PARP and Oxidative Stress

ROS and nitric oxide that are produced by activated macrophages are involved in DNA damage leading to PARP activation [66] , In addition, PARP would regulate inflammation by expression-inducible nitric oxide synthase (iNOS) [ 66]. X-ray repair cross-complementing 1 (XRCC1), which is a DNA repair protein, is recruited by PARP1 to damaged sites following DNA damage caused by ROS [95]. Besides the effect of OS on DNA damage, it can also impair histones. Ullrich et al. explained that the 20s proteosome which is involved in degrading oxidized damaged histones can be activated by PARP. When ROS exceeds the level of the repair capacity, cleaved PARP1 is catalyzed by caspase 3 activation and initiates apoptosis [96].

Shiraishi et al. demonstrated that elevated scrotal temperature is associated with OS, impaired spermatogenesis, and apoptosis of germ cells in human testis with varicocele [97] .

El-Domyati et al. showed higher level of caspase 3 and cleaved PARP1 in varicocele patients compared to fertile group expressed [ 51[ , In another research by Chang et al., it has been shown that expression of active PARP was more in varico-cele patient than in normal fertile donors [ 49] . Tekcan et al. showed that after varicocele induction in rat testis, PAR and PARP1 and 4-HNE expressions in germ cells increased and explained that increased level of oxidative stress and PARP overexpression caused testicular dysfunction, which is associated with varicocele [98],

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