Potenza Lucia, Calcabrini Cinzia, De Bellis Roberta, Guescini Michele, Mancini Umberto, Cucchiarini Luigi, Nappo Gennaro, Alloni Rossana, Coppola Roberto, Dugo Laura, Dacha Marina
Dipartimento di Scienze Biomolecolari, Universita degli Studi di Urbino, Carlo bo, Urbino.
Can J Gastroenterol. 2011 Aug;25(8):433-9. doi: 10.1155/2011/741073.
Anastomotic dehiscence is one of the most severe complications of colorectal surgery. Gaining insight into the molecular mechanisms responsible for the development of anastomotic dehiscence following colorectal surgery is important for the reduction of postoperative complications.
Based on the close relationship between surgical stress and oxidative stress, the present study aimed to determine whether a correlation exists between increased levels of reactive oxygen species and colorectal anastomotic dehiscence.
Patients who underwent surgical resection for colorectal cancer were divided into three groups: patients with anastomotic dehiscence (group 1); patients without dehiscence who underwent neoadjuvant radiochemotherapy (group 2); and patients without anastomotic dehiscence who did not undergo neoadjuvant radiochemotherapy (group 3). Quantitative polymerase chain reaction and real-time polymerase chain reaction assays were performed to measure nuclear DNA and mitochondrial DNA (mtDNA) content, and possible oxidative damage to nonmalignant colon and rectal tissues adjacent to the anastomoses.
mtDNA content was reduced in the colon tissue of patients in groups 1 and 2. Rectal mtDNA was found to be more damaged than colonic mtDNAs in all groups. The 4977 bp common deletion was observed in the mtDNA of tissues from both the colon and rectum of all patients.
Patients in groups 1 and 2 were more similar to one another than to group 3, probably due to higher levels of reactive oxygen species in the mitochondria; the greater damage found in the rectum suggests that dehiscence originates primarily from the rectal area.
The present study of mtDNA analyses of normal human colon and rectal tissues from patients with colorectal cancer is among the first of its kind.
吻合口漏是结直肠手术最严重的并发症之一。深入了解结直肠手术后吻合口漏发生发展的分子机制对于减少术后并发症至关重要。
基于手术应激与氧化应激之间的密切关系,本研究旨在确定活性氧水平升高与结直肠吻合口漏之间是否存在相关性。
接受结直肠癌手术切除的患者分为三组:吻合口漏患者(第1组);接受新辅助放化疗且无吻合口漏的患者(第2组);未接受新辅助放化疗且无吻合口漏的患者(第3组)。采用定量聚合酶链反应和实时聚合酶链反应测定法测量核DNA和线粒体DNA(mtDNA)含量,以及吻合口附近非恶性结肠和直肠组织可能存在的氧化损伤。
第1组和第2组患者的结肠组织中mtDNA含量降低。在所有组中,直肠mtDNA的损伤比结肠mtDNA更严重。在所有患者的结肠和直肠组织的mtDNA中均观察到4977 bp的常见缺失。
第1组和第2组患者彼此之间比与第3组患者更相似,这可能是由于线粒体中活性氧水平较高;直肠中发现的更大损伤表明吻合口漏主要起源于直肠区域。
本研究对结直肠癌患者正常人类结肠和直肠组织进行mtDNA分析,属同类研究中的首次尝试。