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)

Trivalent chromium (Cr(III)) preadministered intraperitoneally (5 mg Cr/kg body weight) to rats and mice protected these animals from acute lethal toxicity of carbon tetrachloride (CCl4). Some other metals, Cr(VI), Cu(II), and Zn(II), had no effect on CCl4 lethal toxicity. DL-alpha-tocopherol, one of the antioxidative agents, showed similar protective effects to Cr(III). Activities of serum GOT and GPT in mice were increased sharply by the administration of CCl4, but these elevations were depressed by Cr(III) preadministration. Serum glucose levels of mice increased transiently after CCl4 administration and then in the control group fell to hypoglycemic levels after 6 hr, whereas the Cr(III)-pretreated group kept to homeostatic levels. Lipid peroxidation of microsomes in mice 24 hr after Cr(III) administration was lower than that of the control. These results suggest that Cr(III) preadministered to mice might act as a radical scavenger to CCl4 to form trichloromethyl radicals which are a major initial product of CCl4 in liver cells.
...
PMID:Protective effect of chromium(III) on acute lethal toxicity of carbon tetrachloride in rats and mice. 164 94

Human intrahepatic biliary epithelial cells are important immune targets in a variety of hepatobiliary diseases particularly primary biliary cirrhosis and primary sclerosing cholangitis. The ability to isolate and maintain these cells in short term primary tissue culture has permitted us to develop an in vitro cytotoxicity assay for the study of these cells as potential targets to a variety of toxic stimuli. We have therefore established a chromium-51 (51Cr) release cytotoxicity assay for use with primary cultures of human intrahepatic biliary epithelial cells. The method is simple, reproducible and is more sensitive than dye exclusion, light microscopy and release of lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase.
...
PMID:A 51Cr release cytotoxicity assay for use with human intrahepatic biliary epithelial cells. 167 52

A comparison of the effects of intraperitoneal and subcutaneous routes of administration of sodium dichromate on nephrotoxicity in rats was studied. Dichromate when injected subcutaneously (SC group) produced a higher degree of nephrotoxicity than when administered intraperitoneally (IP group). It caused severe progressive proteinuria followed by polyuria and glucosuria, reaching maximum levels at 3 days after treatment in the SC group, whereas it produced mild proteinuria without glucosuria in the IP group. The dose-dependent increases in blood urea nitrogen (BUN) and creatinine concentrations, shown in the SC group, were not observed in the IP group. However, between the two groups, there were no great differences in either the urinary excretion rate of chromium or the electrophoretic patterns of urinary protein in the day 1 urine specimens. Pretreatment of phenobarbital (PB) had no remarkable effect on the dichromate-induced nephrotoxicity. In contrast, it potentiated dichromate-induced hepatotoxicity, the indices of which were the elevation in serum alanine aminotransferase (ALT) activity and hepatic lipid peroxide formation. These results suggest that the dependence of dichromate-induced nephrotoxicity on the route of administration is related to the chemical forms of chromium reaching the kidney, and the necrotizing property of dichromate results from its metabolic fate in vivo.
...
PMID:Nephrotoxicity of sodium dichromate depending on the route of administration. 178 35

Oral administration of L-triiodothyronine (L-T3) (0.015-1 mg/kg) for 30 days to mature rats or cynomolgus monkeys resulted in both species in a high mortality at 1 mg/kg (after 2 weeks of treatment) and a progressive loss in body weight. Dose-related elevations in plasma marker enzymes occurred, mainly after 1-2 weeks of treatment. The approximate no-effect dose for these changes was around 0.015-0.020 mg/kg for both rat and primate. The large elevations of leucine aminopeptidase (LAP) at 1 mg/kg L-T3 in monkey indicated hepatocellular toxicity although in the rat such large increases in alanine aminotransferase (ALT) and glutamate dehydrogenase (GLDH) were not seen. L-T3 also showed little toxicity to rat hepatocytes in vitro. High concentrations of L-T3 (7 x 10(-9) to 7 x 10(-7) M) had minimal effects on parameters of cell viability such as lactate dehydrogenase (LDH) leakage, chromium-51 release and [3H]leucine incorporation. Urinary enzymes in the rat showed a similar profile to those in plasma. Large rises in alkaline phosphatase (AKP) and N-acetyl glucosaminidase (NAG) at 1 mg/kg indicated possible proximal tubular damage although this was not supported histologically. Clinically, in both species L-T3 appeared more toxic to males than females but this was not supported histologically. The histological lesions observed were different in the 2 species. In the monkeys there was extensive lipid vacuolation of hepatocytes and changes in thyroid and adrenal cortex. In the rat there was fine, non-lipid vacuolation of hepatocytes and thyroid changes. In the rat, 2 previously unreported lesions were also noted. There were multinucleated cells in the renal distal tubular epithelium, and focal fibroplasia of serosal surfaces of abdominal viscera.
...
PMID:Comparison of the toxicity of orally administered L-triiodothyronine (T3) in rat and cynomolgus monkey. 320 78

The Authors have studied AST and ALT enzymatic activities in the workers of two firms, the former of which (tannery) with a high and the latter (boot and shoe factory) with a low level of hepatic-toxic risk. The influence of various trouble factors such as age, sex and seniority was eliminated through appropriate statistical techniques. A significant difference was evidenced between AST and ALT levels in two firms, chiefly attributable to the quantity and quality of the substances utilized in the two technological cycles: trichloroethylene, chromium, sulphuric acid, mineral oils, ammonia, N-hexane, pentanes acetone, ciclo hexane, methanol, ethyl acetate, isopropyl acetate, toluene, methylene chloride.
...
PMID:[Levels of aspartate aminotransferase and alanine aminotransferase in two factories with various hepato-toxic risks]. 734 21

The intravenous injection of zinc chloride immediately before and 15 minutes after alloxan or dithizone prevented the usual hyperglycaemia observed 24 hours after induction of diabetes. The intravenous injection of manganese chloride prevented any marked rise of blood glucose, while chromium and cobalt chlorides lowered the blood glucose level to a certain extent. In alloxan diabetic rats, serum GOT and GPT levels were significantly higher than normal. The serum GOT levels were higher in animals injected with chromium than cobalt, zinc and manganese; while serum GPT levels were higher in cobalt than in chromium, zinc and manganese. In dithizone diabetes, serum GOT and GPT were increased in animals injected with cobalt than chromium, zinc and manganese. Alloxan diabetic rats showed lower serum alkaline phosphatase levels and higher in animals injected with cobalt than chromium, zinc and manganese. For dithizone, there are statistically significant differences in all cases. In alloxan diabetes, coeruloplasmin was higher than normal, while intravenous injection of dithizone was without effect on serum coeruloplasmin.
...
PMID:Serum enzyme changes due to trace amounts of some transition metal ions on the induction of experimental diabetes. 742 63

Urinary biochemical indicators of renal injury were examined in 84 male and 38 female ferrochromium-producing workers exposed to water-soluble chromium compounds [Cr(VI)]. The indicators examined included urinary chromium (U-Cr), alkaline phosphatase (ALP), gamma-glutamyl transferase (gamma-GT), glutamic-oxalacetic and glutamic-pyruvic transaminases (GOT & GPT), lactate dehydrogenase (LDH), N-acetyl-beta-D-glucosaminidase (NAG), total protein (TPr) and beta 2-microglobulin (beta 2-MG). The U-Cr levels in the exposed group were approximately 1.8 times that of the control group. Compared to controls, the activities of gamma-GT, NAG, ALP, GOT and LDH in the urine of workers were significantly increased whenever U-Cr concentration exceeded 45 microgram/g creatinine. The activities of gamma-GT, GOT and NAG were elevated in workers employed for longer than ten years. However, no clear dose-response relationships nor time-effect relationships were found. The present results suggest that long-term exposure to water-soluble chromium [Cr(VI)] produces chronic renal injury. The site of the injury appears to mainly involve the proximal tubule. U-Cr concentrations of > 15 microgram/g creatinine can be proposed as a threshold dosage for nephrotoxicity, and gamma-GT, NAG and ALP are early sensitive indicators of the most valuable for evaluating the renal injury.
...
PMID:Chromium-induced early changes in renal function among ferrochromium-producing workers. 791 62

Activated sludge is a rich source of nitrogenous matter and has been recommended as cheap supplement in animal feed. It has been incorporated into cattle and poultry feed. It is well known that sewage of purely domestic origin is also contaminated with heavy metals, pesticides, and other organic pollutants. A study was undertaken to determine the toxic effects of heavy metal-contaminated domestic sewage sludge on young male Wistar rats by supplementing dehydrated activated sludge in their diet at concentrations of 5, 10, 15 and 20%. The sludge was found to be contaminated with 1.820 (zinc), 0.273 (nickel), 0.017 (lead), 0.053 (copper), 0.006 (chromium), and 0.005 (cadmium)mg/g of dry sludge, by analysis by atomic absorption spectroscopy. The toxic effects of sludge-supplemented diets on individual groups of rats were assessed by assaying various enzyme activities in serum, liver, muscle, and brain. Levels of serum and liver alanine aminotransferase and succinate dehydrogenase (SDH) were significantly low in all the sludge-supplemented diet-fed (SSDF) rats. Similarly, serum lactate dehydrogenase (LDH) and muscle SDH activity were also significantly reduced in the SSDF rats. On the other hand, liver and muscle LDH, serum and liver aspartate aminotransferase, and serum and muscle alkaline phosphatase activities were significantly higher in all the SSDF animals. Brain and muscle acetylcholinesterase activity was significantly high in all the SSDF groups. This study indicates that even though the sludge is a rich source of nitrogenous matter, its supplementation in poultry and animals feed should be done with caution. Otherwise, the contaminants found in the sludge will biomagnify in the food chain and lead to various toxicological hazards.
...
PMID:A study of toxic effects of heavy metal contaminants from sludge-supplemented diets on male Wistar rats. 1005 66

The ability of chromium (Cr) salts to increase metallothionein (MT) levels in rat liver, kidney and pancreas, and its relationship with the presence of toxic effects are reported here. Rats were injected subcutaneously with 0, 10, 20, 30, 40, or 50 mg K2Cr2O7/kg and sacrificed 24 h later. Total Cr accumulation followed a dose-dependent pattern, levels in kidney being higher than those in liver or pancreas, suggesting different tissue bioavailabilities and accumulation patterns. Cr(IV) administration resulted in a tissue-specific MT induction: pancreas and liver showed five- and 3.5-fold MT increases, respectively; no increase was observed in the kidney. A positive correlation was observed between zinc and MT concentrations in liver, and between total Cr and MT concentrations in pancreas. Serum alpha-amylase activity showed a dose-dependent increase starting from 20 mg/kg, whereas serum glucose levels increased at doses higher than 30 mg/kg. Serum aspartate aminotransferase and alanine aminotransferase activities were increased in a dose-dependent manner, from 20 and 30 mg/kg, respectively. Our results showed that treatment with Cr(VI) can induce MT synthesis in pancreas and suggests a subsequent binding of Cr to MT. Also, pancreas is a target organ for Cr toxicity, and the usefulness of alpha-amylase activity as a sensitive biomarker of Cr toxicity in human exposed populations merits further study.
...
PMID:Chromium increases pancreatic metallothionein in the rat. 1068 10

The purpose of this study was to evaluate the interactive toxicity of ethanol with potassium dichromate (K2Cr2O7-chromium). Young, male Wistar rats (100-120 g) were divided into four groups of five or six animals each and were dosed, through water, with 10% ethanol (vol./vol.) or 25 ppm chromium or were dosed with a combination of ethanol+chromium at the same concentrations for a period of 22 weeks ad libitum and were maintained on normal diet. Control animals were maintained on a normal diet and water for the same period. The serum succinate dehydrogenase and liver total triglyceride levels were significantly reduced in the three treated groups. The serum alkaline phosphatase levels were significantly reduced in ethanol-treated rats, and there was no significant change in the acid phosphatase activity. Serum aspartate and alanine aminotransferase levels in the three treated groups were significantly increased. The liver glycogen significantly decreased in both the ethanol-treated and the chromium-treated rats. There was a significant increase in liver total cholesterol levels in chromium-treated rats. Total glutathione levels were significantly decreased in the livers of ethanol-treated and ethanol+chromium-treated rats. To further substantiate these findings, a histological examination of the liver and kidneys was undertaken. The livers of alcohol-treated animals showed altered hepatic architecture in the centrilobular and periportal areas, with increased sinusoidal space (space of Disse), vacuolation, and necrosis of hepatocytes. Similar changes were observed in a histological examination of the livers of chromium-treated rats, except that the damage to the hepatocytes was more confined to the periportal area. Moreover, histological examination of the livers of ethanol+chromium-treated rats revealed uniform damage in the centrilobular and periportal areas, as was observed in the groups treated either with ethanol or chromium. The histological examination of the kidneys in the three treated groups revealed significant damage to the renal tubules and Bowman's capsule, which showed vacuolation and degeneration of the basement membrane. These findings correlate well with the serum enzyme levels found in the treated groups. It is evident from this study that chronic ethanol consumption sensitizes the liver to the toxic action of agents such as chromium. It leads to impairment of the biochemical functions in the liver, and it causes liver and kidney damage. Long-term simultaneous exposure to ethanol and chromium may cause severe health problems in people who are alcoholics and work in chrome-plating and leather-tanning industries.
...
PMID:A subtoxic interactive toxicity study of ethanol and chromium in male Wistar rats. 1133 Nov 7


1 2 3 4 5 6 Next >>

---