glucose 6 phosphatase/necrosis

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Activity of glucose-6-phosphatase in regenerating tubular epithelium in rat kidney after necrosis induced with mercuric chloride: a light and electronmicroscopical study.

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The activity of glucose-6-phosphatase was investigated in the renal proximal tubules of male albino rats after necrosis induced with mercuric chloride. Between the 3rd and 14th days an active zone could be observed in the inner cortex, which in the control animals was inactive. As regeneration

Tumor necrosis factor inhibits the transcriptional rate of glucose-6-phosphatase in vivo and in vitro.

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Recombinant human tumor necrosis factor-alpha (TNF) injection in mice was associated with a reduced blood glucose level, already manifest 6 hours following cytokine administration. Insulin levels were not affected. Glycogen content was decreased in a dose-dependent and time-response manner. The

Tumour necrosis factor alpha decreases glucose-6-phosphatase gene expression by activation of nuclear factor kappaB.

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The key insulin-regulated gluconeogenic enzyme G6Pase (glucose-6-phosphatase) has an important function in the control of hepatic glucose production. Here we examined the inhibition of G6Pase gene transcription by TNF (tumour necrosis factor) in H4IIE hepatoma cells. TNF decreased

Studies on necrosis of mouse liver in vitro. Alterations in activities of succinoxidase, succinic dehydrogenase, glutamic dehydrogenase, acid phosphatase, uricase, glucose-6-phosphatase and NAD-pyrophosphorylase.

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[Glucose-6-phosphatase activity in kidney tubule regeneration after sublimate necrosis. Light and electron microscopy].

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Late preventive effects of trifluoperazine on carbon tetrachloride-induced hepatic necrosis.

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As a very preliminary test for a possible role of calmodulin in CCl4-induced hepatic injury, we studied the effects of the anticalmodulin drug trifluoperazine (TFP) on several deleterious actions of CCl4 on the liver. TFP administrated 30 min before or 6 or 10 hr after CCl4 significantly prevented

Effect of tumor necrosis factor on enzymes of gluconeogenesis in the rat.

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The effect of human recombinant tumor necrosis factor (TNF)-alpha on enzymes of gluconeogenesis in the rat was investigated by determining the activity of glucose 6-phosphatase, fructose 1,6-diphosphatase (FDP), and phosphoenolpyruvate carboxykinase in the liver and kidney of fed and fasted rats.

[Electron histochemical characteristics of laser necrosis].

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Linear or dot-shaped lesions were inflicted on rat liver with Nd:YAG laser, and fine structural alterations of hepatocytes were studied in the specimens processed for an endoplasmic reticulum (ER) marker glucose-6-phosphatase (GP). 5-7 s after irradiation a severe cell damage and GP inhibition

Carbon tetrachloride-induced early biochemical alterations but not necrosis in pigeon's liver.

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In contrast to what is well known to occur in rats, pigeons receiving CCl4 (1 ml/kg i.p.) were not susceptible to necrogenic effects of the hepatotoxin at 24 h. There were, however, other early biochemical alterations observable, such as depression of glucose 6 phosphatase activity, decrease in the

Experimental acetaminophen-induced hepatic necrosis: biochemical and electron microscopic study of cysteamine protection.

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In an attempt to elucidate the biochemical mechanism of acetaminophen-induced hepatic necrosis, the present study in hamsters was undertaken to evaluate the possible changes in lipid peroxidation and microsomal enzyme activities. The protective action of cysteamine was likewise assessed in the light

Further studies on the mechanism of the late protective effects of phenylmethylsulfonyl fluoride on carbon tetrachloride-induced liver necrosis.

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We previously reported that phenylmethylsulfonyl fluoride (PMSF) administration to rats (100 mg/kg, ip in olive oil) as late as 6 or 10 hr after CCl4 (1 ml/kg, ip as a 20% v/v solution in olive oil) can partially prevent the necrogenic response to the hepatotoxin at 24 hr. Here we confirm that

Imipramine prevention of carbon tetrachloride-induced liver necrosis at late states of the intoxication process.

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Imipramine administration (50 mg kg-1, i.p.) to Sprague-Dawley male rats (240-290 g) 6 or 10 h after CCl4 (1 ml kg-1, i.p.) partially prevents liver necrosis induced by the hepatotoxin. When imipramine is given 30 min before CCl4, it inhibits in part the CCl4-induced lipid peroxidation and the

Lethal hypoglycemia and hypothermia induced by administration of low doses of tumor necrosis factor to adrenalectomized rats.

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An increased sensitivity of adrenalectomized (Adex) rats to intravenous (IV) injection of recombinant human tumor necrosis factor (rHuTNF) was manifested by a marked increase in the rate of mortality. The rats that died exhibited severe hypoglycemia and hypothermia. Administration of 2.5 or 10

Daily injection of tumor necrosis factor-{alpha} increases hepatic triglycerides and alters transcript abundance of metabolic genes in lactating dairy cattle.

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To determine whether inflammation can induce bovine fatty liver, we administered recombinant bovine tumor necrosis factor-alpha (rbTNF) to late-lactation Holstein cows. Cows (n = 5/treatment) were blocked by feed intake and parity and randomly assigned within block to control (CON; saline), rbTNF at

Enterically transmitted non-A, non-B hepatitis in cynomolgus monkeys: morphology and probable mechanism of hepatocellular necrosis.

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Two cynomolgus monkeys were inoculated with a stool extract originally derived from patients suffering from enterically transmitted non-A, non-B hepatitis. Subsequently, the primates developed self-limiting acute hepatitis and their liver tissues were obtained sequentially by needle biopsy or at

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