Journal Article

Studies of chemopreventive effects of budenoside on benzo[a]pyrene-induced neoplasia of the lung of female A/J mice.

L W Wattenberg and R D Estensen

in Carcinogenesis

Volume 18, issue 10, pages 2015-2017
Published in print October 1997 | ISSN: 0143-3334
Published online October 1997 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/18.10.2015
Studies of chemopreventive effects of budenoside on benzo[a]pyrene-induced neoplasia of the lung of female A/J mice.

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The objective of the present investigation was to determine conditions under which the synthetic glucocorticoid, budenoside, will inhibit benzo[a]pyrene (BaP)-induced pulmonary carcinogenesis when administered in the post-initiation period. For this purpose, female A/J mice were employed. The animals were given three administrations of 2 mg of BaP by oral intubation during a 1-week period. Budenoside was fed in the diet subsequent to the last dose of BaP. Using this format, two experiments were carried out to determine the effects of varying the time of administration of budenoside on the magnitude of the inhibition obtained. In both experiments, one group of mice was fed budenoside (1.5 mg/kg of diet) from 1 week after the last dose of BaP until the termination of the experiment, 15 weeks later. The reduction of pulmonary tumor formation under these conditions was 89% in the first experiment and 78% in the second (average 84%). In the first experiment the effects of feeding budenoside only during weeks 1-5 after BaP administration was studied. Under these conditions, inhibition of pulmonary tumor formation was 35%. In the second experiment, the effects of postponing the start of feeding budenoside was determined. In mice in which the budenoside feeding was delayed until 5 weeks after the last dose of BaP and then continued for the duration of the protocol, a 67% inhibition of tumor formation was found. The data obtained indicate that budenoside will produce inhibition of pulmonary adenoma formation when fed either early or late in the post-initiation stage of carcinogenesis, and that feeding throughout the entire post-initiation period gives maximum inhibition.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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