4.3 Article

Effect of Dietary Methylseleninic Acid and Se-Methylselenocysteine on Carcinogen-Induced, Androgen-Promoted Prostate Carcinogenesis in Rats

Journal

NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
Volume 74, Issue 10, Pages 3761-3768

Publisher

ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
DOI: 10.1080/01635581.2022.2093387

Keywords

-

Funding

  1. National Institutes of Health [R01 CA172169]

Ask authors/readers for more resources

Selenomethionine did not prevent prostate cancer in both clinical and rat models, but the next-generation selenium forms MSeA and MSeC showed inhibitory effects in mouse models and human prostate cancer cells. However, in a chemically induced-androgen promoted carcinogenesis rat model where selenomethionine was not effective, MSeA and MSeC feeding did not show preventive effects. Possible reasons for the contrast between these findings could be differences in carcinogenic mechanisms, selenium dosage, delivery mode, and pharmacokinetics, or fundamental differences in selenium metabolism between rats and mice.
Selenomethionine (SeMet) did not prevent prostate cancer in the SELECT trial and in two hormone-driven rat models. However, we have shown that daily oral bolus administration of next-generation selenium forms, methylseleninic acid (MSeA) and Se-methylselenocysteine (MSeC) at 3 mg Se/kg body weight, inhibits prostate carcinogenesis in the TRAMP and pten-deficient mouse models and In Vivo growth of human prostate cancer cells. Here, we determined whether these Se forms prevent prostate cancer in a chemically induced-androgen promoted carcinogenesis rat model in which SeMet was not preventive. WU rats were treated with methylnitrosourea, and one week later, slow-release testosterone implants when they were randomized to groups fed AIN-93M diet supplemented with 3 ppm selenium as MSeA or MSeC or control diet. Mean survival, tumor incidence in all accessory sex glands combined (dorsolateral and anterior prostate plus seminal vesicle) and the incidence of tumors confined to dorsolateral and/or anterior prostate were not statistically significantly different among the groups. Thus, MSeA and MSeC feeding was not preventive in this model. The contrast with the inhibitory effects of MSeA and MSeC in mouse models may be due to differences in carcinogenic mechanisms, selenium dosage, delivery mode, and pharmacokinetics or fundamental rat-mouse differences in selenium metabolism.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.3
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available