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nitrosodimethylamine/necrosis
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 19 risultati
Hyaluronic acid-tumor necrosis factor-related apoptosis-inducing ligand conjugate for targeted treatment of liver fibrosis.
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Liver fibrosis is a chronic liver disease caused by viral infection and/or metabolic, genetic and cholestatic disorders. The inhibition of hepatic stellate cell (HSC) activation and the selective apoptosis of activated HSCs can be a good strategy to treat liver fibrosis. The activated HSCs are known
Effects of ethanol consumption on bioactivation and hepatotoxicity of N-nitrosodimethylamine in rats.
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To study the effects of ethanol on the hepatotoxicity of N-nitrosodimethylamine (NDMA), 5 mg NDMA/kg body weight was injected intraperitoneally 3 times a week for 6 weeks into rats pair-fed liquid diets containing 36% of energy either as ethanol or as additional carbohydrates. Another group of rats
Calcium transport, thiol status, and hepatotoxicity following N-nitrosodimethylamine exposure in mice.
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The hepatotoxicant N-nitrosodimethylamine (NDMA) is presumed to exert toxicity through reactive metabolites. NDMA is similar in this respect to numerous other hepatotoxicants, for which hepatotoxicity is also associated with a rapid depletion of soluble and/or protein thiols, and an inhibition of
Sequential study in rats of nasal and hepatic lesions induced by N-nitrosodimethylamine and N-nitrosopyrrolidine.
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Female Sprague-Dawley rats were given an ip dose of N-nitrosodimethylamine (NDMA) and N-nitrosopyrrolidine (NPYR), singly or in combination, and the sequential development of lesions in the liver and nasal cavity was characterized. Liver and nasal tissues were collected from rats given either NDMA
Expression of hyaluronic acid in N-nitrosodimethylamine induced hepatic fibrosis in rats.
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Hyaluronic acid (HA) plays prominent role in the pathogenesis of liver fibrosis. The mechanism of increased serum and liver HA during hepatic fibrosis was studied in rats. Liver injury was induced by intraperitoneal injections of N-nitrosodimethylamine (NDMA) for 7 consecutive days. A group of
Expression of selected proteins of the extrinsic and intrinsic pathways of apoptosis in human leukocytes exposed to N-nitrosodimethylamine.
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N-nitrosodimethylamine (NDMA) is a xenobiotic widespread in human environment capable of regulating the lifespan of immune cells. In this study, we examined the roles of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)/death receptor 5 (DR5) complex and the Fas molecule in the
Tissue levels and biological effects of N-nitrosodimethylamine in mice during chronic low or high dose exposure with or without ethanol.
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In a study of the metabolism, disposition, and hepatotoxicity of the environmental carcinogen N-nitrosodimethylamine (NDMA), as a function of dose in the drinking water and of concomitant administration of ethanol, outbred Swiss mice were given NDMA for 1-4 weeks at levels of 50-0.5 ppm, with or
Protection from N-nitrosodimethylamine-mediated liver damage by indole-3-carbinol.
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Indole-3-carbinol (I-3-C) was examined for its ability to protect mice against 24-hr N-nitrosodimethylamine (NDMA)-mediated hepatotoxicity. NDMA (20 mg/kg body weight) alone produced extensive hemorrhagic and centrolobular necrotic lesions, with a necrotic severity index of 3.0 +/- 0.4 (scale of
Ameliorative effect of silibinin against N-nitrosodimethylamine-induced hepatic fibrosis in rats.
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The protective effect of silibinin (SBN) against hepatic fibrosis induced by repeated intermittent administration of N-nitrosodimethylamine (DMN) was investigated in rats. Oral administration of SBN recovered body and liver weight loss and reversed the elevation of serum AST, ALT and ALP accompanied
MMP-13 deletion decreases profibrogenic molecules and attenuates N-nitrosodimethylamine-induced liver injury and fibrosis in mice.
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Connective tissue growth factor (CTGF) is involved in inflammation, pathogenesis and progression of liver fibrosis. Matrix metalloproteinase-13 (MMP-13) cleaves CTGF and releases several fragments, which are more potent than the parent molecule to induce fibrosis. The current study was aimed to
Potentiation of the hepatotoxicity of N-nitrosodimethylamine by fasting, diabetes, acetone, and isopropanol.
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Previous studies indicate that pretreatment with acetone or isopropanol, fasting, and streptozotocin-induced diabetes enhance hepatic microsomal nitroso-dimethylamine (NDMA) demethylase in rats. This study demonstrates that these same treatments also potentiate the hepatotoxicity of NDMA as
Studies on the mechanism of the acute and carcinogenic effects of N-nitrosodimethylamine on mink liver.
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Outbreaks of liver necrosis and liver hemangiosarcoma were detected in a mink breeding colony in Argentina. Analysis of the Minks' food revealed the presence of 2.6 ppm dimethylnitrosamine (NDMA) in it, apparently as a result of the addition of nitrite as preservative. Previous studies gave evidence
[Possibility of N-dimethylnitrosamine formation after parenteral administration of amidopyrine and nitrite to rats].
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The intravenous or intraperitoneal injection of amidopyrine and sodium nitrite to rats induces liver necrosis caused by endogenic synthesis of carcinogenic N-nitrosodimethylamine (NDMA). Ascorbic acid, which inhibits this synthesis when injected intravenously, phenobarbital, which is an inductor of
The role of hepatocyte heterogeneity in the initiation of hepatocarcinogenesis.
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N-Nitrosodimethylamine (NDMA) is a carcinogen in rat liver while N-nitrosomethylbenzylamine (NMBzA) produces no liver tumors but is a potent esophageal carcinogen in the rat. Both nitrosamines, however, are metabolically activated in the liver and methylate hepatic DNA. The reasons for their
[Histopathological studies of the acute and chronic toxic effects of 2 N-nitroso compounds on the blue mussel (Mytilus edulis)].
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The acute and chronic effects of two N-Nitroso compounds (N-Nitrosodimethylamine) (DMN) and N-Methyl-N-Nitro-N-Nitrosoguanidine (MNNG) were studied by light microscopy after injection of the chemicals into the foot of the mussel, Mytilus edulis. Acute toxic effects: DMN produced dose-dependent (0.1
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