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Synergistic neurotoxic effects of styrene oxide and acrylamide: glutathione-independent necrosis of cerebellar granule cells.
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Conjugation with glutathione (GSH) is a mechanism of detoxification of acrylamide (ACR); hence, prior depletion of GSH might be expected to exacerbate ACR's neurotoxicity. GSH levels in female rats were reduced by ip administration of styrene oxide (SO; 250 mg/kg), diethylmaleate (DEM; 0.5 ml/kg),
Styrene inhalation toxicity studies in mice. II. Sex differences in susceptibility of B6C3F1 mice.
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Styrene is a commercially important chemical used in the production of plastics and resins. In initial short-term styrene inhalation studies, toxicity was significantly greater in male B6C3F1 mice than in females, suggesting that males may metabolize styrene more extensively and/or may be less able
Styrene-induced hepatotoxicity in mice depleted of glutathione.
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In mice depleted of glutathione (GSH) by pretreatment with an inhibitor of GSH synthesis, buthionine sulfoximine (BSO; 1 hr before styrene, 2 mmol/kg or higher doses, ip), styrene (0.96-5.76 mmol/kg, po) produced hepatotoxicity characterized by an increase in serum alanine transaminase activity and
Tissue protective effect of xanthine oxidase inhibitor, polymer conjugate of (styrene-maleic acid copolymer) and (4-amino-6-hydroxypyrazolo[3,4-d]pyrimidine), on hepatic ischemia-reperfusion injury.
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The detrimental role of superoxide anion (O(2)(-)) has been well documented in the pathogenesis of ischemia-reperfusion (I/R) injury. Our and other studies suggested that one critical source of O(2)(-) generation may be xanthine oxidase (XO). We thus hypothesized that I/R injury could be protected
Estimation of the styrene 7,8-oxide-detoxifying potential of epoxide hydrolase in glutathione-depleted, perfused rat livers.
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The importance of epoxide hydrolase in preventing styrene 7,8-oxide-induced hepatoxicity was studied in isolated perfused rat livers depleted of GSH. GSH depletion was accomplished by treating the rats with diethyl maleate 45 min before surgical removal of their livers. Diethyl maleate itself caused
The effects of styrene on lung cells in female mice and rats.
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Styrene has been shown to cause an increase in the incidence of lung tumors in CD-1 mice following chronic exposure at 40 and 160 ppm, whereas no treatment-related increase in tumors in any organ was seen in rats chronically exposed to up to 1000 ppm styrene. So far most of the mechanistic studies
Comparison of styrene hepatotoxicity in B6C3F1 and Swiss mice.
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Inhalation exposure to styrene at concentrations that cause metabolic saturation results in significantly greater hepatotoxicity in B6C3F1 mice than in Swiss mice; females of both strains are more susceptible than males. These studies were conducted to investigate the mouse strain and gender
Effects of various pretreatments on the hepatotoxicity of inhaled styrene in the B6C3F1 mouse.
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1. The roles of cytochrome P450 monooxygenases (P450) and glutathione (GSH) in styrene hepatotoxicity were investigated in mice by pretreating with either phenobarbital (PB; P450 inducer), SKF 525A (P450 inhibitor), N-acetylcysteine (NAC; GSH precursor), or saline (vehicle control) prior to a 6-h
Protective effect of N-acetyl-L-cysteine (L-NAC) against styrene-induced cochlear injuries.
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CONCLUSIONS
Styrene exposure causes hair cell death through both apoptotic and necrotic pathways and treatment with N-acetyl-L-cysteine (L-NAC) reduces styrene ototoxicity.
OBJECTIVE
Exposure to styrene causes hearing loss and hair cell death in the middle frequency region in the cochlea. The
Serum hepatic biochemical activity in two populations of workers exposed to styrene.
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OBJECTIVE
To determine whether hepatic biochemical changes, as measured by routinely available tests indicative of hepatocellular necrosis, cholestasis, or altered hepatic clearance of bilirubin, occur in association with low to moderate exposure to styrene commonly experienced in industrial
Block copolymer nanotemplating of tobacco mosaic and tobacco necrosis viruses.
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This paper examines the interaction between a block copolymer and a virus. A poly(styrene-b-4-vinylpyridine) block copolymer was loaded with nickel, and cast from a selective solvent mixture to form a cylindrical microstructure (PS/P4VP-Ni). The nickel ions were confined within the P4VP block of the
CYP2F2-generated metabolites, not styrene oxide, are a key event mediating the mode of action of styrene-induced mouse lung tumors.
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Styrene induces lung tumors in mice but not in rats. Although metabolism of styrene to 7,8-styrene oxide (SO) by CYP2E1 has been suggested as a mediator of styrene toxicity, lung toxicity is not attenuated in CYP2E1 knockout mice. However, styrene and/or SO metabolism by mouse lung Clara
Characterization of hepatocellular resistance and susceptibility to styrene toxicity in B6C3F1 mice.
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Short-term inhalation exposure of B6C3F1 mice to styrene causes necrosis of centrilobular (CL) hepatocytes. However, in spite of continued exposure, the necrotic parenchyma is rapidly regenerated, indicating resistance by regenerated cells to styrene toxicity. These studies were conducted to test
Styrene inhalation toxicity studies in mice. III. Strain differences in susceptibility.
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Inhalation toxicity studies were conducted to evaluate mouse strain differences in the susceptibility to styrene vapors. Male and female B6C3F1, C57BL/6, Swiss, and DBA/2 mice (8 weeks old) were exposed to 0, 125, 250, or 500 ppm styrene 6 hr/day, for 4 days (20/sex/dose). Histopathological changes
Total necrosis of hepatocellular carcinoma with a combination therapy of arterial infusion of chemotherapeutic lipiodol and transcatheter arterial embolization: report of 14 cases.
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Combination therapy consisting of Lipiodol (Laboratoire Guerbet, Villepinte, France) containing styrene maleic acid neocarzinostatin and transcatheter arterial embolization (L-TAE) has been an important conservative therapy for hepatocellular carcinoma (HCC). We examined the clinical and pathologic
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