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鼠伤寒沙门氏菌感染期间肠道黏膜抗氧化防御系统的损伤

Impairment of intestinal mucosal antioxidant defense system during Salmonella typhimurium infection.

作者信息

Mehta A, Singh S, Ganguly N K

机构信息

Department of Pediatrics, Postgraduate Institute of Medical Education & Research, Chandigarh, India.

出版信息

Dig Dis Sci. 1998 Mar;43(3):646-51. doi: 10.1023/a:1018887813713.

Abstract

The mucosal pathology of Salmonella typhimurium infection may in part be due to the excessive production of reactive oxygen species (ROS). The influence of S. typhimurium infection on the intestinal mucosal antioxidant defense system was investigated. We injected ligated rat ileal loops with Salmonella live culture or toxin. After 18 hr of infection, the animals were killed and enterocytes isolated from the ileal loops. The enterocyte-reduced glutathione (GSH) content and activities of the enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase, glutathione-S-transferase (GST), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PDH) were spectrophotometrically estimated. The vitamin E and A contents were determined by high-performance liquid chromatography (HPLC). In both the Salmonella live culture and toxin-treated groups, the enterocyte GSH and vitamin E contents and activities of the enzymes SOD, GSH-Px, catalase, GR, and G6PDH were significantly decreased as compared to the control group. However there was a significant increase in the enterocyte activity of GST. There was no change in the vitamin A content of the enterocytes. These findings might indicate a decreased endogenous intestinal protection against ROS in S. typhimurium-mediated infection, which could contribute to the pathogenesis of the disease.

摘要

鼠伤寒沙门氏菌感染的黏膜病理可能部分归因于活性氧(ROS)的过量产生。研究了鼠伤寒沙门氏菌感染对肠道黏膜抗氧化防御系统的影响。我们向结扎的大鼠回肠肠袢注射沙门氏菌活菌培养物或毒素。感染18小时后,处死动物并从回肠肠袢分离肠上皮细胞。用分光光度法测定肠上皮细胞还原型谷胱甘肽(GSH)含量以及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶、谷胱甘肽-S-转移酶(GST)、谷胱甘肽还原酶(GR)和葡萄糖-6-磷酸脱氢酶(G6PDH)的活性。通过高效液相色谱法(HPLC)测定维生素E和A的含量。与对照组相比,在沙门氏菌活菌培养组和毒素处理组中,肠上皮细胞GSH和维生素E含量以及SOD、GSH-Px、过氧化氢酶、GR和G6PDH的活性均显著降低。然而,肠上皮细胞GST活性显著增加。肠上皮细胞的维生素A含量没有变化。这些发现可能表明在鼠伤寒沙门氏菌介导的感染中,肠道内源性对ROS的保护作用降低,这可能有助于该疾病的发病机制。

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