4
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Revisiting carotenoids as dietary antioxidants for human health and disease prevention.

      1
      Food & function
      Royal Society of Chemistry (RSC)

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Humans are unique indiscriminate carotenoid accumulators, so the human body accumulates a wide range of dietary carotenoids of different types and to varying concentrations. Carotenoids were once recognized as physiological antioxidants because of their ability to quench singlet molecular oxygen (1O2). In the 1990s, large-scale intervention studies failed to demonstrate that supplementary β-carotene intake reduces the incidence of lung cancer, although its antioxidant activity was supposed to contribute to the prevention of oxidative stress-induced carcinogenesis. Nevertheless, the antioxidant activity of carotenoids has attracted renewed attention as the pathophysiological role of 1O2 has emerged, and as the ability of dietary carotenoids to induce antioxidant enzymes has been revealed. This review focuses on six major carotenoids from fruit and vegetables and revisits their physiological functions as biological antioxidants from the standpoint of health promotion and disease prevention. β-Carotene 9',10'-oxygenase-derived oxidative metabolites trigger increases in the activities of antioxidant enzymes. Lutein and zeaxanthin selectively accumulate in human macular cells to protect against light-induced macular impairment by acting as antioxidants. Lycopene accumulates exclusively and to high concentrations in the testis, where its antioxidant activity may help to eliminate oxidative damage. Dietary carotenoids appear to exert their antioxidant activity in photo-irradiated skin after their persistent deposition in the skin. An acceptable level of dietary carotenoids for disease prevention should be established because they can have deleterious effects as prooxidants if they accumulate to excess levels. Finally, it is expected that the reason why humans are indiscriminate carotenoid accumulators will be understood soon.

          Related collections

          Most cited references256

          • Record: found
          • Abstract: found
          • Article: not found

          Ferroptosis: an iron-dependent form of nonapoptotic cell death.

          Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferroptosis is dependent upon intracellular iron, but not other metals, and is morphologically, biochemically, and genetically distinct from apoptosis, necrosis, and autophagy. We identify the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes. Indeed, erastin, like glutamate, inhibits cystine uptake by the cystine/glutamate antiporter (system x(c)(-)), creating a void in the antioxidant defenses of the cell and ultimately leading to iron-dependent, oxidative death. Thus, activation of ferroptosis results in the nonapoptotic destruction of certain cancer cells, whereas inhibition of this process may protect organisms from neurodegeneration. Copyright © 2012 Elsevier Inc. All rights reserved.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Age-related macular degeneration

            Age-related macular degeneration is a leading cause of visual impairment and severe vision loss. Clinically, it is classified as early-stage (medium-sized drusen and retinal pigmentary changes) to late-stage (neovascular and atrophic). Age-related macular degeneration is a multifactorial disorder, with dysregulation in the complement, lipid, angiogenic, inflammatory, and extracellular matrix pathways implicated in its pathogenesis. More than 50 genetic susceptibility loci have been identified, of which the most important are in the CFH and ARMS2 genes. The major non-genetic risk factors are smoking and low dietary intake of antioxidants (zinc and carotenoids). Progression from early-stage to late-stage disease can be slowed with high-dose zinc and antioxidant vitamin supplements. Intravitreal anti-vascular endothelial growth factor therapy (eg, ranibizumab, aflibercept, or bevacizumab) is highly effective at treating neovascular age-related macular degeneration, and has markedly decreased the prevalence of visual impairment in populations worldwide. Currently, no proven therapies for atrophic disease are available, but several agents are being investigated in clinical trials. Future progress is likely to be from improved efforts in prevention and risk-factor modification, personalised medicine targeting specific pathways, newer anti-vascular endothelial growth factor agents or other agents, and regenerative therapies.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease.

              Observational studies suggest that people who consume more fruits and vegetables containing beta carotene have somewhat lower risks of cancer and cardiovascular disease, and earlier basic research suggested plausible mechanisms. Because large randomized trials of long duration were necessary to test this hypothesis directly, we conducted a trial of beta carotene supplementation. In a randomized, double-blind, placebo-controlled trial of beta carotene (50 mg on alternate days), we enrolled 22,071 male physicians, 40 to 84 years of age, in the United States; 11 percent were current smokers and 39 percent were former smokers at the beginning of the study in 1982. By December 31, 1995, the scheduled end of the study, fewer than 1 percent had been lost to follow-up, and compliance was 78 percent in the group that received beta carotene. Among 11,036 physicians randomly assigned to receive beta carotene and 11,035 assigned to receive placebo, there were virtually no early or late differences in the overall incidence of malignant neoplasms or cardiovascular disease, or in overall mortality. In the beta carotene group, 1273 men had any malignant neoplasm (except nonmelanoma skin cancer), as compared with 1293 in the placebo group (relative risk, 0.98; 95 percent confidence interval, 0.91 to 1.06). There were also no significant differences in the number of cases of lung cancer (82 in the beta carotene group vs. 88 in the placebo group); the number of deaths from cancer (386 vs. 380), deaths from any cause (979 vs. 968), or deaths from cardiovascular disease (338 vs. 313); the number of men with myocardial infarction (468 vs. 489); the number with stroke (367 vs. 382); or the number with any one of the previous three end points (967 vs. 972). Among current and former smokers, there were also no significant early or late differences in any of these end points. In this trial among healthy men, 12 years of supplementation with beta carotene produced neither benefit nor harm in terms of the incidence of malignant neoplasms, cardiovascular disease, or death from all causes.
                Bookmark

                Author and article information

                Journal
                Food Funct
                Food & function
                Royal Society of Chemistry (RSC)
                2042-650X
                2042-6496
                Aug 29 2023
                : 14
                : 17
                Affiliations
                [1 ] Faculty of Medicine, Tokushima University, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan. terao@tokushima-u.ac.jp.
                Article
                10.1039/d3fo02330c
                37593767
                911a2c73-3c6d-430c-9f85-ea465dd78ef9
                History

                Comments

                Comment on this article