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

Marañón G, Manley W, Cayado P, García C, de la Muela MS, Vara E - BMC Vet. Res. (2009)

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Horsepital SL, Villanueva del Pardillo, Madrid, Spain. gonzamara@yahoo.es

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.

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Related in: MedlinePlus

Nitric oxide (NO) and carbon monoxide (CO) level in jejunum homogenates.
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Related In: Results  -  Collection

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Figure 5: Nitric oxide (NO) and carbon monoxide (CO) level in jejunum homogenates.

Mentions: The NO and CO content (released by) in mitochondria gave higher values in the proximal portion as compared with the distal group (Fig. 5). No differences were observed between distal portion and healthy horses.


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

Marañón G, Manley W, Cayado P, García C, de la Muela MS, Vara E - BMC Vet. Res. (2009)

Nitric oxide (NO) and carbon monoxide (CO) level in jejunum homogenates.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2664797&req=5

Figure 5: Nitric oxide (NO) and carbon monoxide (CO) level in jejunum homogenates.
Mentions: The NO and CO content (released by) in mitochondria gave higher values in the proximal portion as compared with the distal group (Fig. 5). No differences were observed between distal portion and healthy horses.

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Horsepital SL, Villanueva del Pardillo, Madrid, Spain. gonzamara@yahoo.es

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.

Show MeSH
Related in: MedlinePlus