A role for Pms2 in the prevention of tandem CC → TT substitutions induced by ultraviolet radiation and oxidative stress

DNA Repair ◽  
2005 ◽  
Vol 4 (1) ◽  
pp. 51-57 ◽  
Author(s):  
Chi Y. Shin-Darlak ◽  
Amy M. Skinner ◽  
Mitchell S. Turker
2018 ◽  
Vol 3 (3) ◽  
pp. 839-845
Author(s):  
BAKI Oladimeji Ibraheem ◽  
OYEDUN Ifeoluwa Oluwagbenga ◽  
OWOLABI Olamide Tawa ◽  
OGUNSHOLA Olawale Jacob ◽  
ADISA Babatunde Ibrahim

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Uraiwan Panich ◽  
Gunya Sittithumcharee ◽  
Natwarath Rathviboon ◽  
Siwanon Jirawatnotai

Skin is the largest human organ. Skin continually reconstructs itself to ensure its viability, integrity, and ability to provide protection for the body. Some areas of skin are continuously exposed to a variety of environmental stressors that can inflict direct and indirect damage to skin cell DNA. Skin homeostasis is maintained by mesenchymal stem cells in inner layer dermis and epidermal stem cells (ESCs) in the outer layer epidermis. Reduction of skin stem cell number and function has been linked to impaired skin homeostasis (e.g., skin premature aging and skin cancers). Skin stem cells, with self-renewal capability and multipotency, are frequently affected by environment. Ultraviolet radiation (UVR), a major cause of stem cell DNA damage, can contribute to depletion of stem cells (ESCs and mesenchymal stem cells) and damage of stem cell niche, eventually leading to photoinduced skin aging. In this review, we discuss the role of UV-induced DNA damage and oxidative stress in the skin stem cell aging in order to gain insights into the pathogenesis and develop a way to reduce photoaging of skin cells.


1995 ◽  
Vol 122 (1) ◽  
pp. 41-51 ◽  
Author(s):  
J. M. Shick ◽  
M. P. Lesser ◽  
W. C. Dunlap ◽  
W. R. Stochaj ◽  
B. E. Chalker ◽  
...  

Author(s):  
Hasan Haci Yeter ◽  
Berfu Korucu ◽  
Elif Burcu Bali ◽  
Ulver Derici

Abstract. Background: The pathophysiological basis of chronic kidney disease and its complications, including cardiovascular disease, are associated with chronic inflammation and oxidative stress. We investigated the effects of active vitamin D (calcitriol) and synthetic vitamin D analog (paricalcitol) on oxidative stress in hemodialysis patients. Methods: This cross-sectional study was composed of 83 patients with a minimum hemodialysis vintage of one year. Patients with a history of any infection, malignancy, and chronic inflammatory disease were excluded. Oxidative markers (total oxidant and antioxidant status) and inflammation markers (C-reactive protein and interleukin-6) were analyzed. Results: A total of 47% (39/83) patients were using active or analog vitamin D. Total antioxidant status was significantly higher in patients with using active or analog vitamin D than those who did not use (p = 0.006). Whereas, total oxidant status and oxidative stress index were significantly higher in patients with not using vitamin D when compared with the patients who were using vitamin D preparation (p = 0.005 and p = 0.004, respectively). On the other hand, total antioxidant status, total oxidant status, and oxidative stress index were similar between patients who used active vitamin D or vitamin D analog (p = 0.6; p = 0.4 and p = 0.7, respectively). Conclusion: The use of active or selective vitamin D analog in these patients decreases total oxidant status and increases total antioxidant status. Also, paricalcitol is as effective as calcitriol in decreasing total oxidant status and increasing total antioxidant status in patients with chronic kidney disease.


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