Radiation and DNA Methylation Mechanisms

Budak, Metin

doi:10.5772/intechopen.92189

Cited by 3 publications

(3 citation statements)

References 63 publications

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“…These molecules contain reactive oxygen species (ROS) and reactive nitrogen types (RNSs) such as hydrogen peroxide (H 2 O 2 ) and nitric oxide (NO). Low concentrations of these molecules are used for adaptive intracellular signaling, and high concentrations are used for defense mechanisms against microorganisms [23,24]. But, physiological concentrations of these molecules need to be precisely regulated, and Nrf2-Keap1 play important role in this signaling.…”

Section: Basal State Induction and Cellular Positionsmentioning

confidence: 99%

“…Different types of stressors react differently with the cysteine residues in Keap1, suggesting that the residues of cysteine in some way contribute to activity of Keap1 individually or in combination (23,24). This indicates that Nrf2-Keap1 mechanism is not a simple "on" or "off " button mechanism but can instead respond with different mechanisms by various stress factors [23,35].…”

Section: Keap1-nrf2-are Signalingmentioning

confidence: 99%

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Two Faces of Nrf2 in Cancer

Yıldız¹,

Segmen²

2022

Molecular Mechanisms in Cancer

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Nuclear factor erythroid 2–related factor 2 (Nrf2) serves as a “main regulator” in response to internal or external cell stressors through coordinated induction of a wide range of cytoprotective genes. In cancer cells, Nrf2 increases expression of cytoprotective genes and, as a result, promotes proliferation through inhibition of apoptosis and metabolic reprogramming. Therefore, the activation of Nrf2 is an important regulator for prevention of cancer triggered by stresses and toxins. Defense system is activated by cellular pathways to ensure that response to stresses and toxins is sufficient for needs of the body. Nrf2 is a regulator of genes mediated by antioxidant response elements. Nrf2 is a pleiotropic gene that represents highly researched strategy in cancers. During recent decades, emerging evidence shows that Nrf2 is generally activated in many types of cancer by many mechanisms. Nrf2 has been showed to contribute to chemoresistance of cancer cells, as well as carcinogenesis due to inflammation, in recent studies. This review provides an overview of current mechanisms of regulation of Nrf2 in normal cells and its dual effects in cancer. This chapter aims to rationalize these double roles by criticizing dependence of Nrf2 functions and methods behind these contradictory data.

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Section: Basal State Induction and Cellular Positionsmentioning

confidence: 99%

Section: Keap1-nrf2-are Signalingmentioning

confidence: 99%

Two Faces of Nrf2 in Cancer

Yıldız¹,

Segmen²

2022

Molecular Mechanisms in Cancer

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“…ROS accumulation, by increasing the irradiation dose during RT, affects the redox potential of cells and leads to a series of membrane peroxidations and other chain reactions that finally causes non-reversed damage [21,22]. For higher RT-dose administration, DNA in vitro and in vivo studies have shown that phosphorylation and methylations are some of the early irradiation effects among intermediate products [2,[23][24][25][26][27].…”

Section: Introductionmentioning

confidence: 99%

The Effect of Irradiation on the Skin upon Breast Cancer Radiotherapy Studied by FTIR Spectroscopy

Markouizou¹,

Michali²,

Mamareli³

et al. 2022

OBM Geriatr

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Breast cancer affects the female population worldwide. Radiotherapy (RT) is part of the therapeutic modality in the management of breast cancer, after radical mastectomy or conserving surgery. The FTIR spectroscopic “marker bands” will lead us to approach the mechanism of skin damage due to the interaction of ionizing radiation and skin, on a molecular level at the very early stages. FT-IR spectroscopy, breast digital pictures, and ImageJ software were used in the study. Healthy breast skin was irradiated ex-vivo with a 4 Gy dose of a γ-60Co course Gammachamber 4000A. The FT-IR spectra showed that the low-dose irradiation induces skin dehydration, collagen secondary structure changes and advanced glycation end products (AGEs) as a result of free radicals as mediated products. The infrared “marker bands” at about 1743, 1160, and 870 cm-1 are characteristic, indicating the development of inflammation, glycations, and peroxidations respectively, due to ionizing radiation-induced oxidative stress. ImageJ analysis provided the sharp surface of the skin after RT irradiation in contrast to the smooth surface of the non-irradiated healthy skin. The most important damages, induced by radiotherapy, were connective tissue lesions, glycosylation, and phosphorylation processes in the skin. The reactive oxygen species (ROS) free radicals prefer to abstract H atoms from lipids, sugar rings of glycoproteins, and base ribose of DNA. The produced intermediate free radicals, as a result of ROS reactions, led to the formation of AGEs and peroxides.

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