Dibenz[a,c]anthracene: A potent inhibitor of skin-tumor initiation by 7,12-dimethylbenz[a]anthracene

T. J. Slaga; A. Viaje; S. G. Buty; W. M. Bracken

Dibenz[a,c]anthracene: A potent inhibitor of skin-tumor initiation by 7,12-dimethylbenz[a]anthracene

T. J. Slaga, A. Viaje, S. G. Buty, W. M. Bracken

Research output: Contribution to journal › Article › peer-review

Abstract

The mechanism by which the weak tumor initiator dibenz[a,c]anthracene (DB[a,c]A) inhibits the skin-tumor-initiating activity of 7,12-dimethylbenz[a]anthracene (DMBA) was investigated. DB[a,c]A was found to be a potent inhibitor of DMBA initiation when given either 5 min, or 1, 12, or 36 hr before DMBA. Pretreatment of mice with unlabeled DB[a,c]A at either 1, 12, or 36 hr before killing increased the in vitro epidermally mediated covalent binding of [³H]DMBA to DNA more than pretreatment with unlabeled DMBA at comparable times. Only when the tumor experiments were mimicked did a decrease in DMBA covalent binding to DNA in vitro occur. The results suggest that some competition at the level of polycyclic hydrocarbon metabolism or at the genome level may exist between metabolites of the weak carcinogen and those of the strong carcinogen.

Original language	English (US)
Pages (from-to)	477-483
Number of pages	7
Journal	Research Communications in Chemical Pathology and Pharmacology
Volume	19
Issue number	3
State	Published - Dec 1 1978
Externally published	Yes

ASJC Scopus subject areas

Pathology and Forensic Medicine
Toxicology
Pharmacology
Pharmacology, Toxicology and Pharmaceutics(all)

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@article{c7ac248797f9480c9a1a5d1396e61219,

title = "Dibenz[a,c]anthracene: A potent inhibitor of skin-tumor initiation by 7,12-dimethylbenz[a]anthracene",

abstract = "The mechanism by which the weak tumor initiator dibenz[a,c]anthracene (DB[a,c]A) inhibits the skin-tumor-initiating activity of 7,12-dimethylbenz[a]anthracene (DMBA) was investigated. DB[a,c]A was found to be a potent inhibitor of DMBA initiation when given either 5 min, or 1, 12, or 36 hr before DMBA. Pretreatment of mice with unlabeled DB[a,c]A at either 1, 12, or 36 hr before killing increased the in vitro epidermally mediated covalent binding of [3H]DMBA to DNA more than pretreatment with unlabeled DMBA at comparable times. Only when the tumor experiments were mimicked did a decrease in DMBA covalent binding to DNA in vitro occur. The results suggest that some competition at the level of polycyclic hydrocarbon metabolism or at the genome level may exist between metabolites of the weak carcinogen and those of the strong carcinogen.",

author = "Slaga, {T. J.} and A. Viaje and Buty, {S. G.} and Bracken, {W. M.}",

year = "1978",

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journal = "Research Communications in Chemical Pathology and Pharmacology",

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T2 - A potent inhibitor of skin-tumor initiation by 7,12-dimethylbenz[a]anthracene

AU - Slaga, T. J.

AU - Viaje, A.

AU - Buty, S. G.

AU - Bracken, W. M.

PY - 1978/12/1

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N2 - The mechanism by which the weak tumor initiator dibenz[a,c]anthracene (DB[a,c]A) inhibits the skin-tumor-initiating activity of 7,12-dimethylbenz[a]anthracene (DMBA) was investigated. DB[a,c]A was found to be a potent inhibitor of DMBA initiation when given either 5 min, or 1, 12, or 36 hr before DMBA. Pretreatment of mice with unlabeled DB[a,c]A at either 1, 12, or 36 hr before killing increased the in vitro epidermally mediated covalent binding of [3H]DMBA to DNA more than pretreatment with unlabeled DMBA at comparable times. Only when the tumor experiments were mimicked did a decrease in DMBA covalent binding to DNA in vitro occur. The results suggest that some competition at the level of polycyclic hydrocarbon metabolism or at the genome level may exist between metabolites of the weak carcinogen and those of the strong carcinogen.

AB - The mechanism by which the weak tumor initiator dibenz[a,c]anthracene (DB[a,c]A) inhibits the skin-tumor-initiating activity of 7,12-dimethylbenz[a]anthracene (DMBA) was investigated. DB[a,c]A was found to be a potent inhibitor of DMBA initiation when given either 5 min, or 1, 12, or 36 hr before DMBA. Pretreatment of mice with unlabeled DB[a,c]A at either 1, 12, or 36 hr before killing increased the in vitro epidermally mediated covalent binding of [3H]DMBA to DNA more than pretreatment with unlabeled DMBA at comparable times. Only when the tumor experiments were mimicked did a decrease in DMBA covalent binding to DNA in vitro occur. The results suggest that some competition at the level of polycyclic hydrocarbon metabolism or at the genome level may exist between metabolites of the weak carcinogen and those of the strong carcinogen.

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