Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging
Recent advances in vitamin D research indicate that this vitamin, a secosteroid hormone, has beneficial effects on several body systems other than the musculoskeletal system. Both 25 dihydroxy vitamin D [25(OH)<sub>2</sub>D] and its active hormonal form, 1,25-dihydroxyvitamin D [1,25(OH)...
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| Format: | Article |
| Language: | English |
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MDPI AG
2019-05-01
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| Series: | Biology |
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| Online Access: | https://www.mdpi.com/2079-7737/8/2/30 |
| _version_ | 1797762663664582656 |
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| author | Sunil J. Wimalawansa |
| author_facet | Sunil J. Wimalawansa |
| author_sort | Sunil J. Wimalawansa |
| collection | DOAJ |
| description | Recent advances in vitamin D research indicate that this vitamin, a secosteroid hormone, has beneficial effects on several body systems other than the musculoskeletal system. Both 25 dihydroxy vitamin D [25(OH)<sub>2</sub>D] and its active hormonal form, 1,25-dihydroxyvitamin D [1,25(OH)<sub>2</sub>D] are essential for human physiological functions, including damping down inflammation and the excessive intracellular oxidative stresses. Vitamin D is one of the key controllers of systemic inflammation, oxidative stress and mitochondrial respiratory function, and thus, the aging process in humans. In turn, molecular and cellular actions form 1,25(OH)<sub>2</sub>D slow down oxidative stress, cell and tissue damage, and the aging process. On the other hand, hypovitaminosis D impairs mitochondrial functions, and enhances oxidative stress and systemic inflammation. The interaction of 1,25(OH)<sub>2</sub>D with its intracellular receptors modulates vitamin D–dependent gene transcription and activation of vitamin D-responsive elements, which triggers multiple second messenger systems. Thus, it is not surprising that hypovitaminosis D increases the incidence and severity of several age-related common diseases, such as metabolic disorders that are linked to oxidative stress. These include obesity, insulin resistance, type 2 diabetes, hypertension, pregnancy complications, memory disorders, osteoporosis, autoimmune diseases, certain cancers, and systemic inflammatory diseases. Vitamin D adequacy leads to less oxidative stress and improves mitochondrial and endocrine functions, reducing the risks of disorders, such as autoimmunity, infections, metabolic derangements, and impairment of DNA repair; all of this aids a healthy, graceful aging process. Vitamin D is also a potent anti-oxidant that facilitates balanced mitochondrial activities, preventing oxidative stress-related protein oxidation, lipid peroxidation, and DNA damage. New understandings of vitamin D-related advances in metabolomics, transcriptomics, epigenetics, in relation to its ability to control oxidative stress in conjunction with micronutrients, vitamins, and antioxidants, following normalization of serum 25(OH)D and tissue 1,25(OH)<sub>2</sub>D concentrations, likely to promise cost-effective better clinical outcomes in humans. |
| first_indexed | 2024-03-12T19:31:37Z |
| format | Article |
| id | doaj.art-8ac7f77dcb1b468bb85491799b210cf2 |
| institution | Directory Open Access Journal |
| issn | 2079-7737 |
| language | English |
| last_indexed | 2024-03-12T19:31:37Z |
| publishDate | 2019-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biology |
| spelling | doaj.art-8ac7f77dcb1b468bb85491799b210cf22023-08-02T04:30:10ZengMDPI AGBiology2079-77372019-05-01823010.3390/biology8020030biology8020030Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and AgingSunil J. Wimalawansa0Professor of Medicine, Endocrinology & Nutrition, Cardio Metabolic and Endocrine Institute, NJ 08873, USARecent advances in vitamin D research indicate that this vitamin, a secosteroid hormone, has beneficial effects on several body systems other than the musculoskeletal system. Both 25 dihydroxy vitamin D [25(OH)<sub>2</sub>D] and its active hormonal form, 1,25-dihydroxyvitamin D [1,25(OH)<sub>2</sub>D] are essential for human physiological functions, including damping down inflammation and the excessive intracellular oxidative stresses. Vitamin D is one of the key controllers of systemic inflammation, oxidative stress and mitochondrial respiratory function, and thus, the aging process in humans. In turn, molecular and cellular actions form 1,25(OH)<sub>2</sub>D slow down oxidative stress, cell and tissue damage, and the aging process. On the other hand, hypovitaminosis D impairs mitochondrial functions, and enhances oxidative stress and systemic inflammation. The interaction of 1,25(OH)<sub>2</sub>D with its intracellular receptors modulates vitamin D–dependent gene transcription and activation of vitamin D-responsive elements, which triggers multiple second messenger systems. Thus, it is not surprising that hypovitaminosis D increases the incidence and severity of several age-related common diseases, such as metabolic disorders that are linked to oxidative stress. These include obesity, insulin resistance, type 2 diabetes, hypertension, pregnancy complications, memory disorders, osteoporosis, autoimmune diseases, certain cancers, and systemic inflammatory diseases. Vitamin D adequacy leads to less oxidative stress and improves mitochondrial and endocrine functions, reducing the risks of disorders, such as autoimmunity, infections, metabolic derangements, and impairment of DNA repair; all of this aids a healthy, graceful aging process. Vitamin D is also a potent anti-oxidant that facilitates balanced mitochondrial activities, preventing oxidative stress-related protein oxidation, lipid peroxidation, and DNA damage. New understandings of vitamin D-related advances in metabolomics, transcriptomics, epigenetics, in relation to its ability to control oxidative stress in conjunction with micronutrients, vitamins, and antioxidants, following normalization of serum 25(OH)D and tissue 1,25(OH)<sub>2</sub>D concentrations, likely to promise cost-effective better clinical outcomes in humans.https://www.mdpi.com/2079-7737/8/2/3025(OH)D1,25(OH)<sub>2</sub>Dagingcytokinesinflammationmorbidity and mortalitypreventionreactive oxygen speciesultraviolet |
| spellingShingle | Sunil J. Wimalawansa Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging Biology 25(OH)D 1,25(OH)<sub>2</sub>D aging cytokines inflammation morbidity and mortality prevention reactive oxygen species ultraviolet |
| title | Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging |
| title_full | Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging |
| title_fullStr | Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging |
| title_full_unstemmed | Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging |
| title_short | Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging |
| title_sort | vitamin d deficiency effects on oxidative stress epigenetics gene regulation and aging |
| topic | 25(OH)D 1,25(OH)<sub>2</sub>D aging cytokines inflammation morbidity and mortality prevention reactive oxygen species ultraviolet |
| url | https://www.mdpi.com/2079-7737/8/2/30 |
| work_keys_str_mv | AT suniljwimalawansa vitaminddeficiencyeffectsonoxidativestressepigeneticsgeneregulationandaging |