Research paperAlterations of nitric oxide synthase and xanthine oxidase activities of human keratinocytes by ultraviolet B radiation: Potential role for peroxynitrite in skin inflammation☆
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2024, Spectrochimica Acta - Part A: Molecular and Biomolecular SpectroscopySkin photo-protection with phytochemicals against photo-oxidative stress, photo-carcinogenesis, signal transduction pathways and extracellular matrix remodeling—An overview
2020, Ageing Research ReviewsCitation Excerpt :These on further react with proteins, DNA, RNA, and lipids, incurring oxidative damages to these macromolecules (Perluigi et al., 2010). Moreover, UVB induces the release of nitric oxide (NO˙), peroxynitrite (ONOO), nitric oxide synthase (NOS), xanthine oxidase (XO) and constitutive nitric oxide synthase (cNOS), exerting cytotoxic effects on keratinocytes (de Jager et al., 2017; Deliconstantinos et al., 1996; Wu et al., 2010). The absorption of high-energy UVB radiation by nucleic acid leads to DNA mutations preferably at cytosines containing dipyrimidine sequences (Pfeifer et al., 2005).
Vitamin E therapy beyond cancer: Tocopherol versus tocotrienol
2016, Pharmacology and TherapeuticsThe cross-talk between electrophiles, antioxidant defence and the endocannabinoid system in fibroblasts and keratinocytes after UVA and UVB irradiation
2016, Journal of Dermatological SciencePathophysiology of circulating xanthine oxidoreductase: New emerging roles for a multi-tasking enzyme
2014, Biochimica et Biophysica Acta - Molecular Basis of DiseaseCitation Excerpt :Such a transition can be shown by an elevated XO/XDH activity ratio and has been the object of numerous studies in the last forty years. The increase of ROS-producing enzyme forms has been reported in burn injury [121]; haematoporphyrin derivative-mediated cutaneous photosensitisation [122]; in vivo and in vitro ethanol intoxication [119,123,124]; glutathione depletion [125]; endothelial stimulation with C5a, TNF, a chemotactic N-formyl peptide [126] or activated neutrophils [127,128]; kainic acid [60] or glutamate neurotoxicity [129]; ricin hepatotoxicity [130]; in a rat model of nephropathy [131]; ultraviolet B radiation [132]; irradiation with gamma rays [133]; hepatocellular injury induced by iron accumulation [134] or cholestasis [135]; in gut mucosal lining of experimental cirrhotic rats [136]; and in rat brain following in vivo acute ammonia intoxication [137]. Additionally, reversible or irreversible XDH/XO conversion was observed in a variety of hypoxic/ischaemic conditions in rat tissues, including the liver, kidney, heart, and lung [138], liver and kidney [139], intestine [140], liver [141], and brain [106,142–144].
Inhibition of UVB-induced skin phototoxicity by a grape seed extract as modulator of nitrosative stress, ERK/NF-kB signaling pathway and apoptosis, in SKH-1 mice
2013, Food and Chemical ToxicologyCitation Excerpt :The main enzyme involved in the generation of large amounts of NO following UVB exposure, is iNOS (Lee et al., 2000). Data in literature, concerning the role of NO in apoptosis process, are rather contradictory and generally assert that NO has a dualistic role, protecting either the keratinocytes against apoptosis (Deliconstantinos et al., 1996; Weller et al., 2003) or inducing cellular toxicity by proteins nitration with further alteration of their functions (Poderoso et al., 1996). Therefore, inhibition of NO production by iNOS expression or blockage of its activity may be a useful tool in the neutralization of NO-related undesired conditions.
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This work was supported by grants from the Ministry of Research and Technology (92 SYN 17) and from the University of Athens.