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Oxidative Stress and DNA Damage in Obesity-Related Tumorigenesis

Part of the Advances in Experimental Medicine and Biology book series (AEMB,volume 824)

Abstract

Reactive oxygen species induce oxidative modification of critical macromolecules. Oxygen derived free radicals may act as potential cytotoxic intermediates inducing inflammatory and degenerative processes, or as signal messengers for the regulation of gene expression. This dual effect mainly depends on the availability of free radicals in terms of concentration, as well as on the environmental characteristics in which they are produced. The formation of free radicals has been proposed to be the linking factor between certain metabolic disturbances and cancer. Circulating mononuclear cells of patients with high cholesterol levels, insulin resistance, metabolic syndrome or obesity present lower levels of antioxidant enzymes and increased concentrations of oxidative stress by-products such as isoprostanes or the DNA oxidized and highly mutagenic base 8-oxo-7,8-dihydro-2′-deoxyguanosine. Overweight or obese subjects also exhibit hormonal changes as a consequence of the increase of mass fat, and these hormonal alterations have been implicated in the alteration of different signal transduction mechanisms and in cell growth and differentiation. A significant correlation has been found between body mass index and cancer. The biological factors and molecular mechanisms implicated in obesity associated cancer susceptibility will be reviewed.

Keywords

  • Cancer
  • DNA damage
  • Free radicals
  • Obesity

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Fig. 2.1

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Acknowledgements

GTS thanks grants from Conselleria de Sanitat de la Generalitat de València and Instituto de Salud Carlos III: ACOM/2012/238; PI10/00802; PI13/01848; CIBEROBN 12/03/30016

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Cerdá, C. et al. (2014). Oxidative Stress and DNA Damage in Obesity-Related Tumorigenesis. In: Camps, J. (eds) Oxidative Stress and Inflammation in Non-communicable Diseases - Molecular Mechanisms and Perspectives in Therapeutics. Advances in Experimental Medicine and Biology, vol 824. Springer, Cham. https://doi.org/10.1007/978-3-319-07320-0_2

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