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Mechanism of inhibition of estrogen-induced renal carcinogenesis in male Syrian hamsters by
Title:
vitamin C.
Author: Liehr, J G : Roy, D : Gladek, A
Citation: Carcinogenesis. 1989 Nov; 10(11): 1983-8
Dietary supplementation of vitamin C to diethylstilbestrol (DES)- or estradiol-treated male
Syrian hamsters is known to inhibit renal carcinogenesis by approximately 50%. To elucidate the
mechanism of inhibition, the influence of administration of vitamin C on a series of previously
described biochemical markers of kidney carcinogenesis was investigated. Hamsters were
stratified into four groups: (i) untreated controls; (ii) vitamin C-treated; (iii) estrogen-treated; and
(iv) estrogen plus vitamin C-treated animals. Concomitant administration of vitamin C and
diethylstilbestrol (DES) decreased concentrations of the major DES-DNA adduct by 70-90% in
liver, kidney and testis than those receiving DES only. Diethylstilbestrol-4',4"-quinone has
Abstract: previously been shown to be the genotoxic metabolite of DES responsible for DNA adduct
formation in vivo. In vitro, vitamin C reduced diethylstilbestrol-4',4"-quinone to cis- and
trans-diethylstilbestrol in a dose-dependent fashion. Changes in activities of quinone reductase,
catalase, superoxide dismutase and of glutathione metabolizing enzymes (glutathione peroxidase,
glutathione reductase, gamma-glutamyl transpeptidase and glucose-6-phosphate dehydrogenase) in
response to vitamin C were not observed or not sufficiently large to account for the 50% decrease
in tumor incidence. No differences were detected in indirect estrogen-induced kidney DNA adducts
in response to vitamin C treatment. It is concluded that vitamin C inhibits estrogen-induced
carcinogenesis by reducing concentrations of estrogen quinone metabolites and their DNA adducts.
Review
None
References:
Notes: None
Language: English
Publication
Journal-Article
Type:
 Ascorbic Acid pharmacology : Estrogens : Glutathione metabolism : Kidney Neoplasms chemically
Keywords:
induced
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