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The DNA of a cell is vulnerable to the damaging effect of oxidative free radicals produced as byproducts of cellular metabolism. DNA damage occurring in oocytes, if not repaired, can be lethal and result in reduced fecundity and loss of potential progeny.
The response of oocytes to DNA double-strand break damage involves a pathway hierarchy in which ATR kinase signals to CHEK2 which then activates p53 and p63 proteins. [ 15 ] In the fruit fly Drosophila , irradiation of germ line cells generates double-strand breaks that result in cell cycle arrest and apoptosis .
Oxidative stress mechanisms in tissue injury. Free radical toxicity induced by xenobiotics and the subsequent detoxification by cellular enzymes (termination).. Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. [1]
XthA (exonuclease III, a DNA repair enzyme) and KatE (catalase) are known to play important roles in the defense against oxidative stress but KatF regulon genes are not induced by oxidative stress. [2] There is an overlap between oxidative stress response and other regulatory networks like heat shock response, SOS response.
The integrated stress response can be triggered within a cell due to either extrinsic or intrinsic conditions. Extrinsic factors include hypoxia, amino acid deprivation, glucose deprivation, viral infection and presence of oxidants. The main intrinsic factor is endoplasmic reticulum stress due to the accumulation of unfolded proteins.
Cellular stress response is the wide range of molecular changes that cells undergo in response to environmental stressors, including extremes of temperature, exposure to toxins, and mechanical damage. Cellular stress responses can also be caused by some viral infections. [1]
These reactive chemical species can reach DNA by diffusion and the bimolecular reaction damages the DNA (oxidative stress). Unlike direct DNA damage which causes sunburn, indirect DNA damage does not result in any warning signal or pain in the human body. The bimolecular reactions that cause the indirect DNA damage are illustrated in the figure:
The SOS response was articulated by Evelyn Witkin. [3] [4] Later, by characterizing the phenotypes of mutagenised E. coli, she and post doctoral student Miroslav Radman detailed the SOS response to UV radiation in bacteria. [3] [5] The SOS response to DNA damage was a seminal discovery because it was the first coordinated stress response to be ...