The antioxidants vitamins A and E and selenium do not reduce the incidence of asbestos-induced disease in a mouse model of mesothelioma

Our plain-English summary of The antioxidants vitamins A and E and selenium do not reduce the incidence of asbestos-induced disease in a mouse model of mesothelioma, by C. Robinson, S. Woo, A. Walsh, et al (Nutrition and Cancer, 2012).

The study

• Authors: C. Robinson, S. Woo, A. Walsh, A.K. Nowak, R.A. Lake
• Journal: Nutrition and Cancer
• Published: 2012;64(2):315-22
• Cited by: 19 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Epidemiological evidence indicates that supplementation with some dietary factors is associated with a lower incidence of cancer. An effective cancer prevention strategy for the millions of people worldwide who have been exposed to asbestos could have enormous benefit. We tested whether dietary supplementation of the antioxidants vitamin A, E, and selenium could alter the pattern of disease in the MexTAg transgenic mouse model, in which mice uniformly develop mesothelioma after asbestos exposure. We focused on antioxidants because one of the most widely accepted hypotheses for the mechanism by which asbestos fibers cause cancer proposes the involvement of reactive oxygen and nitrogen species. We compared the survival of MexTAg mice that had been inoculated with asbestos fed on diets supplemented with 250,000 IU/kg vitamin A (retinoic acid), or 1,000 mg/kg vitamin E (α-tocopherol acetate) or 3 mg/kg selenium, or both vitamin E and selenium concurrently and, additionally, diets deficient in each antioxidant. We found that neither the time to develop symptoms of disease nor overall survival times were altered by any of the diets. We conclude that the data do not support the notion that dietary antioxidants will moderate the rate of mesothelioma in asbestos-exposed populations.

In plain English

In this animal experiment, the authors used MexTAg 299h transgenic mice, which develop mesothelioma after asbestos exposure. Groups of 10 to 25 mice were injected in the peritoneum (abdominal cavity) with two 3 mg doses of Wittenoom Gorge crocidolite, one month apart. Some mice were fed diets with extra vitamin A (retinoic acid), vitamin E, selenium, or vitamin E plus selenium, at 10 times the human recommended daily amount. Others got diets deficient in one nutrient; the vitamin E-deficient diet still held 3 mg/kg, against 75 mg/kg in the control diet. Both were compared with mice on a control diet. Test diets began 2 weeks before, or 8 or 12 weeks after, the injections. No diet changed survival. With vitamin A started 12 weeks after exposure, median survival was 33 weeks versus 32.5 on the control diet (P = 0.95). Survival after first signs of disease also did not differ. The authors concluded that the data do not support the idea that dietary antioxidants will lower mesothelioma rates in asbestos-exposed people. They noted that transgenic mice may not respond to antioxidants as humans do.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Animal experiment using a transgenic mouse model of asbestos-induced mesothelioma
• Who was studied: MexTAg 299h transgenic mice, adults aged 3 to 6 months, in groups of 10 to 25 matched for age and gender, studied at the University of Western Australia, Perth. These mice develop mesothelioma only after asbestos exposure.
• Exposure: Crocidolite asbestos (IUCC reference sample from Wittenoom Gorge, Western Australia), given as 2 injections of 3 mg into the peritoneum, 1 month apart. Diets were supplemented with vitamin A (250,000 IU/kg retinoic acid), vitamin E (1,000 mg/kg alpha tocopherol acetate), selenium (3 mg/kg sodium selenite), or vitamin E plus selenium. Other diets were deficient in vitamin A, vitamin E or selenium. The vitamin E-deficient diet still contained 3 mg/kg vitamin E, compared with 75 mg/kg in the control diet. All diets were compared with a control diet.
• Main results:
  • Vitamin A diet started 12 weeks after asbestos exposure: median survival was 33 weeks in the supplemented group and 32.5 weeks in the control group (P = 0.95). All mice developed mesothelioma.
  • Vitamin A diets started 2 weeks before asbestos exposure: median survival was 29.5 weeks (supplemented), 33.5 weeks (deficient) and 32 weeks (control) (P = 0.4).
  • Vitamin E diet started 8 weeks after asbestos exposure: median survival was 28 weeks (control) and 29 weeks (supplemented) (P = 0.53).
  • Vitamin E diet started 2 weeks before asbestos exposure: median survival was 33.5 weeks (supplemented) and 32 weeks (control) (P = 0.20). The vitamin E-deficient group had a median of 33 weeks, and survival did not differ across the three diets overall (P = 0.23).
  • Selenium diet started 8 weeks after asbestos exposure did not change survival compared with the control diet (n = 10, P = 0.25).
  • Selenium diets started 2 weeks before asbestos exposure: median survival was 33 weeks (supplemented), 32 weeks (control) and 29 weeks (deficient), with no statistical difference (P = 0.67).
  • Combined vitamin E and selenium diet started 8 weeks after asbestos exposure: median survival was 27 weeks, compared with 28 weeks for the control group (P = 0.74).
  • Survival from first diagnosis (first sign of fluid in the abdomen) to the endpoint did not differ between diet groups in any experiment (P = 0.38 for vitamin A, 0.24 for vitamin E, 0.43 for selenium, 0.83 for the combined diet).
  • Blood levels: after 8 weeks on the supplemented diets, serum vitamin E and selenium were significantly higher than in mice on the control diet.
  • Serum vitamin A did not track the diet. Mice on the vitamin A-deficient diet for 34 weeks had significantly higher serum levels than mice on the vitamin A-supplemented diet for 34 weeks (P = 0.0039).
• The authors' conclusion: The authors concluded that the data do not support the idea that dietary antioxidants will reduce the rate of mesothelioma in asbestos-exposed populations.
• Limitations the authors state:
  • The transgenic mice are genetically different and may not respond to antioxidants in the same way as humans or ordinary (wild-type) mice.
  • The authors did not measure vitamin A stores in the liver, so they could not judge how well the diets depleted or increased vitamin A. Serum vitamin A was not greatly affected by the diets.
  • The particular chemical forms of vitamin E and selenium used may matter for any cancer-prevention effect. Other forms were not tested in this mesothelioma model.

Mines named here

Asbestos mines this study is about. Each mine's page says who ran it, when it worked, and what it produced.

• Wittenoom, Western Australia

All asbestos mines

Topics

The National Library of Medicine indexes this study under subjects our site covers: Mesothelioma.

Medical terms in this study, explained in our Lexicon: Mesothelioma, Asbestos Exposure, Overall Survival.

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• Plasma retinol, carotene and vitamin E concentrations and lung function in a crocidolite-exposed cohort from Wittenoom, Western Australia: a cohort study — H.S. Alfonso, L. Fritschi, et al. (2005)
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