Table 3: Examples from the literature of vitamins’ effects in cell culture and on genomic stability.

MicronutrientMain effects on cell viability and genomic stabilityCell typeAdditional information regarding the form and concentration of the micronutrient evaluatedStatus in relation to physiological concentrationReferences

Vitamin AEnhanced the levels of 8-oxo-dG DNA damage but significantly inhibited M1dG formation especially after induction of M1dG by H2O2 or B[a]P; increased production of reactive oxygen species and formation of promutagenic DNA lesionsLung epithelial cellsBeta-carotene (5  mol/L)Similar[159, 160]
Caused oxidation of dG and cytotoxicity, giving rise to an almost complete cell deathLeukemia cells (HL-60)Retinol (2  mol/L) and ascorbic acid (50  mol/L)Similar[161]
Induced apoptosis by increasing apoptotic protein p53 and decreasing antiapoptotic Bcl-2 as well as nuclear ATM; also induced DNA fragmentationGastric cancer cells (AGS)Beta-carotene (100  mol/L)Higher[162]
DNA damage on HepG2 which was also concordant to increased apoptosis and necrosis of cells Hepatocarcinoma cells (HepG2)Beta-carotene (4  mol/L) and 8  mol/L)Similar [163, 164]
Reduced levels of total DNA adducts and increased apoptosis levels in cells coexposed to benzo(a)pyrene and retinoic acidRetinoic acid (1  mol/L)Lower

Vitamin B7 (biotin)Increased strand breaks and cellular response to strand breaks T-lymphocyte cell line (Jurkat) mol/L and
0.01  mol/L
Lower and higher[75]
Affects biotinylation of proteins, gene expression, and metabolism of interleukin-2; rates of proliferation and apoptosis were not affected by biotin status mol/L, mol/L and 0.01  mol/LLower and higher[165]

Vitamin B9Increased levels of excision repair and apoptosisLymphocytesFolate ( mol/L)Lower[166, 167]
Decreased apoptosis and increased cell proliferationNeural stem cells (NSCs)Folic acid ( mol/L)Higher[168, 169]
High concentration accelerated growth; increased metabolic activity, proliferation, and apoptosis; decreased differentiationHuman colon cancer cells (HT29)Folic acid (0.021  mol/L and 0.21  mol/L) with other micronutrients involved in folate-methionine cycleSimilar and higher[56]

Vitamin B12Reduced cell proliferation and increased differentiationNeuroblastoma cells (NIE115)Vitamin B12 (total absence)Lower[89]
Chronic exposure inhibited neurotoxicityRetina cells (primary cultures from fetal rats)Methylcobalamin (1  mol/L)Higher[170]
Absence is likely to result both in reduced cell proliferation and in cell death, as inhibition of DNA synthesis generally results in apoptosis Human erythroleukemic (K562) and murine lymphoma (BW5147) cell linesCobalamin (total absence and
mol/L)
Lower and higher[171]

Physiological concentrations of AA were not toxic, while high concentrations of AA induced DNA strand breakage in a dose-dependent manner, whereas AA2P were not genotoxicHuman dermal fibroblasts (HDFs)Ascorbic acid (AA) and ascorbic acid 2-Phosphate (AA2P) (total absence or 20, 100, and 500  mol/L)Lower, similar, and higher[172]
Vitamin CEnhanced DNA-protein crosslinks and cytotoxicityChinese hamster cells (V79)Ascorbic acid (1000  mol/L)Higher[173]
Decreased number of 8-hydroxydeoxyguanosine adductsMouse keratinocyte cell lineAscorbic acid (2,27  mol/L and 4,54  mol/L)Lower[174]
Protective effect against DNA damage induced by X-ray treatmentHuman lymphoblastoid cells (Raji)Ascorbic acid (60  mol/L)Similar[175]

Protective effect against DNA damage induced by H2O2 treatmentRaji cells -Tocopherol (30  mol/L)Similar[175]
Vitamin EReduced DNA fragmentation and apoptotic body formation, possibly favoring DNA repairAfrican green monkey kidney (Vero), human colon carcinoma (Caco-2), and dysplastic oral keratinocyte (DOK) cellsVitamin E (25  mol/L)Similar[176]
Reduced apoptosis and autophagyCultured trophoblasts and villous explants obtained from human placentas at termVitamin E (50  mol/L) with vitamin C (50  mol/L)Higher[177]