Nonenzymatic β-Carotene Degradation in Provitamin A-Biofortified Crop Plants

Our plain-English summary of Nonenzymatic β-Carotene Degradation in Provitamin A-Biofortified Crop Plants, by P. Schaub, F. Wüst, J. Koschmieder, et al (Journal of Agricultural and Food Chemistry, 2017).

The study

• Authors: P. Schaub, F. Wüst, J. Koschmieder, Q. Yu, P. Virk, J. Tohme, P. Beyer
• Journal: Journal of Agricultural and Food Chemistry
• Published: 2017;65(31):6588-6598
• Cited by: 45 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Provitamin A biofortification, the provision of provitamin A carotenoids through agriculture, is regarded as an effective and sustainable intervention to defeat vitamin A deficiency, representing a global health problem. This food-based intervention has been questioned in conjunction with negative outcomes for smokers and asbestos-exposed populations of the CARET and ATBC trials in which very high doses of β-carotene were supplemented. The current notion that β-carotene cleavage products (apocarotenoids) represented the harmful agents is the basis of the here-presented research. We quantitatively analyzed numerous plant food items and concluded that neither the amounts of apocarotenoids nor β-carotene provided by plant tissues, be they conventional or provitamin A-biofortified, pose an increased risk. We also investigated β-carotene degradation pathways over time. This reveals a substantial nonenzymatic proportion of carotene decay and corroborates the quantitative relevance of highly oxidized β-carotene polymers that form in all plant tissues investigated.

In plain English

This was a laboratory food chemistry study, not a study of people or asbestos. Its background noted that the CARET and ATBC trials of very high-dose β-carotene had negative outcomes for smokers and asbestos-exposed participants. This study did not re-examine those trials. The authors measured β-carotene and its breakdown products (apocarotenoids) in 102 Philippine food items, in biofortified crops from Zambia and Uganda, and in Golden Rice stored up to 215 days. All possible nonvolatile breakdown products were found in foods with substantial β-carotene. Stored Golden Rice lost β-carotene (31 to 2.7 micrograms per gram) while apocarotenoids stayed near 400 nanograms per gram. The authors concluded that breakdown was mainly non-enzymatic and that much β-carotene formed oxidized polymers. Comparing the amounts of each food needed to meet the same vitamin A requirement, with assumed conversion ratios, the authors estimated apocarotenoid exposure from Golden Rice as similar to green leafy vegetables, or up to 4 times higher in the leafy vegetables. The authors saw "no reason for concern" about diets, noting that high-dose supplements may represent a different scenario.

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: Laboratory chemical analysis of food items, with storage time-course experiments and calculated estimates of dietary exposure; no human subjects
• Who was studied: 102 plant food items bought on markets in the greater Manila area, Philippines, plus some soft drinks. Also biofortified orange maize and yellow cassava from Zambia, orange-fleshed sweet potato from Uganda, and greenhouse-grown Golden Rice 2 (cv. Kaybonnet) and wild-type rice
• Exposure: β-carotene and its cleavage products (apocarotenoids, including retinal, β-apo-14′-carotenal and β-apo-13-carotenone) and oxidized β-carotene polymers in foods. Asbestos appears only in the background description of the CARET and ATBC trials, which used high-dose β-carotene supplements
• Main results:
  • In food samples with substantial β-carotene, all possible nonvolatile β-carotene-derived apocarotenoids were detected
  • In stored Golden Rice, apocarotenoids stayed fairly constant at about 400 ng per gram, while β-carotene fell from 31 to 2.7 μg per gram after 215 days
  • In orange-fleshed sweet potato, sun drying and oven drying increased apocarotenoids 1.6-fold and 1.7-fold. However, the apocarotenoids formed accounted for only 0.3 to 0.4% of the β-carotene lost
  • In Golden Rice, parboiling, which inactivates enzymes, did not slow β-carotene decay, and there was no decay in grains stored without oxygen. The authors took this as showing the breakdown was mainly non-enzymatic
  • Geronic acid, which the authors used as a marker of oxidized β-carotene polymer, was detected in stored Golden Rice but not in wild-type grains of the same cultivar
  • The authors calculated the daily amounts needed to reach the same requirement of 500 μg retinol activity equivalents, using assumed conversion ratios and 80% cooking retention. On that basis, Golden Rice stored 29 days needed 141 g daily. The resulting apocarotenoid exposure was in a very similar range to green leafy vegetables, or up to 4 times higher in the green leafy vegetables, depending on the conversion ratio used
  • Matching the 30 mg per day supplement dose would require eating 441 g of carrots or 306 g of orange-fleshed sweet potato daily. After applying conversion ratios, the effective daily intake would be 3.3 kg of carrots or 2 kg of orange-fleshed sweet potato
• The authors' conclusion: The authors concluded that β-carotene cleavage products and oxidized polymers occur in all plant sources, whether biofortified or not, and form mainly through non-enzymatic breakdown. They found no pronounced differences between biofortified and non-biofortified foods when each is used to attain a given vitamin A requirement, and saw no reason for concern about diets. They suggested that high-dose supplementation may represent a different scenario
• Limitations the authors state:
  • The shorter breakdown products β-cyclocitral and β-ionone could not be measured quantitatively
  • Apocarotenoid 5,6-epoxides could not be quantified
  • Retinoic acid could not be identified with certainty because it was present at very low levels
  • No single analytical method exists for measuring the oxidized β-carotene polymers
  • The authors knew of no reports on what happens to retinal eaten in the diet
  • The supplement formulations used in the CARET, ATBC and Physicians' Health studies were not defined with respect to bioavailability

Related studies

• No dose-dependent increase in fracture risk after long-term exposure to high doses of retinol or beta-carotene — G.L. Ambrosini, A.P. Bremner, et al. (2013)
• Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Retinol Efficacy Trial — G.S. Omenn, G.E. Goodman, et al. (1996)
• Vitamin A and cancer prevention II: comparison of the effects of retinol and beta-carotene — N.H. de Klerk, A.W. Musk, et al. (1998)
• The protective effect of beta-carotene and retinol on ventilatory function in an asbestos-exposed cohort — P. Chuwers, S. Barnhart, et al. (1997)
• Analytical tools for the analysis of β-carotene and its degradation products — H. Stutz, N. Bresgen, et al. (2015)
• Beta carotene: from biochemistry to clinical trials — W.A. Pryor, W. Stahl, et al. (2000)

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