According to a new Australian review, zinc plays a critical role in the regulation of DNA repair mechanisms, cell proliferation, differentiation and cell death.
The review focused on studies investigating the role of zinc in the maintenance of genome integrity and the effects of deficiency or excess on genomic stability events and cell death (1). The majority of studies suggest that zinc deficiency may influence DNA damage via two different mechanisms: by increasing oxidative stress resulting in increased DNA damage and/or by impairing DNA damage responses. Zinc seems to be an essential cofactor or structural component for important antioxidant defense proteins and DNA repair enzymes and may also affect activities of enzymes involved in methylation reactions.
The researchers commented that it would be important to determine dietary reference values for a micronutrient, such as zinc, based on DNA damage prevention. However, an optimal concentration range would differ depending on alterations in geno- and phenotype. As there is limited information on the relationship between zinc status and DNA damage/chromosomal instability, there would be an urgent need to conduct robust and reproducible intervention in vivo studies with well-validated biomarkers of DNA integrity.
The involvement of genomic stability in the development of cancer has been well-established. Cancer is recognized as a disease of altered gene expression caused by genome and epigenome alterations. Apart from the effect of environmental gene toxins, one of the key components in cancer initiation is a loss of genome stability due to nutritional imbalances and their interaction with certain genes. Recent research has focused on the involvement of micronutrients and their role in fundamental processes such as DNA synthesis, DNA methylation, DNA repair and cell death (2). It has been shown that dietary deficiencies in certain micronutrients, such as folate, and antioxidant vitamins, such as vitamin C or E, can result in DNA-strand breaks and DNA base lesions similar to those induced by carcinogenic doses of ionizing radiation (3).