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Indian J Biochem Biophys ; 2014 Dec ; 51 (6): 552-558
Article in English | IMSEAR | ID: sea-156536

ABSTRACT

Ultraviolet C (UVC) irradiation (λ: 200-280 nm) causes release of several secretory cytokines responsible for inflammation. Our objective was to investigate whether inflammatory response was also induced in bystander cells. For this purpose, the conditioned medium containing the released factors from UVC irradiated A375 cells was used in this study to evaluate the expression of inflammatory markers, such as tumour necrosis factor alpha (TNFα), nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) and p38 mitogen-activated protein kinase (p38 MAPK) in its bystander cells. Inflammatory responses in bystander cells subjected to further irradiation by UVC or other damaging agent like H2O2 were also examined. It was observed that TNFα, NFκB and p38 MAPK were not induced in UVC-bystander cells, but their expression was suppressed in the UVC-bystander cells treated with UVC or H2O2. This lowering in inflammatory response might be due to smaller depletion in the reduced glutathione (GSH) content present in these treated bystander cells. The study indicated that UVC-induced bystander effect was an intrinsic protective response in cells, capable of suppressing inflammation induced in cells on exposure to damaging agents.


Subject(s)
Bystander Effect/drug effects , Bystander Effect/immunology , Bystander Effect/radiation effects , Cell Line, Tumor , Cytokines/immunology , Humans , Hydrogen Peroxide/pharmacology , Inflammation/immunology , /immunology , Radiation Dosage , Ultraviolet Rays
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