Hepatic Gamma-glutamyl Transpeptidase Activity Research Articles

Dietary effects of marine food intake on intestinal and hepatic enzyme activities in rats.

Dietary effects of two diets high in protein from two marine species (Haliotis tuberculata and Anemonia viridis) as compared to a high-quality patron protein such as casein (or casein supplemented with olive oil) on intestinal and hepatic enzymes were studied. After 23 days, the two marine species as diet compared to casein increased the disaccharidase and alkaline phosphatase activities. Feeding Haliotis tuberculata meal produced a decrease on intestinal leucine aminopeptidase activity. The hepatic gamma-glutamyltranspeptidase activity decreased slightly in animals fed Haliotis tuberculata meal. Supplementation of casein with olive oil tended to decrease the intestinal and hepatic enzyme activity.

Nutritive value of protein from sea urchin, and its effects on intestinal leucine aminopeptidase and intestinal and hepatic gamma-glutamyltranspeptidase

Seafoods are a rich source of easily digestible protein that also provides polyunsaturated fatty acids, vitamins and minerals for human nutrition. The purpose of this study was to determine the nutritive value of diets high in protein from two species of sea urchin (Paracentrotus lividus and Echinus esculentus) as compared to a high-quality reference protein such as casein, as well as the effects of these diets on leucine aminopeptidase and gamma-glutamyltranspeptidase, intestinal and hepatic enzymes. The test was carried out on three groups of male rats fed these diets for 23 days. The result of the nutritive parameters indicated that sea urchin, Echinus esculentus, were significantly lower than the casein protein except for food intake, and the nutritive parameters of sea urchin, Paracentrotus lividus, were similar to the values obtained for casein protein except for digestibility and net protein utilization. Intestinal leucine aminopeptidase activity was significantly lower (P < 0.05) in the group fed Paracentrotus lividus as compared to the group fed casein. Intestinal gamma-glutamyltranspeptidase showed a significantly higher activity in the group fed E. esculentus than in the two other groups and the hepatic gamma-glutamyltranspeptidase activity in the groups fed the two species of sea urchin were lower. Nutritive values suggested that these marine species are a good protein source and similar to casein. The activity of the enzymes under study must have been affected by the amino acid composition of the protein.

Efeito da restrição energética na atividade hepática da gama-glutamiltranspeptidase e nos níveis de glutationa

Avaliou-se o efeito da restrição energética aguda (crescimento pós-desmame) e crônica (lactantes desnutridas desde o período pré-natal e seus filhotes) na atividade da gama-glutamiltranspeptidase e nos níveis de glutationa. O consumo da dieta foi ad libitum (controle) ou com restrição de 30% (desnutrido), tendo-se conduzido dois ensaios, um de desnutrição aguda e outro de desnutrição crônica. A restrição aguda provocou redução significativa no ganho ponderal dos ratos em crescimento, mas as mães cronicamente desnutridas ganharam significativamente mais peso/filhote, pois apresentaram menor número de filhotes. Não foram observadas alterações significativas nos níveis de glutationa, na atividade da gama-glutamiltranspeptidase e mesmo na concentração de proteína hepática sob o efeito da restrição energética, aguda ou crônica. Menor desequilíbrio no perfil de aminoácidos plasmáticos e na síntese protéica, conseqüente à desnutrição energética e não à protéica, pode justificar estes resultados.

Hypothyroidism-evoked shifts in hippocampal adrenergic receptors: implications to ischemia-induced hippocampal damage.

Hypothyroidism was induced in a group of male Fischer 344 rats by administration of 0.05% propylthiouracil (PTU) in the drinking water for 12 weeks. Control rats were not treated. Plasma levels of thyroid hormones indicated that PTU treatment had produced severe thyroid hormone deficiency. In PTU-treated rats compared to control rats, levels of total T3 and total T4 were reduced 54.5% and 53.7%; while levels of free T3 and free T4 were reduced 87.1% and 96.5%. Functional hypothyroidism was demonstrated by: (i) a 49.1% decrease in hepatic plasma membrane alpha1-adrenergic receptor binding, and (ii) a 11.2-fold increase in hepatic gamma-glutamyltranspeptidase activity; relative to the expression of these parameters in control rats. Membranes were isolated from hippocampi of control, PTU-induced hypothyroid and thyroxine-replaced rats and specific adrenergic receptor binding determined by radioligand binding techniques. Hypothyroidism resulted in a shift in the balance of alpha1 and beta2 adrenergic receptor binding by evoking: an increase in alpha1-adrenergic receptor binding to 1.57-fold of control levels; and, a decrease in beta2-adrenergic receptor binding to 64% of control levels. Thyroid hormone replacement carried out in PTU-treated hypothyroid rats at 30 microg/kg s.c. per day for the last 3 days of the 12 week PTU-treatment protocol, which reversed physical and functional hypothyroidism, reversed the observed changes in hippocampal adrenergic receptor binding, indicating them to be thyroid hormone, and not PTU, -dependent. This receptor shift evoked by hypothyroidism may, in part, explain the protective effect of hypothyroidism on ischemia-induced hippocampal damage by favoring inhibitory input and limiting excitotoxic input by catecholamines.

Experimental murine schistosomiasis: reduced hepatic morbidity after pre- and/or post-infection treatment with ibuprofen or diclofenac sodium.

Arachidonic-acid metabolites appear to participate in skin penetration by and transformation of schistosome cercariae and in the pathogenesis of schistosomiasis. With this in mind, mice were treated with one of two cyclooxygenase inhibitors before and/or after infection with Schistosoma mansoni. The effects of the treatment on liver morbidity and the parasitic infection were then evaluated, using infected, untreated and uninfected, treated mice as controls. Treatment with ibuprofen (20 mg/kg.day) or diclofenac sodium (2.5 mg/kg.day) for 7 days before infection led to significantly lower liver weights, worm loads and hepatic hydroxyproline contents than in the untreated mice. If treatment with either drug was continued after infection, for 28 days, there was an additional significant decrease in hepatic gamma-glutamyl transpeptidase activity. All these parameters except liver weight were similarly affected when treatment with either drug was begun on the day of infection and continued for 28 days. There was no significant change in liver weight or worm load when treatment was delayed until day 28 post-infection but faecal egg counts were reduced in the treated groups. In additional experiments, using a smaller dose of diclofenac sodium (1.25 mg/kg.day), all the measured parameters of infection were significantly decreased when the treatment was initiated 7 days before infection and continued until day 28 post-infection. The results indicate that the treatment of S. mansoni-infected mice with ibuprofen or diclofenac sodium was effective in reducing the severity of infection and in attenuating hepatic fibrosis, particularly when the treatment was started early in relation to the time of infection.

Ontogeny of hepatobiliary secretion: Role of glutathione

The ontogeny of hepatic synthesis and biliary secretion of glutathione was characterized and correlated with hepatic gamma glutamyl transpeptidase, bile flow rate, biliary bile acids and amino acids in Sprague-Dawley rats at 18 days of gestation and postnatally at ages 7, 14, 21, 28 and 54 days. Bile was collected by bile duct cannulation under intraperitoneal anesthesia with nembutal/ketamine. Glutathione, gamma glutamyl transpeptidase and bile acids were analyzed enzymatically and amino acids by high-performance liquid chromatography using established methods. Hepatic glutathione was low in the fetus, but increased to approximate adult levels by 7 days postnatally (2.77 mumol/gm liver). Hepatic gamma glutamyl transpeptidase activity, high in the fetus, declined to adult levels by day 7 (0.03 mumol/mg protein). In contrast, significant efflux of glutathione and its constituent amino acids into bile did not occur until weaning (21 days of age). During weaning, there was a fivefold increase in the biliary glutathione and with a twofold increase in bile flow rate. Biliary bile acids concentration remained constant throughout development, with only a 30% to 50% increase in its secretion rate. The data suggest that the developmentally related increase in bile flow rate was principally a result of the increase in bile acid independent flow from 1.1 microliters/(min.100 gm body wt) in the suckling to 4.3 microliters/(min.100 gm body wt) in the post-weanling animal.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of aging on metabolic zonation in rat liver: Acinar distribution of GSH metabolism

The effect of age on the glutathione antioxidant system and its acinar distribution in rat liver was studied. GSH/GSSG ratio in blood and liver was lower in old than in young rats. Hepatic glutathione peroxidase and glutathione S-transferase activities were higher in old than in young rats, whereas hepatic gamma-glutamyl transpeptidase activity was lower in old than in young rats. Glutathione reductase and glucose-6-phosphate dehydrogenase activities did not change with age in rat liver. Total glutathione levels and glutathione peroxidase activity were higher in periportal than in perivenous areas of young rats, but this heterogeneous distribution did not occur in old rats. No change with age was found in hepatic zonation of glutathione reductase and glucose-6-phosphate dehydrogenase.

Experimental treatment of thioacetamide-induced liver cirrhosis by metenolone acetate. A morphological and biochemical study

The influence of metenolone acetate (1 mg/kg b.m. orally) on intact and chronically thioacetamide-injured rat liver (experimental liver cirrhosis) was investigated over 14 d. Histological examination revealed nodular transformation of liver structure according to cirrhosis like lesions with hepatocellular and cholangiocellular proliferations. These structural alterations were more serious in the group treated with metenolone compared with the group without metenolone. Metanolone administration to animals with thioacetamide-induced experimental liver cirrhosis led to an increase in liver injury. This treatment seems to promote hepatic preneoplastic lesions induced by thioacetamide reflected by histology and induction of gamma-glutamyltranspeptidase and 7-ethoxycoumarin O-deethylase in injured livers. Metenolone did not interfere directly with the processes of connective tissue synthesis and degradation after thioacetamide pretreatment. Only little changes of the investigated biochemical parameters were seen after metenolone administration to animals with intact liver function: increases in serum cholinesterase and tissue N-acetyl-beta-D-glucosaminidase activity; decreases in N-acetyl-beta-D-glucosaminidase in serum, liver hydroxyproline content and hepatic gamma-glutamyltranspeptidase activity. The observed changes reflect hepatic adaption processes under the influence of metenolone. The results of this study indicate that the risk of anabolic steroids in adjuvant therapy of liver cirrhosis cannot be calculated at present.

Mechanism of γ–Glutamyl Transpeptidase Release in Serum During Intrahepatic and Extrahepatic Cholestasis in the Rat: A Histochemical, Biochemical and Molecular Approach

The mechanism of the elevation of serum gamma-glutamyl transpeptidase activity in cholestasis is not clear. We therefore analyzed rat gamma-glutamyl transpeptidase activities in liver, bile and serum during intrahepatic cholestasis induced by a single dose of alpha-naphthyl isothiocyanate (20 mg/100 gm body weight) and during extrahepatic cholestasis after bile duct ligation. At days 1 and 2 after alpha-naphthyl isothiocyanate ingestion, we saw a fivefold and a 60-fold increase in serum and bile gamma-glutamyl transpeptidase activities, respectively. These increases were associated with a decrease in hepatic gamma-glutamyl transpeptidase activity and of corresponding mRNA. Simultaneously, necrosis of the biliary epithelium appeared in portal tracts. From day 2 to day 14, gamma-glutamyl transpeptidase activity in bile and serum progressively returned to basal levels; in the liver, cholangiolar proliferation was mild and was associated with moderate elevation of the gamma-glutamyl transpeptidase activity and of its corresponding mRNA. In extrahepatic cholestasis, a 10-fold increase in serum gamma-glutamyl transpeptidase activity was detected between day 0 and day 14. This increase was associated with major cholangiolar proliferation and with a progressive rise in hepatic gamma-glutamyl transpeptidase activity and in specific mRNA; in bile, gamma-glutamyl transpeptidase activity was slightly elevated. In these two models of cholestasis, histochemically detected gamma-glutamyl transpeptidase activity was largely predominant in biliary cells. We found no significant induction of gamma-glutamyl transpeptidase activity in hepatocytes. These results suggest that in these two models of cholestasis, the increase in serum gamma-glutamyl transpeptidase activity is of biliary cell origin and does not originate from hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)