Abstract
Helicobacter pylori (H. pylori) infection has been associated with gastric carcinogenesis, but responsible and detail mechanisms are insufficient by the absence of adequate data. To obtain direct evidence regarding the carcinogenicity of H. pylori, we investigated the initiating and promoting activity of H. pylori water extract (HPE) in two-stage mouse skin carcinogenesis model. HPE treatment, as an initiation, significantly enhanced tumor formation compared with control group. Moreover, HPE treatment increased production of 8-hydroxydeoxyguanosine in epidermal cells and HPE-initiated/TPA-promoted papillomas demonstrated a point mutation of the Ha-ras gene. These results suggest an initiating activity of HPE on two-stage mouse skin carcinogenesis.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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8-Hydroxy-2'-Deoxyguanosine
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Alleles
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Animals
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Carcinogens / isolation & purification
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Carcinogens / toxicity*
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Cell Fractionation
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Cocarcinogenesis
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Codon / drug effects
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DNA / drug effects
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DNA / genetics
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DNA Adducts / analysis
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DNA Damage
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Deoxyguanosine / analogs & derivatives*
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Deoxyguanosine / analysis
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Disease Progression
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Female
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Genes, ras / drug effects
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Helicobacter pylori / chemistry*
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Luminescent Measurements
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Mice
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Mice, Inbred SENCAR
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Oxidative Stress
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Papilloma / chemically induced*
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Papilloma / genetics
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Peroxidase / analysis
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Point Mutation
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Skin / drug effects
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Skin / enzymology
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Skin Neoplasms / chemically induced*
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Skin Neoplasms / genetics
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Superoxides / metabolism
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Tetradecanoylphorbol Acetate / toxicity
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Water
Substances
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Carcinogens
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Codon
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DNA Adducts
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Water
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Superoxides
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8-Hydroxy-2'-Deoxyguanosine
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DNA
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Peroxidase
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Deoxyguanosine
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Tetradecanoylphorbol Acetate