Enhancement of BOP‐induced pancreatic carcinogenesis in selenium‐fed Syrian Golden hamsters under specific dietary conditions

Birt, Diane F.; Julius, Alan D.; Runice, Christopher E.; White, Lenora T.; Lawson, Terence; Pour, Parviz M.

doi:10.1080/01635588809513966

Cited by 40 publications

(11 citation statements)

References 23 publications

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“…Dietary supplementation with Se inhibits cancer induction in a number of in vivo carcinogenesis models, including animal models for neoplasms of the skin, mammary gland, liver, and colon (reviewed in 13). However, Se compounds are not universally active as chemopreventive agents: negative results and/or enhancement of carcinogenesis have been reported in animal models for cancer of the pancreas, liver, and skin (14–16). …”

Section: Introductionmentioning

confidence: 99%

Null Activity of Selenium and Vitamin E as Cancer Chemopreventive Agents in the Rat Prostate

McCormick

Rao

Johnson

et al. 2010

Cancer Prevention Research

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To evaluate the potential efficacy of selenium and vitamin E as inhibitors of prostate carcinogenesis, four chemoprevention studies using a common protocol were done in a rat model of androgen-dependent prostate cancer. After stimulation of prostate epithelial cell proliferation by a sequential regimen of cyproterone acetate followed by testosterone propionate, male Wistar-Unilever rats received a single i.v. injection of N-methyl-N-nitrosourea (MNU) followed by chronic androgen stimulation via subcutaneous implantation of testosterone pellets. At 1 week post-MNU, groups of carcinogen-treated rats (39-44/group) were fed either a basal diet or a basal diet supplemented with L-selenomethionine (3 or 1.5 mg/kg diet; study 1), DL-α-tocopherol (vitamin E, 4,000 or 2,000 mg/kg diet; study 2), L-selenomethionine + vitamin E (3 + 2,000 mg/kg diet or 3 + 500 mg/kg diet; study 3), or selenized yeast (target selenium levels of 9 or 3 mg/kg diet; study 4). Each chemoprevention study was terminated at 13 months post-MNU, and prostate cancer incidence was determined by histopathologic evaluation. No statistically significant reductions in prostate cancer incidence were identified in any group receiving dietary supplementation with selenium and/or vitamin E. These data do not support the hypotheses that selenium and vitamin E are potent cancer chemopreventive agents in the prostate, and when considered with the recent clinical data reported in the Selenium and Vitamin E Cancer Prevention Trial (SELECT), show the predictive nature of this animal model for human prostate cancer chemoprevention. Cancer Prev Res; 3(3);

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Section: Introductionmentioning

confidence: 99%

Null Activity of Selenium and Vitamin E as Cancer Chemopreventive Agents in the Rat Prostate

McCormick

Rao

Johnson

et al. 2010

Cancer Prevention Research

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“…The chemopreventive activity of Se compounds has been demonstrated most convincingly in animal models for breast cancer; both inorganic (selenite, selenate) and organic (selenomethionine [SeMet], selenocysteine, Se-methylselenocysteine [MSC]) forms of Se demonstrate useful preventive activity against cancer induction in the rodent mammary gland. It should be noted, however, that although chemoprevention studies in many animal tumor systems demonstrate inhibition of carcinogenesis by Se compounds, a few have shown no effect (e.g., Lijinsky et al, 1989;McCormick and Rao, 1999), and at least one study demonstrated an enhancement of carcinogenesis by Se supplementation (Birt et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Subchronic oral toxicity studies of Se-methylselenocysteine, an organoselenium compound for breast cancer prevention

Johnson

Morrissey

Kapetanović

et al. 2008

Food and Chemical Toxicology

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Se-methylselenocysteine (MSC) is an organoselenium compound being developed for breast cancer chemoprevention. To characterize MSC toxicity, CD rats received daily gavage doses of 0, 0.5, 1.0, or 2.0 mg/kg/day (0, 3, 6, or 12 mg/m 2 /day), and beagle dogs received daily gavage doses of 0, 0.15, 0.3, or 0.6 mg/kg/day (0, 3, 6, or 12 mg/m 2 /day) for 28 days. In rats, MSC induced dose-related hepatomegaly in both sexes; mild anemia, thrombocytopenia, and elevated liver enzymes were observed in high dose females only. Microscopic pathology included hepatocellular degeneration (high dose males, all doses in females); arrested spermatogenesis (high dose males); and atrophy of corpora lutea (middle and high dose females). In dogs, MSC induced mild anemia in middle and high dose males, and in high dose females. Toxicologically significant microscopic lesions in dogs were seen only in the liver (peliosis and vacuolar degeneration in high dose males, midzonal necrosis in males in all dose groups). Based on liver pathology seen in female rats in all dose groups, the No Observed Adverse Effect Level [NOAEL] for MSC in rats is < 0.5 mg/kg/day. Based on alterations in hematology parameters and liver morphology in male dogs in all dose groups, the NOAEL for MSC in dogs is <0.15 mg/kg/day.

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“…Although the gene products and the general mechanisms of DNA repair are understood fairly well in prokaryotes, knowledge of mammalian repair systems has only recently accumulated, and little is known about the influence of dietary factors on these processes. Calorie restriction [39,40], EGCG [41], and selenium [42] have shown enhancing effects on unscheduled DNA synthesis and other measures related to repair capacity. In addition, folate deficiency has been associated with hypomethylation and decreased DNA repair capacity [43].…”

Section: Dna Repair Processesmentioning

confidence: 99%

Nutritional Modulation of the Carcinogenesis Process: Targets and Examples

Hursting¹

2000

Cancer &Amp; Nutrition

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Enhancement of BOP‐induced pancreatic carcinogenesis in selenium‐fed Syrian Golden hamsters under specific dietary conditions

Cited by 40 publications

References 23 publications

Null Activity of Selenium and Vitamin E as Cancer Chemopreventive Agents in the Rat Prostate

Null Activity of Selenium and Vitamin E as Cancer Chemopreventive Agents in the Rat Prostate

Subchronic oral toxicity studies of Se-methylselenocysteine, an organoselenium compound for breast cancer prevention

Nutritional Modulation of the Carcinogenesis Process: Targets and Examples

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