通过³²P后标记法测定迷走神经切断术后胃内的DNA损伤。
DNA damage in the stomach after vagotomy measured by 32P-postlabelling.
作者信息
Dyke G W, Craven J L, Hall R, Garner R C
机构信息
Jack Birch Unit for Environmental Carcinogenesis, Department of Biology, University of York.
出版信息
Gut. 1993 Dec;34(12):1683-7. doi: 10.1136/gut.34.12.1683.
This study analysed gastric mucosal DNA by 32P-postlabelling in a series of patients who have had previous vagotomy for benign peptic ulcer disease. DNA adduct levels were found to be significantly higher in patients who had had previous truncal vagotomy than in those who had had previous highly selective vagotomy (p < 0.001). Intragastric bile concentrations were also considerably higher in patients after truncal vagotomy but there was no correlation between intragastric bile concentrations and DNA adduct levels. These results suggest that, although duodenogastric reflux may be a cause of gastric mucosal DNA damage in the stomach after vagotomy, measurement of total intragastric bile does not accurately reflect genotoxic insult.
本研究通过³²P后标记法分析了一系列曾因良性消化性溃疡疾病接受迷走神经切断术的患者的胃黏膜DNA。结果发现，既往接受过全胃迷走神经切断术的患者的DNA加合物水平显著高于既往接受过高选择性迷走神经切断术的患者（p<0.001）。全胃迷走神经切断术后患者的胃内胆汁浓度也明显更高，但胃内胆汁浓度与DNA加合物水平之间无相关性。这些结果表明，虽然十二指肠-胃反流可能是迷走神经切断术后胃黏膜DNA损伤的一个原因，但胃内总胆汁的测量并不能准确反映基因毒性损伤。
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