Impact of Selenium on Biomarkers and Clinical Aspects Related to Ageing. A Review

Alehagen, Urban; Opstad, Trine Baur; Alexander, Jan; Larsson, Anders; Aaseth, Jan

doi:10.3390/biom11101478

Cited by 38 publications

(36 citation statements)

References 119 publications

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“…Most of the human selenoproteins are oxidoreductases containing the amino acid selenocysteine (SeCys) at their catalytic site [ 439 ]. In the antioxidant enzymes GPXs, SeCys residues catalyse the reduction of hydrogen peroxide and peroxide radicals using glutathione as a substrate, thus lowering free radicals and consequent DNA damage [ 440 , 441 ]. A second crucial family of proteins containing SeCys and involved in redox biology is thioredoxin reductases (TRs), which contribute to the regulation of gene expression of multiple transcription factors implicated in inflammatory and cell cycle pathways (e.g., NF-kB and p53) [ 442 ], as well as in the recycling of antioxidant molecules [ 441 ].…”

Section: Resultsmentioning

confidence: 99%

The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence

et al. 2022

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Cellular senescence is an irreversible state of cell cycle arrest occurring in response to stressful stimuli, such as telomere attrition, DNA damage, reactive oxygen species, and oncogenic proteins. Although beneficial and protective in several physiological processes, an excessive senescent cell burden has been involved in various pathological conditions including aging, tissue dysfunction and chronic diseases. Oxidative stress (OS) can drive senescence due to a loss of balance between pro-oxidant stimuli and antioxidant defences. Therefore, the identification and characterization of antioxidant compounds capable of preventing or counteracting the senescent phenotype is of major interest. However, despite the considerable number of studies, a comprehensive overview of the main antioxidant molecules capable of counteracting OS-induced senescence is still lacking. Here, besides a brief description of the molecular mechanisms implicated in OS-mediated aging, we review and discuss the role of enzymes, mitochondria-targeting compounds, vitamins, carotenoids, organosulfur compounds, nitrogen non-protein molecules, minerals, flavonoids, and non-flavonoids as antioxidant compounds with an anti-aging potential, therefore offering insights into innovative lifespan-extending approaches.

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Section: Resultsmentioning

confidence: 99%

The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence

et al. 2022

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“…Relevant here are the previous studies showing that pro-inflammatory cytokines, such as IGF-1, TNFα, and interleukin-6, induce increased FGF-23 synthesis [41,42]. It is also known that there is a close connection between general inflammation and development of cardiovascular disease [28,29,43].…”

Section: Discussionmentioning

confidence: 74%

Decreased Concentration of Fibroblast Growth Factor 23 (FGF-23) as a Result of Supplementation with Selenium and Coenzyme Q10 in an Elderly Swedish Population: A Sub-Analysis

Alehagen

Aaseth

Larsson

et al. 2022

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There is a reduced intake of selenium in many countries due to low levels of selenium in the soil. This results in an increased cardiovascular risk. Fibroblast growth factor 23 (FGF-23) is active mainly in the metabolism of vitamin D and phosphorus. However, there are indications that FGF-23 may also provide information both on cardiovascular function and prognosis. The aim of the study was to evaluate the effect of supplementation with selenium and coenzyme Q10 on the FGF-23 concentration in an elderly population with low concentrations of both selenium and coenzyme Q10 and in which the supplementation improved cardiac function and mortality. In a randomised double-blind placebo-controlled trial, FGF-23 was measured in 219 individuals at the start and after 48 months. Selenium yeast (200 µg/day) and coenzyme Q10 (200 mg/day) (n = 118) or placebo (n = 101) were given as a dietary supplement. The intervention time was 48 months. t-Tests, repeated measures of variance, and ANCOVA analyses were used to evaluate the differences in FGF-23 concentration. Following supplementation with selenium and coenzyme Q10, a significantly lower level of FGF-23 could be seen (p = 0.01). Applying 10 years of follow-up, those who later died a cardiovascular death had a significantly higher FGF-23 concentration after 48 months compared with those who survived (p = 0.036), and a significantly lower FGF-23 concentration could be seen in those with a normal renal function compared to those with an impaired renal function (p = 0.027). Supplementation with selenium and coenzyme Q10 to an elderly community-living population low in both substances prevented an increase of FGF-23 and also provided a reduced cardiovascular risk.

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“…If we can curb the oxidative stress with antioxidants, the favourable effects of increased levels of serotonin may render positive the overall effect of administering tryptophan as a dietary supplement. A diet high in acetylcysteine, selenium, and natural antioxidants appears to be associated with reduced risk of chronic diseases [ 109 , 110 ] and constitutes an insufficiently investigated possibility for reducing pain- or mood-related problems and age-associated dementia [ 97 ]. Clinical evaluation of this approach requires several years of follow-up, however, and such a preventive treatment must be initiated before severe motor or cognitive symptoms have developed—in the early stages of Parkinson’s disease [ 69 ], for example.…”

Section: Discussionmentioning

confidence: 99%

The Role of Tryptophan Dysmetabolism and Quinolinic Acid in Depressive and Neurodegenerative Diseases

et al. 2022

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Emerging evidence suggests that neuroinflammation is involved in both depression and neurodegenerative diseases. The kynurenine pathway, generating metabolites which may play a role in pathogenesis, is one of several competing pathways of tryptophan metabolism. The present article is a narrative review of tryptophan metabolism, neuroinflammation, depression, and neurodegeneration. A disturbed tryptophan metabolism with increased activity of the kynurenine pathway and production of quinolinic acid may result in deficiencies in tryptophan and derived neurotransmitters. Quinolinic acid is an N-methyl-D-aspartate receptor agonist, and raised levels in CSF, together with increased levels of inflammatory cytokines, have been reported in mood disorders. Increased quinolinic acid has also been observed in neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, and HIV-related cognitive decline. Oxidative stress in connection with increased indole-dioxygenase (IDO) activity and kynurenine formation may contribute to inflammatory responses and the production of cytokines. Increased formation of quinolinic acid may occur at the expense of kynurenic acid and neuroprotective picolinic acid. While awaiting ongoing research on potential pharmacological interventions on tryptophan metabolism, adequate protein intake with appropriate amounts of tryptophan and antioxidants may offer protection against oxidative stress and provide a balanced set of physiological receptor ligands.

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Impact of Selenium on Biomarkers and Clinical Aspects Related to Ageing. A Review

Cited by 38 publications

References 119 publications

The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence

The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence

Decreased Concentration of Fibroblast Growth Factor 23 (FGF-23) as a Result of Supplementation with Selenium and Coenzyme Q10 in an Elderly Swedish Population: A Sub-Analysis

The Role of Tryptophan Dysmetabolism and Quinolinic Acid in Depressive and Neurodegenerative Diseases

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