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谷胱甘肽代谢的改变可能与马缺血诱导的小肠细胞损伤有关。

Alterations in the glutathione metabolism could be implicated in the ischemia-induced small intestinal cell damage in horses.

作者信息

Marañón Gonzalo, Manley William, Cayado Patricia, García Cruz, de la Muela Mercedes Sánchez, Vara Elena

机构信息

Horsepital SL, Villanueva del Pardillo, Madrid, Spain.

出版信息

BMC Vet Res. 2009 Mar 18;5:10. doi: 10.1186/1746-6148-5-10.

Abstract

BACKGROUND

Colic could be accompanied by changes in the morphology and physiology of organs and tissues, such as the intestine. This process might be, at least in part, due to the accumulation of oxidative damage induced by reactive oxygen (ROS) and reactive nitrogen species (RNS), secondary to intestinal ischemia. Glutathione (GSH), being the major intracellular thiol, provides protection against oxidative injury. The aim of this study was to investigate whether ischemia-induced intestinal injury could be related with alterations in GSH metabolism.

RESULTS

Ischemia induced a significant increase in lipid hydroperoxides, nitric oxide and carbon monoxide, and a reduction in reduced glutathione, and adenosine triphosphate (ATP) content, as well as in methionine-adenosyl-transferase and methyl-transferase activities.

CONCLUSION

Our results suggest that ischemia induces harmful effects on equine small intestine, probably due to an increase in oxidative damage and proinflammatory molecules. This effect could be mediated, at least in part, by impairment in glutathione metabolism.

摘要

背景

绞痛可能伴有器官和组织(如肠道)形态和生理的变化。这一过程可能至少部分归因于肠道缺血继发的活性氧(ROS)和活性氮(RNS)诱导的氧化损伤积累。谷胱甘肽(GSH)作为主要的细胞内硫醇,可提供抗氧化损伤保护。本研究的目的是调查缺血诱导的肠道损伤是否与GSH代谢改变有关。

结果

缺血导致脂质氢过氧化物、一氧化氮和一氧化碳显著增加,还原型谷胱甘肽、三磷酸腺苷(ATP)含量以及甲硫氨酸-腺苷转移酶和甲基转移酶活性降低。

结论

我们的结果表明,缺血对马的小肠产生有害影响,可能是由于氧化损伤和促炎分子增加所致。这种影响可能至少部分由谷胱甘肽代谢受损介导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ab1/2664797/42b82c8b12bc/1746-6148-5-10-1.jpg

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