Mitogenic and apoptotic signaling by carotenoids: involvement of a redox mechanism

Our plain-English summary of Mitogenic and apoptotic signaling by carotenoids: involvement of a redox mechanism, by P. Palozza, S. Serini, F. Di Nicuolo, et al (IUBMB Life, 2001).

The study

• Authors: P. Palozza, S. Serini, F. Di Nicuolo, G. Calviello
• Journal: IUBMB Life
• Published: 2001;52(1-2):77-81
• Type of article: Review
• Cited by: 16 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The potential for carotenoids to modulate tumor growth is currently under investigation. Although epidemiological studies evidence that a high intake of vegetables, rich in carotenoids, decreases cancer incidence and mortality, clinical trials demonstrate that supplementation of beta-carotene to chronic smokers or to asbestos workers increases the risk for lung cancer. These contradictory findings have renewed interest in elucidating the mechanism of action of carotenoids in biological systems. In this review, we show evidence for mitogenic and apoptotic effects of carotenoids and we support the hypothesis that these molecules may act as anticarcinogens or as procarcinogens through a redox mechanism. In particular, we report demonstrations for the anti-oxidant or pro-oxidant effects of carotenoids in vitro and in vivo, focusing our attention on the relationship existing between cell growth and redox status.

In plain English

This article was a review, not an original study. The authors summarized laboratory and animal evidence on how beta-carotene and other carotenoids (plant pigments) affect cell growth, cell death (apoptosis) and the balance of oxidation inside cells. Asbestos appeared only as background: the authors noted that clinical trials had reported increased lung cancer after beta-carotene supplementation among chronic smokers or individuals suffering from asbestosis. The review reported no new data on asbestos-exposed people. Studies reviewed reported that carotenoids inhibited tumor cell growth in cell cultures. In ferrets exposed chronically to tobacco smoke, high-dose beta-carotene increased lung tumor formation, while low doses showed no potentially detrimental effects. In the authors' own cell experiments, beta-carotene reduced production of reactive oxygen species at low concentrations and increased it at high concentrations. These increases coincided with cell death and halted cell division. The authors concluded that the increased lung cancer seen in the trials could be the result of a pro-oxidant effect of beta-carotene. They added that further studies are required to verify this in living organisms.

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: Review (described as a 'Critical Review') of laboratory, animal and trial evidence on carotenoids, cell growth and redox status
• Who was studied: No study population of its own. The review covered cell culture studies, animal studies and the authors' own earlier experiments in human colon adenocarcinoma cells and HL-60 leukemia cells.
• Exposure: Beta-carotene and other carotenoids. Asbestos is not studied. It is mentioned only because clinical trials reported increased lung cancer after beta-carotene supplementation in chronic smokers or individuals suffering from asbestosis.
• Main results:
  • Studies reviewed: in ferrets exposed chronically to tobacco smoke, beta-carotene at high doses increased lung tumorigenesis. At low doses it had no potentially detrimental effects and may have given weak protection against lung damage.
  • The authors' own work in human colon adenocarcinoma and leukemia cells: increases in reactive oxygen species and/or oxidized glutathione caused by beta-carotene coincided with its ability to induce apoptosis and to arrest cell cycle progression.
  • In the authors' experiments, apoptosis caused by beta-carotene occurred through a p53-independent mechanism.
  • Studies reviewed: at low oxygen tension beta-carotene acted as an anti-oxidant. At higher oxygen tension it auto-oxidized and showed pro-oxidant behavior.
• The authors' conclusion: The authors concluded that carotenoids act as mitogenic and apoptotic agents, possibly through changes in intracellular redox status. They suggested that the enhancement of lung cancer by beta-carotene in clinical trials could be the result of the carotenoid's pro-oxidant effect.
• Limitations the authors state:
  • The dependence of beta-carotene's behavior on oxygen tension has been shown only in laboratory (in vitro) models. The authors state that no evidence is available in living organisms.
  • The authors state that further studies are needed to verify their proposed mechanism in living organisms.

Topics

Medical terms in this study, explained in our Lexicon: Clinical Trial, Lung Cancer.

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