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hydroxytoluene/neoplasms
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Sida 1 från 124 resultat
Changes in pulmonary adenosine triphosphate-binding proteins detected by nucleotide photoaffinity labeling following treatment of mice with the tumor-modulatory agent butylated hydroxytoluene.
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Protein kinases play a central role in the regulation of normal and neoplastic growth. A novel approach to evaluating this role is to apply the photoaffinity analogue of adenosine 5'-triphosphate (ATP), 8-azido[gamma-32P]adenosine 5'-triphosphate (8-N3-[gamma-32P]ATP), to extracts obtained from
Mitogen-activated protein kinase (MAPK) activation by butylated hydroxytoluene hydroperoxide: implications for cellular survival and tumor promotion.
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The mitogen-activated protein kinase (MAPK) cascade plays an important role in carcinogenic development. Herein, we show that the skin tumor promoter butylated hydroxytoluene hydroperoxide (BHTOOH) stimulates a rapid and potent (14- to 20-fold) activation of extracellular signal-regulated kinase
Inhibitory effects of selenium, vitamin A and butylated hydroxytoluene on in vitro growth of human tongue cancer cells.
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The effects of vitamin A, selenium and butylated hydroxytoluene (BHT) on the growth of a human tongue cancer cell line were examined in monolayer cell cultures. A colony-forming assay showed a 50% reduction in the survival rate of the cell line at a concentration of 2.6 micrograms/ml selenium, 60
Selective induction of apoptosis in mouse and human lung epithelial cell lines by the tert-butyl hydroxylated metabolite of butylated hydroxytoluene: a proposed role in tumor promotion.
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Butylated hydroxytoluene (BHT) causes lung injury in mice and promotes tumor formation. Hydroxylation of a tert-butyl group on BHT to yield the metabolite, 6-tert-butyl-2-[2'-(2'-hydroxymethyl)-propyl]-4-methylphenol (BHTOH), may be required. BHTOH is more potent than BHT on an equimolar basis in
The lung tumor promoter, butylated hydroxytoluene (BHT), causes chronic inflammation in promotion-sensitive BALB/cByJ mice but not in promotion-resistant CXB4 mice.
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An inflammatory response accompanies the reversible pneumotoxicity caused by butylated hydroxytoluene (BHT) administration to mice. Lung tumor formation is promoted by BHT administration following an initiating agent in BALB/cByJ mice, but not in CXB4 mice. To assess the contribution of inflammation
Decrease in the protein kinase C-catalyzed phosphorylation of an endogenous lung protein (Mr 36,000) following treatment of mice with the tumor-modulatory agent butylated hydroxytoluene.
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Butylated hydroxytoluene (BHT) causes transient lung damage in mice, and it can either inhibit or enhance carcinogen induction of tumors in internal organs, such as urethan-induced lung adenomas. Since protein kinase C (Pk-C) may mediate the action of one class of tumor-modulatory agents, the
Responses of tumorigenic and non-tumorigenic mouse lung epithelial cell lines to electrophilic metabolites of the tumor promoter butylated hydroxytoluene.
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A model system to investigate the promotion phase of pulmonary carcinogenesis involves chronic exposure of carcinogen-initiated mice to the food additive, butylated hydroxytoluene (BHT). Previous studies strongly suggested that this activity is due to the cytochrome p450-catalyzed formation of
Butylated hydroxytoluene exposure is necessary to induce lung tumors in BALB mice treated with 3-methylcholanthrene.
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Chronic butylated hydroxytoluene (BHT) treatment after a single administration of a carcinogen increases lung tumor multiplicity in some inbred strains of mice. We report that BALB/cOla and BALB/cByJ mice given a low dose (10 microg/g of body weight) of 3-methylcholanthrene (MCA) develop no lung
Intake of butylated hydroxyanisole and butylated hydroxytoluene and stomach cancer risk: results from analyses in the Netherlands Cohort Study.
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Both carcinogenic and anticarcinogenic properties have been reported for the synthetic antioxidants butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT). The association between dietary intake of BHA and BHT and stomach cancer risk was investigated in the Netherlands Cohort Study (NLCS)
Use of a microsome-mediated test system to assess efficacy and mechanisms of cancer chemopreventive agents.
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There is a growing need for short-term assays which can assess the mechanisms and efficacy of cancer chemopreventive agents. In the present study we have employed a microsome-mediated test system concomitantly with DNA adduct detection to assess the efficacy of five chemopreventive agents,
Changes in urine composition, bladder epithelial morphology, and DNA synthesis in male F344 rats in response to ingestion of bladder tumor promoters.
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An investigation of changes in urine composition, morphology of bladder epithelium, and levels of DNA synthesis following 4 or 8 weeks oral administration of bladder tumor promoters or analogs without promotion potential was performed. The sodium salts of L-ascorbate, o-phenylphenate, and
Promotion of lung tumors in mice.
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Several elements of two-stage carcinogenesis apply to the development of lung tumors in Strain A or Swiss-Webster mice. At least three agents which have been identified as promoters in skin, urinary bladder and liver will also enhance tumor formation in lung; phorbol, saccharin and butylated
Overview of tumor promotion in animals.
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Our present understanding of two-stage carcinogenesis encompasses almost four decades of research. Evidence for chemical promotion or cocarcinogenesis was first provided by Berenblum, who reported that a regimen of croton oil (weak or noncarcinogenic) applied alternately with small doses of
Inhibitors of the cytochrome P-450 enzymes block the secretagogue-induced release of corticotropin in mouse pituitary tumor cells.
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A mouse pituitary tumor cell line (AtT-20) releases corticotropin (ACTH) in response to a number of secretagogues, including corticotropin-releasing factor (CRF), beta-adrenergic agents, N6,O2'-dibutyryladenosine 3',5'-cyclic monophosphate (Bt2 cAMP), and potassium. The stimulation of ACTH secretion
Simultaneous inhibition of liver carcinogenicity and enhancement of bladder carcinogenicity of N-2-fluorenylacetamide by butylated hydroxytoluene.
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The effect of butylated hydroxytoluene on the carcinogenicity to rats of concurrently administered N-2-fluorenylacetamide was determined. N-2-Fluorenylacetamide at 200 ppm alone in the diet produced liver neoplasms but no bladder neoplasms after 25 weeks. With simultaneous administration, 6000 ppm
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