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首页> 外文期刊>Биофизика >Activation of poly(ADP-ribose) polymerase inhibited the apoptosis of rat thymocytes induced by short-wavelength ultraviolet irradiation
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Activation of poly(ADP-ribose) polymerase inhibited the apoptosis of rat thymocytes induced by short-wavelength ultraviolet irradiation

机译:聚(ADP-核糖)聚合酶的活化抑制短波紫外线照射诱导的大鼠胸腺细胞凋亡

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摘要

The effect of (i) aphidicolin, a specific inhibitor of #delta#-and #epsilon#-polymerase, and nucleotide excision repair; (ii) 3-aminobenzamide, an inhibitor of poly(ADP-ribose) polymerase and base excision repair; and (iii) actinomycin D and cycloheximide, inhibitors of protein and RNA synthesis, respectively, on the induction of suppression of apoptosis of rat thymocytes by different doses of short-wavelength ultraviolet radiation was studied by flow cytometry. 3-Aminobenzamide suppressed the inhibition of apoptosis induced by the doses of short-wavelength ultraviolet radiation higher than 20 J/m~2, increasing the cell death to a maximum. Thus, the inhibition of apoptosis by high short-wavelength ultraviolet radiation doses depends on the status of poly(ADP-ribose) polymerase and is prevented by 3-aminobenzamide. As opposed to 3-aminobenzamide, aphidicolin did not affect the cell heath at short-wavelength radiation doses higher than 10 J/m~2 but induced the apoptosis of unirradiated cells and cells irradited with short-wavelength ultraviolet radiation doses lower than 10 J/m~2. The inhibitors of protein and RNA synthesis cycloheximide and actinomycin D prevented the induction of apoptosis caused by low and medium doses but did not not abolish the apoptosis-inhibiting activity of high doses of short-wavelength ultraviolet radiation.
机译:(i)aphidicolin,一种#delta#和#epsilon#聚合酶的特异性抑制剂,以及核苷酸切除修复的作用; (ii)3-氨基苯甲酰胺,聚(ADP-核糖)聚合酶的抑制剂和碱基切除修复; (iii)通过流式细胞术研究了放线菌素D和环己酰亚胺,分别是蛋白质和RNA合成的抑制剂,通过不同剂量的短波长紫外线辐射诱导大鼠胸腺细胞凋亡的抑制。 3-氨基苯甲酰胺抑制了高于20 J / m〜2的短波长紫外线辐射对细胞凋亡的抑制作用,使细胞死亡达到最大。因此,高剂量的短波紫外线辐射对细胞凋亡的抑制作用取决于聚(ADP-核糖)聚合酶的状态,并被3-氨基苯甲酰胺所阻止。与3-氨基苯甲酰胺相反,蚜虫灵在短波辐射剂量高于10 J / m〜2时不影响细胞健康,但会诱导未照射的细胞和短波紫外线辐射剂量低于10 J / m的细胞凋亡。 m〜2蛋白质和RNA合成的抑制剂环己酰亚胺和放线菌素D阻止了低剂量和中等剂量引起的细胞凋亡的诱导,但并未消除大剂量短波紫外线辐射的细胞凋亡抑制活性。

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