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Cited by 134Vitamin D Research StudiesParathyroid Disorders and TreatmentsBone Metabolism and Diseases

Vitamin D and genomic stability

Chatterjee, Malay·2001·Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
DOI 10.1016/s0027-5107(01)00080-x
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Abstract

1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] has been shown to act on novel target tissues not related to calcium homeostasis. There have been reports characterizing 1,25(OH)(2)D(3) receptors and activities in diverse tissues such as brain, pancreas, pituitary, skin, muscle, placenta, immune cells and parathyroid. The receptor hormone complex becomes localized in the nucleus, and undergoes phosphorylation by reacting with a kinase. This form of the receptor then interacts with the Vitamin D responsive element of target gene and modifies the transcription of those genes to develop the action. The modulation of gene transcription results in either the induction or repression of specific messenger RNAs (m-RNAs), ultimately resulting in changes in protein expression needed to produce biological responses. Genes for carbonic anhydrase that are expressed at high levels in osteoclast are known to be involved in bone resorption and Id genes role in osteoblast-osteoclast differentiation reflects the genomic effect of Vitamin D on bones. Genomic action of Vitamin D also explains the biosynthesis of oncogenes, polyamines, lymphokines and calcium binding proteins. However, there is a possibility that some of the actions of 1,25(OH)(2)D(3) may be mediated by non-genomic mechanisms and may not require the binding to Vitamin D receptor (VDR). Vitamin D offers a protection from genotoxic effects of Vitamin D deficiency by increasing the insulin receptor gene expression and BSP (bone sialoprotein), bone-remodeling by decreasing the osteopontin (OPN) m-RNAs, maintaining the normal epidermal structure and enamel matrix. Gonadal insufficiency in Vitamin D deficiency was corrected by vitamin mediated direct regulation of the expression of aramotase gene. The supportive role of Vitamin D in placental function is also evident by its influence on human placental lactogen (hpl) gene transcription accompanied by increase hpl m-RNA levels. Further role of Vitamin D is envisaged in identifying cyclin C as an important target for Vitamin D in cell-cycle regulation. Vitamin D at physiological concentration has been found to protect cell proteins and membranes against oxidative stress by inhibiting the peroxidative attack on membrane lipids. Vitamin D, at a concentration range of 2x10(-8)-5x10(-8)M, induces apoptosis in most cancer cells, stabilizes chromosomal structure and prevents DNA double-strand breaks induced either by endogenous or exogenous factors. Vitamin D is also effective in stimulating DNA synthesis in adult alveolar II cells and provides a novel mechanism of modulation of epithelial cell proliferation in the context of lung development and repair against injury. The regulation of various proto-oncogenes (c-myc, c-fos, c-jun), differentiation inducing properties, antiproliferative effects on keratinocytes and inhibitory effects in several human malignancy ranks Vitamin D as a novel hormone that may have physiological and clinical implication in the carcinogenic process.

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  • Treatment with vitamin D stabilizes chromosomal structure and prevents double strand breaks.

    “Treatment with vitamin D has been shown to decrease 8—hydroxy–2—deoxyguanosin, a marker of endogenous oxidative damage to DNA [150], increase Bax, a protein coding gene involved in apoptosis [150], regulates poly-ADP-ribose polymerase activity in the DNA damage response pathway [151], stabilize chromosomal structure and prevent double strand breaks [152].”

    From Vitamin D and Autism Spectrum Disorder: A Literature Review (2016) · cites this paper as [152]

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Authors
Chatterjee, M.
Affiliations
Jadavpur University (IN)
Corresponding author
Chatterjee, Malay
Venue
Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Publisher
Elsevier BV
Published
2001-04
Volume
475
Issue
1-2
Pages
69-88
ISSN
  • 0027-5107 (ISSN-L)
  • 1386-1964
DOI
10.1016/s0027-5107(01)00080-x
OpenAlex
W2124931509
Cited by
134
References
117
Citations by year
2026: 2 · 2025: 1 · 2023: 3 · 2022: 3 · 2021: 4 · 2020: 3 · 2019: 4 · 2018: 7 · 2017: 3 · 2016: 7 · 2015: 5 · 2014: 7 · 2013: 7 · 2012: 6
FWCI
1.06
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Mutation research. Fundamental and molecular mechanisms of mutagenesis (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Vitamin D Research Studies
  • Health Sciences › Medicine › Nephrology › Parathyroid Disorders and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
Keywords
vitamin D, 1,25-dihydroxyvitamin D3, vitamin D receptor, gene transcription, osteoclasts, bone remodeling, insulin receptor, bone sialoprotein, osteopontin, placental lactogen, cyclin C, cell cycle regulation, oxidative stress, apoptosis, DNA double-strand breaks, chromosome stability, genotoxicity, vitamin D deficiency
MeSH terms
Animals, DNA, DNA Damage, Gene Expression Regulation, Humans, Vitamin D, Vitamin D Deficiency

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