title: Attenuation of intestinal ischemia/reperfusion injury with sodium nitroprusside: studies on mitochondrial function and lipid changes.
abstract: Reactive oxygen species have been implicated in cellular injury during ischemia/reperfusion (I/R). Mitochondria are one of the main targets of oxygen free radicals and damage to this organelle leads to cell death. Reports suggest that nitric oxide (NO) may offer protection from damage during I/R. This study has looked at the functional changes and lipid alteration to mitochondria during intestinal I/R and the protection offered by NO. It was observed that I/R of the intestine is associated with functional alterations in the mitochondria as suggested by MTT reduction, respiratory control ratio and mitochondrial swelling. Mitochondrial lipid changes suggestive of activation of phospholipase A(2) and phospholipase D were also seen after (I/R) mediated injury. These changes were prevented by the simultaneous presence of a NO donor in the lumen of the intestine. These studies have suggested that structural and functional alterations of mitochondria are prominent features of I/R injury to the intestine which can be ameliorated by NO.
authors.affiliation: The Wellcome Trust Research Laboratory, Department of Gastrointestinal Sciences, Christian Medical College and Hospital, Vellore, India.
authors.forename: M
authors.initials: M
authors.lastname: Madesh
authors.forename: A
authors.initials: A
authors.lastname: Ramachandran
authors.forename: A
authors.initials: A
authors.lastname: Pulimood
authors.forename: M
authors.initials: M
authors.lastname: Vadranam
authors.forename: K A
authors.initials: KA
authors.lastname: Balasubramanian
mesh_terms: D000818:Animals; D048429:Cell Size; D002784:Cholesterol / Q000378:metabolism; D003250:Constriction; D004734:Energy Metabolism; D004789:Enzyme Activation; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D007421:Intestine, Small / Q000098:blood supply* / Q000648:ultrastructure; D007511:Ischemia / Q000150:complications / Q000188:drug therapy*; D050356:Lipid Metabolism; D008563:Membrane Lipids / Q000378:metabolism; D017538:Mesenteric Artery, Superior; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D020030:Nitric Oxide Donors / Q000627:therapeutic use*; D009599:Nitroprusside / Q000627:therapeutic use*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D010739:Phospholipase D / Q000378:metabolism; D010741:Phospholipases A / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species; D015427:Reperfusion Injury / Q000209:etiology / Q000517:prevention & control*; D014280:Triglycerides / Q000378:metabolism
chemical_list: D005230:Fatty Acids, Nonesterified; D008563:Membrane Lipids; D020030:Nitric Oxide Donors; D010743:Phospholipids; D017382:Reactive Oxygen Species; D014280:Triglycerides; D009599:Nitroprusside; D002784:Cholesterol; D010741:Phospholipases A; D010739:Phospholipase D