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Ultraviolet A(320-400 nm)modulation of ultraviolet B(290-320 nm)-induced immune suppression is mediated by carbon monoxide

机译:一氧化碳介导紫外线A(320-400 nm)对紫外线B(290-320 nm)诱导的免疫抑制的调节

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摘要

Accumulating evidence suggests that suberythemogenic UVA exposure protects against the immunosuppressive effect of UVB radiation or its epidermal photoproduct,ris-urocanic acid(cis-UCA).In skin,UVA photoimmunoprotection is mediated by the inducible antioxidant stress enzyme heme oxygenase-1(HO-1),which degrades heme into carbon monoxide(CO),iron,and biliverdin(reduced to bilirubin),and is important for cell survival under conditions of oxidative stress.The identity of the HO enzymatic product(s)that provide the immunoprotec-tion is unknown.
机译:越来越多的证据表明,暴露于红细胞的UVA可以抵抗UVB辐射或其表皮光产物ris-尿酸(cis-UCA)的免疫抑制作用。在皮肤中,UVA的光免疫保护作用是由诱导性抗氧化应激酶血红素加氧酶-1(HO- 1),它能将血红素降解为一氧化碳(CO),铁和胆绿素(还原为胆红素),对于氧化应激条件下的细胞存活很重要。提供酶促保护作用的HO酶产物的身份位置未知。

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