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dichlorobenzene/некроза
Линкът е запазен в клипборда
Страница 1 от 20 резултата
NTP Toxicology and Carcinogenesis Studies of 1,2-Dichlorobenzene (o-Dichlorobenzene) (CAS No. 95-50-1) in F344/N Rats and B6C3F1 Mice (Gavage Studies).
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The major use of 1,2-dichlorobenzene is as an intermediate in the synthesis of several organic compounds (e.g. 3,4-dichloroaniline) and in the syntheses of the herbicides propanil, diuron, and neburon. It is used as an industrial solvent for toluene diisocyanate, an additive to degreasing agents, a
Target cells for methylsulphonyl-2,6-dichlorobenzene in the olfactory mucosa in mice.
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Previously we reported that methylsulphonyl-2,6-dichlorobenzene, 2, 6-(diCl-MeSO(2)-B), was irreversibly bound to the olfactory mucosa of mice and induced necrosis of the Bowman's glands with subsequent neuroepithelial degeneration and detachment. In this study, autoradiography and histopathology
Localization and comparative toxicity of methylsulfonyl-2,5- and 2,6-dichlorobenzene in the olfactory mucosa of mice.
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Several methylsulfonyl (MeSO2) metabolites formed from chlorinated aromatic hydrocarbons have been identified in human milk, lung, and body fat, as well as in the tissues of Baltic grey seals and arctic polar bears. The tissue localization and nasal toxicity of two methylsulfonyl-substituted
ICE/CED-3 family executes oligodendrocyte apoptosis by tumor necrosis factor.
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Tumor necrosis factor (TNF) is thought to be one of the mediators responsible for the damage of oligodendrocytes (OLGs) in multiple sclerosis (MS). We report here the involvement of the interleukin 1beta-converting enzyme (ICE)/Caenorhabditis elegans gene ced-3 (CED-3) family in TNF-mediated cell
Thirteen-week inhalation toxicity of p-dichlorobenzene in mice and rats.
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Subchronic inhalation toxicity of p-dichlorobenzene (p-DCB) was examined by exposing BDF1 mice and F344 rats of both sexes (6 h/d and 5 d/wk) to inhalation of 25, 55, 120, 270 or 600 ppm (v/v) p-DCB vapor for 13 wk. The exposure to p-DCB vapor retarded the growth rate in the male mice, and induced
Serum-borne factor(s) of 1,1-dichloroethylene and 1,2-dichlorobenzene-treated mice inhibited in vitro antibody forming cell response and natural killer cell activity.
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1,1-Dichloroethylene and 1,2-dichlorobenzene administered to mice produced liver and/or kidney damage which was quantified in this study by a histochemical method. The in vitro effect of sera obtained from these mice on antibody forming cell (AFC) response and natural killer (NK) cell activity was
Inflammatory damage to skin by prolonged contact with 1,2-dichlorobenzene and chloropentafluorobenzene.
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Skin samples from Fischer-344 rats and Hartley guinea pigs exposed dermally to 1,2-dichlorobenzene (DCB) and chloropentafluorobenzene (CPFB) for up to 4 h were examined for chemical-induced damage. Samples were stained with hematoxylin and eosin and scored for polymorphonuclear cell (PMN)
Mitogenic stimulation of hepatocellular proliferation in rodents following 1,4-dichlorobenzene administration.
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1,4-Dichlorobenzene (DCB), a non-DNA-reactive compound, induced hepatocellular carcinomas at 600 mg/kg/day, but not 300 mg/kg/day in male and female B6C3F1 mice in a National Toxicology Program (NTP) bioassay. Cell proliferation studies were performed under conditions of the NTP bioassay to
Persistent olfactory mucosal metaplasia and increased olfactory bulb glial fibrillary acidic protein levels following a single dose of methylsulfonyl-dichlorobenzene in mice: comparison of the 2,5- and 2, 6-dichlorinated isomers.
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Histopathology was used to characterize long-term toxic effects in the olfactory system following a single ip dose (4-65 mg/kg) of methylsulfonyl-2,6-dichlorobenzene, (2,6-(diCl-MeSO(2)-B)), in female NMRI mice. The effects of 2,6-(diCl-MeSO(2)-B) and its 2, 5-chlorinated isomer,
A possible involvement of ion transporter in tumor necrosis factor alpha and cycloheximide-induced apoptosis of endothelial cells.
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We examined the tumor necrosis factor alpha (TNFalpha)-induced apoptosis of vascular endothelial cells from the standpoint of ion channels. Cultured vascular endothelial cells from bovine carotid artery were used. Apoptosis was determined by a propidium iodide assay. Treatment of the endothelial
Acute hepatic and renal toxicity of dichlorobenzene isomers in Fischer 344 rats.
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Studies were conducted to examine acute hepatic and renal toxicity of dichlorobenzene (DCB) structural isomers. Male Fischer 344 (F344) rats were injected with 2, 3 or 4 mmol kg-1 of 1,2-DCB, 1,3-DCB or 1,4-DCB (o-, m-, p-). Pair-fed control (PFC) animals were injected (i.p.) with corn oil (1 ml
Induction of light hydrocarbon nephropathy by p-dichlorobenzene.
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In order to clarify the etiology of a dose-related increase in the incidence of tubular cell adenocarcinomas of the kidney in male rats, the nephrotoxicity of p-dichlorobenzene (p-DCB) was investigated in a subchronic study. Groups of ten male and ten female Fischer 344 rats were dosed by gavage
NTP Toxicology and Carcinogenesis Studies of 1,4-Dichlorobenzene (CAS No. 106-46-7) in F344/N Rats and B6C3F1 Mice (Gavage Studies).
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1,4-Dichlorobenzene is commonly used as a space deodorant in toilets and for moth control. Because of its extensive production and use and the absence of carcinogenicity data, carcinogenesis studies were conducted by administering 1,4-dichlorobenzene (greater than 99% pure) in corn oil by gavage (5
Ten- and ninety-day toxicity studies of 1,2-dichlorobenzene administered by oral gavage to Sprague-Dawley rats.
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Ten- and ninety-day toxicity studies of 1,2-dichlorobenzene (DCB) were conducted in male and female Sprague-Dawley rats to meet the needs of the U.S. Environmental Protection Agency for toxicity data on this chemical for use in their determination of possible health risks related to human exposure.
The differential hepatotoxicity and cytochrome P450 responses of Fischer-344 rats to the three isomers of dichlorobenzene.
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The acute hepatotoxicity and response of hepatic cytochrome P450 to treatment with the three isomers of dichlorobenzene (DCB) have been investigated. The objectives were to estimate the onset of toxicity and to further elucidate the role of cytochrome P450 in the metabolism and toxicity of these
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