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allyl alcohol/betændelse
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Side 1 fra 22 resultater
Synthesis and pharmacological evaluation of 1,3,4-oxadiazole bearing bis(heterocycle) derivatives as anti-inflammatory and analgesic agents.
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A series of novel ether-linked bis(heterocycle)s have been synthesized via [3+2]-cycloaddition reaction of nitrile oxide with allyl alcohol followed by intramolecular 1,3-diploar cycloaddition reaction of nitrile imine with carbonyl group. All the newly synthesized compounds were screened for their
NTP Technical Report on the comparative toxicity studies of allyl acetate (CAS No. 591-87-7), allyl alcohol (CAS No. 107-18-6) and acrolein (CAS No. 107-02-8) administered by gavage to F344/N rats and B6C3F1 mice.
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Allyl acetate, allyl alcohol, and acrolein are used in the manufacture of detergents, plastics, pharmaceuticals, and chemicals and as agricultural agents and food additives. Male and female F344/N rats and B6C3F(1) mice received allyl acetate, allyl alcohol, or acrolein by gavage for 14 weeks.
Modeling inflammation-drug interactions in vitro: a rat Kupffer cell-hepatocyte coculture system.
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Xenobiotic-inflammation interactions lead to hepatotoxicity in vivo. Selected xenobiotic agents (acetaminophen, APAP; chlorpromazine, CPZ; allyl alcohol, AlOH; monocrotaline, MCT) for which this occurs were evaluated for ability to elicit the release of Kupffer cell (KC)-derived inflammatory
Pentoxifylline attenuates bacterial lipopolysaccharide-induced enhancement of allyl alcohol hepatotoxicity.
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Small amounts of exogenous lipopolysaccharide (LPS) (10 ng/kg-100 microg/kg) enhance the hepatotoxicity of allyl alcohol in male Sprague-Dawley rats. This augmentation of allyl alcohol hepatotoxicity appears to be linked to Kupffer cell function, but the mechanism of Kupffer cell involvement is
Influence of caffeine on allyl alcohol-induced hepatotoxicity in rats. I. In vivo study.
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Cotreatment of rats with a low hepatotoxic dose (30.7 mg/kg, i.p.) of allyl alcohol (AA) and a higher, but nontoxic, dose (150 mg/kg, oral) of caffeine (CF) potentiated the hepatotoxicity of AA. This was verified by significantly higher levels of plasma alanine aminotransferase (ALT) activity and
Neutrophils contribute to endotoxin enhancement of allyl alcohol hepatotoxicity.
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Nontoxic doses of endotoxin (lipopolysaccharide, LPS) enhance the hepatotoxicity of many xenobiotic agents, including allyl alcohol. Systemic LPS exposure induces an inflammatory response, including accumulation and activation of neutrophils (PMNs) in the liver. The hypothesis that PMNs play a
Pathological changes of hepatic artery and portal vein, after allyl-alcohol and carbon tetrachloride administration. An experimental study.
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BACKGROUND
Allyl-alcohol (AA) and carbon tetrachloride (CC14) are known to cause peritoneal and pericentral liver necrosis, respectively. This study investigates pathological changes of hepatic artery and portal vein after simultaneous administration of AA and CC14 in rats.
METHODS
The study
Cell kinetics of repair after allyl alcohol-induced liver necrosis in mice.
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The cellular kinetics of repair and scarring which occurs after induction of periportal necrosis in mice by allyl alcohol were examined by histology and immunohistochemistry. Thirty-six six-week-old female C57BI/6J mice were injected intraperitoneally with two doses of allyl alcohol on day 0 and
Involvement of cyclooxygenase-2 in the potentiation of allyl alcohol-induced liver injury by bacterial lipopolysaccharide.
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Bacterial endotoxin (lipopolysaccharide; LPS) augments the hepatotoxicity of a number of xenobiotics including allyl alcohol. The mechanism for this effect is known to involve the inflammatory response elicited by LPS. Upregulation of cyclooxygenase-2 (COX-2) and production of eicosanoids are
Influx of macrophages into livers of rats treated with hepatotoxicants (thioacetamide, allyl alcohol, D-galactosamine) induces expression of HSP25.
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Treatment of rats with a single dose of thioacetamide (TAA) provokes centrilobular inflammation and a significant expression of heat shock protein HSP25 in hepatocytes surrounding the area of inflammation. The HSP25 accumulation in hepatocytes adjacent to inflammatory regions was confirmed by
Acute inhalation study of allyl alcohol for derivation of acute exposure guideline levels.
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An acute, whole-body inhalation study for allyl alcohol in Sprague-Dawley rats was designed to support derivation of AEGL values, with emphasis on establishing NOAELs for irreversible effects of different exposure concentrations and durations. Groups of 10 rats were exposed for 1 hour (0, 50, 200,
Participation of different cell types in the restitutive response of the rat liver to periportal injury induced by allyl alcohol.
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OBJECTIVE
Restitution of periportal liver necrosis induced by allyl alcohol involves proliferation and differentiation of putative liver stem cells. The participation of different non-epithelial cell types required to restore the liver cord structure in this process has not been well documented. The
Irritant dermatitis from diallylglycol carbonate monomer in the optical industry: clinical and experimental studies of cutaneous tolerance and chemical investigations.
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The diallylglycol carbonate monomer causes dermatitis due to irritation in the optical industry. Cutaneous intolerance may effect as many as 70% of the exposed persons employed. Almost all control subjects who where patch-tested showed irritation at a 2% concentration. The histological effects were
Is exposure to bacterial endotoxin a determinant of susceptibility to intoxication from xenobiotic agents?
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Why certain individuals are more susceptible than others to harmful effects of chemical exposure remains incompletely understood. One understudied but potentially important determinant of susceptibility is concurrent or preexisting inflammation that may influence the pathogenic outcome of chemical
Genes related to apoptosis predict necrosis of the liver as a phenotype observed in rats exposed to a compendium of hepatotoxicants.
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BACKGROUND
Some of the biochemical events that lead to necrosis of the liver are well-known. However, the pathogenesis of necrosis of the liver from exposure to hepatotoxicants is a complex biological response to the injury. We hypothesize that gene expression profiles can serve as a signature to
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