALT did not increase significantly after AZA when compared to control. However, the lipid peroxides and GSH levels did not have any significant difference when compared to AZA group. These observations also indicate that the improvement in the GSH levels by NAC is the most significant protective mechanism rather than any other mechanistic profile. The protective effect of AG against the enzyme leakage seems to be through the liver cell membrane permeability restoration and is independent of any effects on liver GSH contents.
...
PMID:A comparison of hepatoprotective activities of aminoguanidine and N-acetylcysteine in rat against the toxic damage induced by azathioprine. 1272 94

Oxidative stress and especially its connection with many diseases has been discussed much recently. Among markers of oxidative stress there appear new and quite specific ones called advanced oxidation protein products (AOPPs). We tried to influence the level of AOPPs by an antioxidant therapy with N-acetylcysteine. Fourteen individuals with many cardiovascular risk factors were examined. All these patients were administered acetylcysteine (NAC) 600 mg/day orally during 20 days. Before starting the therapy we determined AOPP, albumin cobalt binding (ACB), glucose, creatinine, urea, ALT, AST, cholesterol, LDL, HDL and triglycerides values in peripheral venous blood in all individuals. After finishing our intervention we determined AOPP, ACB and glucose level again. Our results show a statistically significant decrease in AOPP levels after 20-day N-acetylcysteine therapy (medians, initially 82.2, at study end 74.3 umol/l, p = 0.039). We demonstrate a significant decrease in AOPP levels after 20-day N-acetylcysteine therapy in dose 600 mg/day.
...
PMID:The antioxidant acetylcysteine reduces oxidative stress by decreasing level of AOPPs. 1574 60

Steatotic livers are highly susceptible to I/R (ischaemia/reperfusion) injury and, therefore, the aim of the present study was to evaluate the in vivo effect of NAC (N-acetylcysteine) on hepatic function in the early and initial late phase of warm liver I/R injury in steatotic rabbits. Twelve New Zealand White rabbits were fed a high-cholesterol (2%) diet. The control group (n=6) underwent lobar liver ischaemia for 1 h, followed by 6 h of reperfusion. In the treated group receiving NAC (n=6), an intravenous infusion of NAC was administered prior to and during the 6 h reperfusion period. Systemic and hepatic haemodynamics were monitored continuously. ALT (alanine aminotransferase) activity and bile production were measured. NMR spectroscopy was used to analyse bile composition. Oxidation of DHR (dihydrorhodamine) to RH (rhodamine) was used as a marker of production of reactive oxygen and nitrogen species. Moderate centrilobular hepatic steatosis was demonstrated by histology. The results showed that NAC administration significantly improved portal flow, hepatic microcirculation, bile composition and bile flow after 5 h of reperfusion. NAC administration was also associated with less hepatocellular injury, as indicated by ALT serum activity, and decreased the oxidation of DHR to RH. In conclusion, NAC administration decreased the extent of I/R injury in the steatotic liver, particularly during the late phase of reperfusion.
...
PMID:N-Acetylcysteine ameliorates the late phase of liver ischaemia/reperfusion injury in the rabbit with hepatic steatosis. 1598 89

3-Butene-1,2-diol (BDD), an allylic alcohol and major metabolite of 1,3-butadiene, has previously been shown to cause hepatotoxicity and hypoglycemia in male Sprague-Dawley rats, but the mechanisms of toxicity were unclear. In this study, rats were administered BDD (250 mg/kg) or saline, ip, and serum insulin levels, hepatic lactate levels, and hepatic cellular and mitochondrial GSH, GSSG, ATP, and ADP levels were measured 1 or 4 h after treatment. The results show that serum insulin levels were not causing the hypoglycemia and that the hypoglycemia was not caused by an enhancement of the metabolism of pyruvate to lactate because hepatic lactate levels were either similar (1 h) or lower (4 h) than controls. However, both hepatic cellular and mitochondrial GSH and GSSG levels were severely depleted 1 and 4 h after treatment and the mitochondrial ATP/ADP ratio was also lowered 4 h after treatment relative to controls. Because these results suggested a role for hepatic cellular and mitochondrial GSH in BDD toxicity, additional rats were administered N-acetyl-l-cysteine (NAC; 200 mg/kg) 15 min after BDD administration. NAC treatment partially prevented depletion of hepatic cellular and mitochondrial GSH and preserved the mitochondrial ATP/ADP ratio. NAC also prevented the severe depletion of serum glucose concentration and the elevation of serum alanine aminotransferase activity after BDD treatment without affecting the plasma concentration of BDD. Thus, depletion of hepatic cellular and mitochondrial GSH followed by the decrease in the mitochondrial ATP/ADP ratio was likely contributing to the mechanisms of hepatotoxicity and hypoglycemia in the rat.
...
PMID:Protection of rats against 3-butene-1,2-diol-induced hepatotoxicity and hypoglycemia by N-acetyl-l-cysteine. 1612 19


1 2 3 4 Next >>

---