Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Streptozotocin-diabetic and non-diabetic rats were given vanadyl sulphate in drinking water at concentrations of 0.5-1.5 mg/ml for one year. It was found that vanadyl treatment did not produce persistent changes in plasma aspartate aminotransferase, alanine aminotransferase, and urea, specific morphological abnormalities in the brain, thymus, heart, lung, liver, spleen, pancreas, kidney, adrenal, or testis, or abnormal organ weight/body weight ratio for these organs in either non-diabetic or diabetic animals. Treatment significantly reduced the incidence of the occurrence of urinary stones in non-diabetic rats. In diabetic animals vanadyl treatment significantly reduced the mortality rate and prevented the elevation of plasma levels of alanine aminotransferase and urea, the increases in organ size, and the occurrence of megacolon but did not affect the development of renal and testicular tumours. Plasma and tissue concentrations of vanadium were determined and found to have the following order of distribution: bone > kidney > testis > liver > pancreas > plasma > brain. Vanadium was retained in these organs at 16 weeks following vanadyl withdrawal while the plasma levels were beneath detection limits. It is concluded that vanadyl sulphate at antidiabetic doses is not significantly toxic to rats following a one-year administration in drinking water, but vanadium may be retained in various organs for months after cessation of treatment.
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PMID:Toxicity studies on one-year treatment of non-diabetic and streptozotocin-diabetic rats with vanadyl sulphate. 787 Jun 97

Streptozotocin (STZ) has drawn attention as a potential source of oxidative stress, which induces genotoxicity. We investigated the effects of STZ on DNA damage in the liver and kidney, as well as the protective effects of antioxidants, by using the alkaline single-cell gel electrophoresis assay, and by measuring the ratio of 8-hydroxy-2'-deoxyguanosine (8-OHdG) to dG. A single intraperitoneal injection of STZ (150 mg/kg) increased serum levels of glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and blood urea nitrogen (BUN), and also caused DNA damage in the liver and kidney, which recovered slowly with time. Antioxidants,(ascorbic acid, trolox and probucol) prevented the STZ-induced elevation of DNA damage in the liver and kidney and inhibited the increase in serum levels of AST, ALT and BUN. Thus ascorbic acid, trolox, and probucol protected the mice against STZ-induced DNA damage that might contribute to the development of hepatic or renal disease.
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PMID:DNA damage and the effect of antioxidants in streptozotocin-treated mice. 1206 20

Fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, and its metabolites have been reported to protect against oxidative DNA damage in vitro. Streptozotocin (STZ) has drawn attention as a potential source of oxidative stress that induces genotoxicity. In order to elucidate the antioxidative effects of fluvastatin in vivo, we investigated the effects of 7-day treatment with fluvastatin on DNA damage in STZ-treated mice, as well as the effects of the main fluvastatin metabolites (M2, M3 and M4) and other inhibitors of the same enzyme, pravastatin and simvastatin. Protective effects against DNA damage in the liver and kidney from STZ-treated mice were assessed by the single-cell gel electrophoresis assay, and by detecting 8-hydroxy-2'-deoxyguanosine. A single intraperitoneal injection of STZ (150 mg/kg) increased serum levels of glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and blood urea nitrogen (BUN), and also caused DNA damage in the liver and kidney. Fluvastatin and its metabolites prevented the STZ-induced elevation of DNA damage and inhibited the increase in serum levels of AST, ALT and BUN. Fluvastatin and its metabolites showed protective effects against DNA damage as potent as that of the reference antioxidants (ascorbic acid, trolox and probucol) though pravastatin and simvastatin still lacked protective activity. Fluvastatin protected the mice against STZ-induced DNA damage, and may reduce the risk of oxidative stress in vivo.
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PMID:Antioxidative effects of fluvastatin and its metabolites against DNA damage in streptozotocin-treated mice. 1238 3

Streptozotocin (STZ)-induced diabetic (DB) mice challenged with single ordinarily lethal doses of acetaminophen (APAP), carbon tetrachloride (CCl4), or bromobenzene (BB) were resistant to all three hepatotoxicants. Mechanisms of protection against APAP hepatotoxicity were investigated. Plasma alanine aminotransferase, aspartate aminotransferase, and liver histopathology revealed significantly lower hepatic injury in DB mice after APAP administration. HPLC analysis of plasma and urine revealed lower plasma t1/2, increased volume of distribution (Vd), and increased plasma clearance (CLp) of APAP in the DB mice and no difference in APAP-glucuronide, a major metabolite in mice. Interestingly, covalent binding of 14C-labeled APAP to liver target proteins; arylation of APAP to 58, 56, and 44 kDa acetaminophen binding proteins (ABPs); and glutathione (GSH) depletion in the liver did not differ between nondiabetic (non-DB) and DB mice in spite of downregulated hepatic microsomal CYP2E1 and 1A2 proteins in the DB mice, known to be involved in bioactivation of APAP. Compensatory cell division measured via 3H-thymidine pulse labeling and immunohistochemical staining for proliferating cell nuclear antigen (PCNA) indicated earlier onset of S-phase in the DB mice after exposure to APAP. Antimitotic intervention of liver cell division by colchicine (CLC) after administration of APAP led to significantly higher mortality in the DB mice suggesting a pivotal role of liver cell division and tissue repair in the protection afforded by diabetes. In conclusion, the resistance of DB mice against hepatotoxic and lethal effects of APAP appears to be mediated by a combination of enhanced APAP clearance and robust compensatory tissue repair.
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PMID:Type 1 diabetic mice are protected from acetaminophen hepatotoxicity. 1270 Apr 23

Increased oxidative stress and impaired antioxidant defense mechanisms are important factors in the pathogenesis and progression of diabetes mellitus and other oxidant-related diseases. This study was designed to determine whether alpha-lipoic acid, which has been shown to have substantial antioxidant properties, when administered (10 mg/kg ip) once daily for 14 days to normal and diabetic female Sprague-Dawley rats would prevent diabetes-induced changes in biomarkers of oxidative stress in liver, kidney and heart. Serum glucose concentrations, aspartate aminotransferase activity, and glycated hemoglobin levels, which were increased in diabetes, were not significantly altered by alpha-lipoic acid treatment. Normal rats treated with a high dose of alpha-lipoic acid (50 mg/kg) survived but diabetic rats on similar treatment died during the course of the experiment. The activity of glutathione peroxidase was increased in livers of normal rats treated with alpha-lipoic acid, but decreased in diabetic rats after alpha-lipoic acid treatment. Hepatic catalase activity was decreased in both normal and diabetic rats after alpha-lipoic acid treatment. Concentrations of reduced glutathione and glutathione disulfide in liver were increased after alpha-lipoic acid treatment of normal rats, but were not altered in diabetics. In kidney, glutathione peroxidase activity was elevated in diabetic rats, and in both normal and diabetic animals after alpha-lipoic acid treatment. Superoxide dismutase activity in heart was decreased in diabetic rats but normalized after treatment with alpha-lipoic acid; other cardiac enzyme activities were not influenced by either diabetes or antioxidant treatment. These results suggest that after 14 days of treatment with an appropriate pharmacological dose, alpha-lipoic acid may reduce oxidative stress in STZ-induced diabetic rats, perhaps by modulating the thiol status of the cells.
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PMID:Effects of alpha-lipoic acid on biomarkers of oxidative stress in streptozotocin-induced diabetic rats. 1283 33

The hypothesis of the present study was that diabetes mellitus might affect brain metabolism. Streptozotocin (STZ)-induced diabetic rats, treated with vanadyl sulphate (V) and sodium tungstate (T) were employed to observe the aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatine kinase (CK) activities in brain homogenates. Significant increases in AST, ALT and CK activities were found in diabetic brain homogenates against controls, suggesting increments of transamination in brain and/or increases in cell membrane permeability to these enzymes. The increase in brain CK possibly expresses alterations in energy production. The decrease in CK activity caused by V and T treatment in diabetic rats suggests that both agents tend to normalize energy consumption. It is also possible that V and T-induced hypoglycemic effects cause metabolic alterations in brain.
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PMID:Enzymatic activities in brains of diabetic rats treated with vanadyl sulphate and sodium tungstate. 1803 59

We investigated the influence of the flavonoid-rich fraction from Spermacoce hispida seed (S-Frf) on PPAR-alpha gene expression, plasma and erythrocyte antioxidants status, protein metabolism, and marker enzymes in diabetic hyperlipidemic rats. Hyperlipidemia was induced by feeding a 20% high fat diet (HFD) to male albino Wistar rats for 66 days. Diabetes was induced on the 17th day by a single i.p. injection of streptozotocin (50 mg/kg). When compared with diabetic hyperlipid-emic rats, plasma TBARS and LOOH levels decreased, the activities of enzymic antioxidants (SOD, CAT, GPx) and plasma GSH levels increased in the S-Frf fed group. The activities of plasma hepatic markers serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, and levels of plasma urea, uric acid, creatinine, globulin, A/G ratio significantly decreased, whereas liver weight, total protein, and albumin increased. Oral administration of S-Frf up-regulates PPAR-alpha (peroxisome proliferator activated receptor alpha) gene expression, activates fatty acid catabolism, and is involved in the control of lipoprotein assembly in liver. The results show that S-Frf has an antihyperlipidemic effect, improves antioxidant status, and alleviates liver and kidney damage associated with HFD-fed-STZ rats by up-regulating PPAR-alpha mRNA.
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PMID:Influence of flavonoid-rich fraction from Spermacoce hispida seed on PPAR-alpha gene expression, antioxidant redox status, protein metabolism and marker enzymes in high-fat-diet fed STZ diabetic rats. 1966 17

The present study is aimed to assess the therapeutic potential of sulfonylurea drug glimepiride in comparison with Nerium oleander plant extract on insulin, glucose levels and some liver enzymes activities in streptozotocin-induced diabetic rats. Rats were rendered diabetic by intraperitoneal injection of a single dose of 50 mg kg(-1) body weight streptozotocin. Rats with serum glucose levels > 200 mg dL(-1) were subdivided into three sub-groups: the first sub-group were remained without treatment and considered as diabetics. The second and third subgroups were orally administered 0.1 mg kg(-1) body weight/day glimepiride and 250 mg kg(-1) body weight/day Nerium oleander, respectively for 4 weeks. Streptozotocin-induced diabetic rats showed hypoinsulinemia and hyperglycemia compared to controls. Strong negative correlation (r = -0.8) was found between serum insulin and glucose levels in diabetic rats. This correlation was +0.4 and -0.3 in glimepiride and Nerium olender-treated rats, respectively implying that glimepiride and plant extract improved insulin and glucose levels with the former was more efficient. The activities of serum aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase were significantly increased in streptozotocin-induced diabetic rats compared to controls. Treatment of diabetic rats with glimepiride or Nerium oleander extract also improved liver enzymes activities.
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PMID:Antidiabetic activity evaluation of glimepiride and Nerium oleander extract on insulin, glucose levels and some liver enzymes activities in experimental diabetic rat model. 2251 88

This study is to observe the effects of sequoyitol on the expression of NADPH oxidase subunits p22 phox and p47 phox in rats with type 2 diabetic liver diseases. The model of high fat and high sugar diet as well as intraperitoneal injection of small dose of streptozotocin (STZ, 35 mg x kg(-1)) induced diabetic rat liver disease was used. After sequoyitol (50, 25 and 12.5 mg x kg(-1)) was administrated for 6 weeks, the contents of blood glucose (BG), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total antioxidant capacity (T-AOC), hydrogen peroxide (H2O2), NO and insulin (Ins) were measured, liver p22 phox and p47 phox mRNA content was determined with real-time PCR and the expression of p22 phox and p47 phox protein was examined by Western blotting. In addition, pathological changes in liver were observed with HE staining. Sequoyitol could reduce the content of fasting blood glucose, ALT, AST, Ins and H2O2, restore insulin sensitive index (ISI) and weight, elevate liver tissue T-AOC and NO content, reduce the NADPH oxidase subunit liver tissue p22 phox and p47 phox mRNA and protein expression, as well as ameliorate liver pathologic lesions. The results showed that sequoyitol can ease the type 2 diabetic rat liver oxidative stress by lowering NADPH oxidase expression.
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PMID:[Effects of sequoyitol on expression of NADPH oxidase subunits p22 phox and p47 phox in rats with type 2 diabetic liver disease]. 2383 34

Diabetes mellitus is a common endocrine disorder. Anti-diabetic agents from natural and synthetic sources are available for the treatment of this disease. Berberis integerrima is a medicinal shrub used in conventional therapy for a number of diseases. The aim of the present study was to investigate the effects of aqueous extract of Berberis integerrima root (AEBI) on some physiological parameters in normal and streptozotocin-induced (STZ-induced) diabetic male Wistar rats. STZ-induced diabetic rats showed significant increases in the levels of blood glucose, triglycerides (TG), total cholesterol (TC), low density lipoprotein LDL-cholesterol (LDL-C), creatinine (Cr), urea, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin while body weight, high density lipoprotein HDL-cholesterol (HDL-C) and total protein levels were significantly decreased compared to normal rats. Treatment of diabetic rats with different doses of aqueous extract of Berberis integerrima root (250 and 500 mg/Kg bw) resulted in a significant decrease in blood glucose, triglycerides, cholesterol, LDL-cholesterol, ALT, AST, ALP, total bilirubin, creatinine and urea while HDL-cholesterol and total protein levels were markedly increased after six weeks compared to untreated diabetic rats. The effects of the AEBI at dose of 500 mg/Kg in all parameters except blood glucose (similar) is more than to the standard drug, glibenclamide (0.6 mg/Kg, p.o.). The results of this study indicate that the tested aqueous extract of Berberis integerrima root possesses hypoglycemic, hypolipidemic and antioxidant effects in STZ-induced diabetic rats.
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PMID:Effects of Aqueous Extract of Berberis integerrima Root on Some Physiological Parameters in Streptozotocin-Induced Diabetic Rats. 2425 Jun 18


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