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chloroform/zea mays
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Pagina 1 a partire dal 69 risultati
Induced regenerative cell proliferation in livers and kidneys of male F-344 rats given chloroform in corn oil by gavage or ad libitum in drinking water.
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These studies were designed to establish the dose response relationships for the induction of cytolethality and regenerative cell proliferation in the liver and kidneys of male F-344 rats given chloroform by gavage or in drinking water. Rats were administered oral doses of 0, 10, 34, 90 or 180
Enhancement of the hepatotoxicity of chloroform in B6C3F1 mice by corn oil: implications for chloroform carcinogenesis.
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A recent study of the ability of chloroform in drinking water to produce cancer reported that male Osborne-Mendel rats developed renal tumors, but that female B6C3F1 mice failed to develop hepatocellular carcinomas. The results obtained in the male Osborne-Mendel rats were comparable to those
Chloroform in drinking water prevents hepatic cell proliferation induced by chloroform administered by gavage in corn oil to mice.
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Chloroform administered by gavage in corn oil, but not when administrated in drinking water, has been shown to induce liver cancer in female B6C3F1 mice and to enhance cell proliferation. Since humans are exposed to chloroform in their drinking water, we evaluated whether exposure by this route
Induced cytotoxicity and cell proliferation in the hepatocarcinogenicity of chloroform in female B6C3F1 mice: comparison of administration by gavage in corn oil vs ad libitum in drinking water.
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Chloroform increases the incidence of liver tumors in B6C3F1 mice when administered in by gavage in corn oil, but not when given in the drinking water at similar daily doses. Since cytotoxicity and regenerative cell proliferation have been implicated in the tumorigenic process for this nongenotoxic
Hepatoprotection by dimethyl sulfoxide. II. Characterization of optimal dose and the latest time of administration for effective protection against chloroform and bromobenzene induced injury.
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Dimethyl sulfoxide (DMSO) has previously been shown to attenuate chloroform (CHCl3) and bromobenzene (BB) induced hepatotoxicity in the rat when a dose of 2.0 ml/kg is given 24 hr after the toxicants. However, the optimal dose of DMSO and the latest time at which DMSO can be administered and still
Re-evaluation of the 2-year chloroform drinking water carcinogenicity bioassay in Osborne-Mendel rats supports chronic renal tubule injury as the mode of action underlying the renal tumor response.
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Chloroform, generally regarded as a non-genotoxic compound, is associated with the induction of liver and/or kidney tumors in laboratory mice and rats. In particular, chloroform produced renal tubule tumors in low incidence in male Osborne-Mendel rats when administered by corn-oil gavage or in the
Dose-dependent liver tissue repair after chloroform plus trichloroethylene binary mixture.
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The aim of the present study was to investigate the hypothesis that liver tissue repair induced by exposure to chloroform (CHCl(3))+trichloroethylene binary mixture (BM) is dose-dependent similar to that elicited by exposure to these compounds individually. Male Sprague-Dawley rats (250-300 g)
Risk assessment of inhaled chloroform based on its mode of action.
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The development of scientifically sound risk assessments based on mechanistic data will enable society to better allocate scarce resources. Inadequate risk assessments may result in potentially dangerous levels of hazardous chemicals, whereas overly conservative estimates can result in unnecessary
Toxicity and cell proliferation in the liver, kidneys and nasal passages of female F-344 rats, induced by chloroform administered by gavage.
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Dose-response relationships were determined for the induction of cytolethality and regenerative cell proliferation in the established target organs (liver, kidneys, and nasal passages) of female F-344 rats given chloroform daily by gavage. Rats were administered chloroform dissolved in corn oil at
Route of administration determines whether chloroform enhances or inhibits cell proliferation in the liver of B6C3F1 mice.
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Chloroform administered by gavage has been shown to induce liver cancer in B6C3F1 mice; however, when administered in the drinking water, chloroform inhibited liver cancer in mice. The effect of chloroform administered by these two routes upon cell proliferation in mouse liver was determined. Female
Dose-response relationships in ketone-induced potentiation of chloroform hepato- and nephrotoxicity.
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Chloroform (CHCl3)-induced hepato- and nephrotoxicity was evaluated in male, Fischer 344 rats pretreated with various dosages (1.0 to 15.0 mmol/kg, po) of acetone (Ac), 2-butanone (Bu), 2-pentanone (Pn), 2-hexanone (Hx), or 2-heptanone (Hp). The CHCl3 challenge dosage (0.5 ml/kg, ip) produced slight
Levels of myc, fos, Ha-ras, met and hepatocyte growth factor mRNA during regenerative cell proliferation in female mouse liver and male rat kidney after a cytotoxic dose of chloroform.
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Chloroform is a liver carcinogen in mice and a kidney carcinogen in rats. It is thought to act through a non-genotoxic-cytotoxic mode of action. Changes in expression of growth control genes accompanying chloroform-induced cytolethality and regeneration may play a part in the development of
The effect of dose and vehicle on early tissue damage and regenerative activity after chloroform administration to mice.
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The relationship between the acute toxicity of orally-administered chloroform and its long-term tumorigenic potential was studied in male mice of the CFLP outbred Swiss albino mouse strain. A single dose of approximately 18 mg CHCl3/kg had no detectable acute toxic effect on the liver or kidneys and
Chloroform-induced olfactory mucosal degeneration and osseous ethmoid hyperplasia are not associated with olfactory deficits in Fischer 344 rats.
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Adult female F-344 rats were trained (avoidance rate > 70%) over four days with a coupled tone- (n = 10 rats/dose) or 2 ppm acetaldehyde-cued (n = 6 rats/dose) foot shock paradigm. Rats were gavaged with chloroform dissolved in corn oil for 5 days/week for 3 week at 0 or 400 (tone-cued) or 0, 34,
Comparison of chloroform-induced toxicity in the kidneys, liver, and nasal passages of male Osborne-Mendel and F-344 rats.
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Chloroform given by gavage in corn oil at 180 mg/kg per day induced kidney tumors in male Osborne-Mendel rats. Chloroform-induced cytotoxicity and regenerative cell proliferation have been observed in the kidneys of male F-344 rats. In order to compare the acute sensitivity of male Osborne-Mendel
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