Protective effect of nitric oxide against oxidative stress under ultraviolet-B radiation

Nitric Oxide ◽  
2005 ◽  
Vol 13 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Suyun Shi ◽  
Gang Wang ◽  
Yading Wang ◽  
Lingang Zhang ◽  
Lixin Zhang
1996 ◽  
Vol 271 (45) ◽  
pp. 28052-28056 ◽  
Author(s):  
Christine Roméro-Graillet ◽  
Edith Aberdam ◽  
Naïma Biagoli ◽  
William Massabni ◽  
Jean-Paul Ortonne ◽  
...  

Forests ◽  
2016 ◽  
Vol 7 (12) ◽  
pp. 251 ◽  
Author(s):  
Haiqing Hu ◽  
Zhenbao Zhou ◽  
Xiaoxin Sun ◽  
Zhonghua Zhang ◽  
Qinghuan Meng

Nitric Oxide ◽  
2008 ◽  
Vol 19 ◽  
pp. 56
Author(s):  
Harminder Pal Singh ◽  
Shalinder Kaur ◽  
Daizy Rani Batish ◽  
Ravinder K Kohli

2003 ◽  
Vol 284 (5) ◽  
pp. C1140-C1148 ◽  
Author(s):  
Richard Weller ◽  
Ann Schwentker ◽  
Timothy R. Billiar ◽  
Yoram Vodovotz

Nitric oxide (NO) can either prevent or promote apoptosis, depending on cell type. In the present study, we tested the hypothesis that NO suppresses ultraviolet B radiation (UVB)-induced keratinocyte apoptosis both in vitro and in vivo. Irradiation with UVB or addition of the NO synthase (NOS) inhibitor N G-nitro-l-arginine methyl ester (l-NAME) increased apoptosis in the human keratinocyte cell line CCD 1106 KERTr, and apoptosis was greater when the two agents were given in combination. Addition of the chemical NO donor S-nitroso- N-acetyl-penicillamine (SNAP) immediately after UVB completely abrogated the rise in apoptosis induced by l-NAME. An adenoviral vector expressing human inducible NOS (AdiNOS) also reduced keratinocyte death after UVB. Caspase-3 activity, an indicator of apoptosis, doubled in keratinocytes incubated with l-NAME compared with the inactive isomer, d-NAME, and was reduced by SNAP. Apoptosis was also increased on addition of 1,H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylate cyclase. Mice null for endothelial NOS (eNOS) exhibited significantly higher apoptosis than wild-type mice both in the dermis and epidermis, whereas mice null for inducible NOS (iNOS) exhibited more apoptosis than wild-type mice only in the dermis. These results demonstrate an antiapoptotic role for NO in keratinocytes, mediated by cGMP, and indicate an antiapoptotic role for both eNOS and iNOS in skin damage induced by UVB.


2014 ◽  
Vol 90 (10) ◽  
pp. 928-935 ◽  
Author(s):  
Mei Jing Piao ◽  
Mee Jung Ahn ◽  
Kyoung Ah Kang ◽  
Ki Cheon Kim ◽  
Jian Zheng ◽  
...  

2012 ◽  
Vol 55 (2) ◽  
pp. 149-158 ◽  
Author(s):  
Mei Jing Piao ◽  
Hee Kyoung Kang ◽  
Eun Sook Yoo ◽  
Young Sang Koh ◽  
Dong Sam Kim ◽  
...  

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