Plasma Glutamic-pyruvic Transaminase Activity Research Articles

Effects of sub-lethal doses of miconazole nitrate on Labeo rohita and its curing efficacy against Saprolegniasis

Miconazole nitrate (MCZ) is an imidazole derivative antifungal drug used as therapeutic and prophylactic agent against fungal outbreak in human and veterinary animals. However, its use in aquaculture industry has not been reported yet. The aim of this study was to evaluate the acute toxicity of MCZ in fish and the effects of sub-lethal doses of MCZ on the haematological and biochemical parameters in Labeo rohita. Different haematological parameters like total blood cell counts, haemoglobin content along with mean corpuscular haemoglobin, mean corpuscular volume and mean corpuscular haemoglobin concentration values were observed. Biochemical parameters like plasma glucose level, plasma glutamic oxaloacetic transaminase and plasma glutamic pyruvic transaminase activity, alkaline phosphatase activity, plasma Na+ and K+ levels were also determined. In this experiment, 32 treatments (4 dose × 8 exposure times) of four MCZ doses (control- 0.0 mgMCZ kgBW−1, T1–6.30 mgMCZ kgBW−1, T2–12.61 mgMCZ kgBW−1 and T3–25.22 mgMCZ kgBW−1) with eight exposure times were set up in triplicates. In the second experiment, fish infected with Saprolegnia parasitica were fed with MCZ based feeds @ 1% BW daily for 21 days and their relative percent survival were recorded. The study revealed that the sublethal doses of MCZ have the significant (p < 0.05) effect on the haematological and biochemical parameters of the fish and also lowered (p < 0.05) the mortalities of saprolegnia infected fish. Fish fed with diet T3 (25.2 mgMCZ kg−BW−1) had maximum survivability with highest curing efficacy without any observable harmful effect on the physiology of fish. Thus, MCZ has an effective role in maintaining the health status of fish and providing protection against oomycetes, S. parasitica infection.

Protection Against Severe Intestinal Ischemia/Reperfusion Injury in Rats by Intravenous Resveratrol

Repetitive enteral or intraperitoneal administration of resveratrol at high doses has recently been found to protect the small intestine against acute ischemia/reperfusion (I/R) injury. In the present work, the protective potential of solvent-free continuous intravenous infusions of small amounts of resveratrol was studied in a model of severe intestinal I/R injury. Mesenteric ischemia was induced in male Wistar rats (six animals/group) by superior mesenteric artery occlusion (SMAO, 90 min) and reperfusion (120 min) by reopening of the microvascular clamp. Resveratrol (0.056 or 0.28 mg/kg) was continuously perfused into the jugular vein (0.014 or 0.07 mg/kg × h) starting 30 min before SMAO; an SMAO control group and sham groups (no SMAO) receiving either 0.9% NaCl solution or resveratrol (0.28 mg/kg) were included. During the experimental procedure, isotonic saline was given at a systolic blood pressure below 90 mmHg, and several parameters including those of biomonitoring and blood gas analysis were measured. Small intestine injury was assessed macroscopically, from released plasma enzyme activities, from the tissue contents of thiobarbituric acid-reactive substances and hemoglobin, from the tissue myeloperoxidase activity, and histopathologically. Resveratrol at only 0.056 mg/kg significantly decreased the macroscopic damage score, the tissue myeloperoxidase activity, the hemoglobin content, the histopathologic score, and the plasma glutamate-pyruvate transaminase activity, but it did not improve the systemic and metabolic parameters. Instead, during reperfusion, significantly higher volumes of saline were administered to animals receiving the polyphenol, although resveratrol did not significantly affect any parameters in sham-operated animals. Low doses of intravenously administered resveratrol considerably protected the rat small intestine against severe I/R injury, despite some adverse effects on blood pressure under these conditions.

TOXICITY AND BIOACCUMULATION OF NICKEL SULFATE IN SPRAGUE-DAWLEY RATS FOLLOWING 13 WEEKS OF SUBCHRONIC EXPOSURE

Adult male Sprague-Dawley rats were given 0, 0.02, 0.05, and 0.1% nickel sulfate (NiSO4 6H2O) or 0, 44.7, 111.75, and 223.5 mg Ni/L, respectively, in their drinking water for 13 wk. Twenty-four hours following the end of such treatment, all animals survived and no apparent clinical signs of toxicity were noted. The final mean body weights of various nickel sulfate-treated rats were not significantly decreased except for the 0.1% nickel sulfate treated group when compared to those in the control. The absolute and relative organ weights were either increased or decreased or remained unchanged, depending on the organ and the dose of nickel sulfate. Total plasma proteins, plasma albumin and globulins, and plasma glutamic pyruvic transaminase activity were all significantly decreased in 0.1% nickel sulfate-treated rats. Lymphocyte subpopulations (T and B cells) were induced at lower dose levels, but suppressed at the highest (0.1 %) dose group. A significant decrease in urine volume and an increase in BUN were observed at the highest dose group. Biochemical analysis of bronchoalveolar lavage fluid and lung tissue showed some lung damage, whereas no damage to the testis or DNA in liver and kidneys were found. No gross or microscopic changes were seen in any of the various tissues examined. The relative order of bioaccumulation of nickel in different organs of rats when treated at 0.1% nickel sulfate (223.5 mg Ni/L) was kidneys > testes > lung = brain > spleen > heart = liver. But with regard to order of toxicity, both immune and pulmonary systems were found to be very sensitive targets, followed by kidney.

Ethanol-induced enhancement of trichloroethylene metabolism and hepatotoxicity: Difference from the effect of phenobarbital

Male Wistar rats pretreated with ethanol (2.0 g in 80 ml liquid diet/day for 3 weeks) or phenobarbital (PB, 80 mg/kg/day ip for 4 days) were exposed by inhalation to 500, 1000, 2000, 4000, or 8000 ppm trichloroethylene (TRI) for 2 or 8 hr, and the blood concentration of TRI and the urinary concentration of TRI metabolites (trichloroethanol (TCE) and trichloroacetic acid (TCA)) were determined at various times. Plasma glutamic-pyruvic transaminase (GPT) activity was measured 22 hr after the end of exposure as an indicator of hepatic damage. Both ethanol and PB enhanced TRI metabolism as evidenced by accelerated disappearance of TRI from the blood and increased excretion of total trichloro compounds (TCE + TCA) in the urine. However, the effects of ethanol and PB were different from each other: ethanol markedly enhanced the metabolism particularly at TRI concentration of 2000 ppm or lower, whereas PB enhanced it only at 4000 ppm or higher. This difference was also reflected in the effect of TRI on liver: ethanol potentiated TRI hepatotoxicity more markedly than did PB when TRI concentration remained 2000 ppm or lower, whereas PB potentiated the toxicity more markedly than ethanol when the concentration was 4000 ppm or higher. It is noteworthy that ethanol potentiated TRI hepatotoxicity at a TRI concentration as low as 500 ppm. The severity of hepatic damage expressed by plasma GPT activity essentially paralleled the urinary excretion rate of total trichloro compounds during and 4 hr after exposure ( r = 0.87 to 0.93). Compared between the contribution of concentration and duration of exposure to the toxicity, a higher concentration of TRI tended to cause more severe liver damage to PB-treated rats than did a prolonged period of exposure, whereas the toxicity in ethanol-treated rats was generally more marked in rats exposed to TRI for a longer period than in rats exposed to a higher concentration.

Plasma Glutathione S-Transferase in Carbon Tetrachrolide Treated Rats and Its Association to Hepatic Cytosolic Isozymes

The effect of carbon tetrachloride (CCI4) treatment on plasma and liver cytosolic glutathione S-transferase (GST) activities was investigated in rats. CCI4 was intraperitoneally administered at a dose of 0.5 ml/kg. The elevation of plasma GST activity paralleled the increase of plasma glutamate pyruvate transaminase activity after the administration of CCI4. Liver cytosolic GST activities were significantly decreased by CCI4 treatment. To establish the relationship of plasma GST with liver cytosolic isozymes, Western blot analysis using antibodies against cytosolic GST 1–2 and 3–4 was performed. The Western blots showed the existence of GST 1–2 and 3–4 in plasma at 24 hr after CCI4 treatment. The data thus strongly suggest that cytosolic GSTs are lost from the liver to plasma as a consequence of liver damage. The Western blot analysis of plasma GST may be useful for monitoring liver damage.

Plasma glutathione S-transferase in carbon tetrachrolide treated rats and its association to hepatic cytosolic isozymes.

The effect of carbon tetrachloride (CCl4) treatment on plasma and liver cytosolic glutathione S-transferase (GST) activities was investigated in rats. CCl4 was intraperitoneally administered at a dose of 0.5 ml/kg. The elevation of plasma GST activity paralleled the increase of plasma glutamate pyruvate transaminase activity after the administration of CCl4. Liver cytosolic GST activities were significantly decreased by CCl4 treatment. To establish the relationship of plasma GST with liver cytosolic isozymes, Western blot analysis using antibodies against cytosolic GST 1-2 and 3-4 was performed. The Western blots showed the existence of GST 1-2 and 3-4 in plasma at 24 hr after CCl4 treatment. The data thus strongly suggest that cytosolic GSTs are lost from the liver to plasma as a consequence of liver damage. The Western blot analysis of plasma GST may be useful for monitoring liver damage.

The Effects of Diethyldithiocarbamate on the Hepatotoxic Action and Antitumor Activity of N-Methylformamide in Mice

The oral administration of diethyldithiocarbamate (DTC) prevented hepatic necrosis induced by N-methylformamide (NMF) in ddY-strain mice, in more susceptible BALB/c mice and in diethylmaleate-treated mice in which NMF-hepatotoxicity was potentiated, as evidenced by suppression of increases of plasma glutamic pyruvic transaminase activity and liver calcium content or by histological observations. Early depletion of liver glutathione following NMF administration was also prevented by DTC. DTC markedly delayed the in vivo metabolism of NMF as indicated by a prolonged retention of plasma and liver NMF levels and an enhancement of urinary excretion of NMF. These observations support a bioactivation mechanism for NMF hepatotoxicity, and the hepatoprotective action of DTC may be due to an inhibition of the metabolic activation of NMF. Hepatotoxic manifestations after repeated administration of NMF also tended to be ameliorated by simultaneous treatment with DTC. Cotreatment with DTC, however, decreased the antitumor activity of NMF against Ehrlich ascites tumors, and Sarcoma 180. This also implies the involvement of a bioactivation mechanism in the antitumor action of NMF, but further studies are necessary to confirm this point. The possible therapeutic value of DTC as a hepatoprotector may be diminished by the suppression of the antitumor activity of NMF.

Toxicity of flavoglaucin from Aspergillus chevalieri in rabbits

Female rabbits were injected intraperitoneally (i.p.) with purified flavoglaucin from Aspergillus chevalieri. After 2 h the rabbits were bled and the livers removed for enzyme assays. No changes were found for plasma lactate dehydrogenase (LDH) and its isozymes or liver transketolase (TK) activities. A small but not statistically significant increase was found in plasma glutamate pyruvate transaminase activity. A highly significant increase in plasma glutamic oxaloacetate transaminase activity was observed along with an increase in liver LDH which was, however, not quite significant. The liver also showed some histological evidence of hepatic damage.

Glutamic-pyruvic transaminase (GPT) in non-human primates II. Implication of the interspecific variation in enzyme activity

Glutamic-pyruvic transaminase (GPT) in plasma of 25 species of non-human primates including one hybrid species was investigated. There were not such significant differences in plasma GPT activities among species as in red cells. The fact that the enzyme activities of GPT in plasma correlate with those in liver s-GPT and the absence of organspecificity of soluble GPT suggest that the significant differences of GPT activity in red cells among species may probably be specific in red cells and reflect the quantitative differences of the enzyme. Moreover, GPT activity was detectable neither in younger red cells nor in reticulocytes obtained from Japanese monkeys (Macaca fuscata) in which red cell GPT activity could not be detected. Therefore, the significant interspecific variation of GPT activity in red cells may result from that of the enzyme quantity synthesized in red cells.

Effect of monocrotaline ingestion on liver, kidney, and lung of rats

Young, male rats were administered monocrotaline (MCT) ad libitum in the drinking water (22 μg/ml) for up to 28 days, and the development of toxicity in lung, liver, and kidney was examined. Clearance of perfused 5-hydroxytrytptamine by isolated lungs of treated rats was decreased as early as 14 days. This was accompanied by increases in lung/body weight ratio and in lactate dehydrogenase activity in cell-free bronchopulmonary lavage fluid. Hypertrophy of the right heart and increased inflow perfusion pressure of isolated lungs were apparent by 21 days of MCT treatment. The magnitude of the changes in all of these parameters increased with duration of treatment. After 28 days of treatment biliary indocyanine green excretion was decreased and plasma glutamic pyruvic transaminase activity was slightly elevated. Twenty-eight days of treatment also resulted in elevated blood urea nitrogen, decreased accumulation of p-aminohippuric acid by kidney slices, and increased accumulation of tetraethylammonium by kidney slices. Thus, lung, liver, and kidney are each affected by this MCT treatment regimen, and functional effects on lung precede effects on other tissues.

Effectiveness of metyrapone in the treatment of acetaminophen toxicity in mice

Metyrapone tartrate, 400 mg/kg i.p. raised the LD 50 for acetaminophen from 340 mg/kg i.p. to 540 mg/kg i.p. in fasting male Swiss white mice. The minimum protective dose of metyrapone was 200 mg/kg. Metyrapone was effective in preventing death when given up to 2 h after acetaminophen administration. The LD 50 for metyrapone tartrate was 760 mg/kg i.p. Metyrapone decreased or prevented acetaminophen induced hepatic damage measured either by histology or plasma glutamate pyruvate transaminase activity. Metyrapone tartrate, 400 mg/kg i.p., inbibited the severe liver glutathione depletion seen with acetaminophen alone. It is proposed that metyrapone protects mice from acetaminophen induced liver toxicity and death by inhibiting the oxidation of acetaminophen to a toxic intermediate.

A note on the combined effects of exercise and food restriction on plasma enzyme activities in the rat.

Plasma activities of malic dehydrogenase (MDH) and glutamic–pyruvic transaminase (GPT) were measured in adult male rats made to swim for 1 h either as a single, acute exercise or in repeated exercises (training) in the presence of a 50% food restriction. Food restriction per se elevated MDH and lowered GPT activities. Food-restricted rats responded to both acute exercise and training by an elevated plasma MDH activity. The effect of exercise on plasma MDH activity in these animals was greater than in rats fed ad libitum and was greater than could be accounted for by the summation of the individual effects of training and of food restriction. Plasma GPT activity was not altered by exercise in rats fed ad libitum or in food-restricted animals. It would appear, as suggested previously, that plasma MDH activity may be a useful biochemical criterion of training.

Alterations in enzyme activities as a consequence of exercise (swimming) in the rat.

SummaryLiver and plasma activities of malic dehydrogenase (MDH) and glutamicpyruvic transaminase (GPT) have been measured in adult, male rats made to swim for 2 hours either as a single, acute exercise or after repeated daily exercises (training). Acute exercise caused a significant increase of both liver and plasma MDH activity. Repeated exercise (training) caused an increased basal MDH activity in liver but not plasma; in the trained rat, a 2-hour swimming exercise did not elicit a further elevation of MDH activity in liver nor did it elicit an elevation in plasma. Neither acute nor repeated exercise caused any alteration in liver or plasma GPT activities. The possibility of using alterations in plasma MDH activity as a criterion of training is suggested.