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liver neoplasms/maïs
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Liver tumor promoting ability of corn oil gavage in B6C3F1 male mice.
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In chronic carcinogenic bioassays, chemicals being tested with low water solubility have been administered via corn oil gavage. The present study examined the effect of chronic corn oil gavage on hepatic tumor formation in the B6C3F1 male mouse. Mice were initiated with diethylnitrosamine (DENA)
Proteome analysis of chemically induced mouse liver tumors with different genotype.
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Mouse liver tumors frequently harbor mutations in Ha-ras, B-raf, or Ctnnb1 (encoding beta-catenin). We conducted a proteome analysis with protein extracts from normal mouse liver and from liver tumors which were induced by a single injection of N-nitrosodiethylamine (DEN) as initiator followed by
PCB 153, a non-dioxin-like tumor promoter, selects for beta-catenin (Catnb)-mutated mouse liver tumors.
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Polychlorinated biphenyls (PCBs) are ubiquitous environmental toxicants which act as liver tumor promoters in rodents and can be classified as either dioxin-like or non-dioxin (phenobarbital [PB])-like inducers of cytochrome P-450. Since we have previously shown that tumor promotion by PB leads to
Dichloroacetate (DCA) dosimetry: interpreting DCA-induced liver cancer dose response and the potential for DCA to contribute to trichloroethylene-induced liver cancer.
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Pharmacokinetic studies with dichloroacetate (DCA) provide insights into the likelihood that trichloroethylene-induced liver cancers arise from formation of DCA as a metabolite and the mode of action by which DCA induces liver cancer. A simple physiologically based pharmacokinetic model was
Long-term exposure to the anti-inflammatory agent phenylbutazone induces kidney tumors in rats and liver tumors in mice.
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Long-term toxicity and carcinogenicity of phenylbutazone, a nonsteroidal anti-inflammatory drug, were evaluated in F344/N rats and B6C3F1 mice. In 2-year studies, phenylbutazone was given in corn oil by gavage 5 days per week to groups of 50 rats of each sex at doses of 0, 50, or 100 mg/kg body
Regenerative hyperplasia is not required for liver tumor induction in female B6C3F1 mice exposed to trihalomethanes.
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Chloroform (TCM), a water disinfection by-product, induced liver tumors in female mice when administered by gavage in corn oil but not when given in drinking water at comparable daily doses. Because short-term studies showed that the gavage doses also induced liver toxicity, it has been suggested
Effect of dietary fat on toad liver tumor induced by DMBA: ultrastructural studies.
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Toads injected with 2 mg 7,12-dimethyl-benza(a)anthracene (DMBA)/toad, 3 times/week for 12 weeks induced liver tumors in 12 out of 50 cases. The electron micrograph of toad liver tumor showed disorganization of the rough endoplasmic reticulum which encircles or partially surrounds the mitochondria.
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
Inhibition of DES-induced DNA adducts by diallyl sulfide: implications in liver cancer prevention.
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Diethylstilbesterol (DES) is known to cause cancer in humans and animals. Diallyl sulfide (DAS), a component of garlic, has been shown to prevent various types of cancer, presumably via metabolic modulation. Previously, we have demonstrated that DAS prevents the oxidation and reduction of DES in
Stunted growth, increased mortality, and liver tumors in offspring of polybrominated biphenyl (PBB) dosed sherman rats.
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Firemaster FF-1, a polybrominated biphenyl (PBB) mixture, was dissolved in corn oil and given as a dose of 200 mg/kg body weight to Sherman rats on d 7 and 14 of pregnancy. Control rats received equivalent doses of corn oil alone. Selected pups and all dams were killed 1 mo after pups were weaned. A
Induction of liver tumors in female Sherman strain rats by polybrominated biphenyls.
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Noninbred Sherman strain rats were given the polybrominated biphenyl mixture Firemaster FF-1 (PBB). Rats given a single dose of 1,000 mg PBB/kg or 12 doses of 100 mg PBB/kg body weight in corn oil by gavage had final (when less than or equal to 26 mo old) liver PBB concentrations of 17.1 and 34.8
Potential role of gut microbiota, the proto-oncogene PIKE (Agap2) and cytochrome P450 CYP2W1 in promotion of liver cancer by alcoholic and nonalcoholic fatty liver disease and protection by dietary soy protein.
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We have previously demonstrated promotion of diethylnitrosamine (DEN) initiated liver tumorigenesis after feeding diets high in fat or ethanol (EtOH) to male mice. This was accompanied by hepatic induction of the proto-oncogene PIKE (Agap2). Switch of dietary protein from casein to soy protein
Dracocephalum: novel anticancer plant acting on liver cancer cell mitochondria.
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Dracocephalum kotschyi Boiss. (Labiatae) is a native Iranian medicinal plant which has been used in combination with Peganum harmala L. as a remedy for many forms of human cancer especially leukemia and gastrointestinal malignancies. Hepatocellular carcinoma (HCC) is the third leading cause of
Effect of diallyl sulfide on rat liver microsomal nitrosamine metabolism and other monooxygenase activities.
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It has been reported that p.o. administration of diallyl sulfide (DAS), a naturally occurring component of garlic (Allium sativum), inhibits 1,2-dimethylhydrazine-induced colon and liver cancer in rodents. A possible mechanism for this protective effect is inhibition of hepatic activation of the
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