Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil; Embrapa Recursos Genéticos e Biotecnologia, Brasília, Distrito Federal, Brazil.
PLoS One. 2014 May 19;9(5):e97526. doi: 10.1371/journal.pone.0097526. eCollection 2014.
Trypanosoma cruzi, the causative agent of Chagas disease, is extremely resistant to ionizing radiation, enduring up to 1.5 kGy of gamma rays. Ionizing radiation can damage the DNA molecule both directly, resulting in double-strand breaks, and indirectly, as a consequence of reactive oxygen species production. After a dose of 500 Gy of gamma rays, the parasite genome is fragmented, but the chromosomal bands are restored within 48 hours. Under such conditions, cell growth arrests for up to 120 hours and the parasites resume normal growth after this period. To better understand the parasite response to ionizing radiation, we analyzed the proteome of irradiated (4, 24, and 96 hours after irradiation) and non-irradiated T. cruzi using two-dimensional differential gel electrophoresis followed by mass spectrometry for protein identification. A total of 543 spots were found to be differentially expressed, from which 215 were identified. These identified protein spots represent different isoforms of only 53 proteins. We observed a tendency for overexpression of proteins with molecular weights below predicted, indicating that these may be processed, yielding shorter polypeptides. The presence of shorter protein isoforms after irradiation suggests the occurrence of post-translational modifications and/or processing in response to gamma radiation stress. Our results also indicate that active translation is essential for the recovery of parasites from ionizing radiation damage. This study therefore reveals the peculiar response of T. cruzi to ionizing radiation, raising questions about how this organism can change its protein expression to survive such a harmful stress.
克氏锥虫,恰加斯病的病原体,对电离辐射具有极强的抗性,可耐受高达 1.5kGy 的伽马射线。电离辐射既能直接损伤 DNA 分子,导致双链断裂,也能间接地产生活性氧物种。在 500Gy 的伽马射线照射后,寄生虫的基因组发生碎片化,但染色体带在 48 小时内得以恢复。在这种情况下,细胞生长停滞长达 120 小时,寄生虫在这段时间后恢复正常生长。为了更好地了解寄生虫对电离辐射的反应,我们使用二维差异凝胶电泳结合质谱法对辐照(辐照后 4、24 和 96 小时)和非辐照的 T. cruzi 进行了蛋白质组分析。共发现 543 个点表达差异,其中 215 个被鉴定。这些鉴定的蛋白点仅代表 53 种蛋白质的不同同工型。我们观察到分子量低于预测值的蛋白质表达上调的趋势,表明这些蛋白质可能经过加工,产生较短的多肽。辐照后出现较短的蛋白质同工型表明发生了翻译后修饰和/或加工,以应对伽马辐射应激。我们的结果还表明,活跃的翻译对于寄生虫从电离辐射损伤中恢复是必不可少的。因此,本研究揭示了 T. cruzi 对电离辐射的特殊反应,提出了关于该生物体如何改变其蛋白质表达以存活于这种有害应激的问题。