title: Antioxidant defenses in rat intestine and mesenteric lymph.
abstract: Dietary oxysterols can reach the circulation and this may contribute to atherosclerosis, where lipid oxidation is thought to be important. There is also evidence that, in rats, peroxidized lipids are absorbed and transported into lymph [Aw TY, Williams MW, Gray L. Absorption and lymphatic transport of peroxidized lipids by rat small intestine in vivo: role of mucosal GSH. Am J Physiol 1992; 262: G99-G106], although the method used to detect lipid peroxides lacked specificity. We tested whether intragastric administration of vegetable oils containing triglyceride hydroperoxides (TG-OOH) to rats resulted in detectable lipid hydroperoxides in mesenteric lymph. Using sensitive HPLC with postcolumn chemiluminescence detection, we were unable to detect hydroperoxides of triglycerides, cholesterylesters or phospholipids during the course of lipid absorption, and lymph levels of ascorbate, urate, alpha-tocopherol and ubiquinol-9 did not change significantly. By contrast, we observed a striking reducing activity judged by the efficient reduction of administered ubiquinones-9 and -10 to the corresponding ubiquinols. Exposure of rat lymph and isolated chylomicrons to aqueous peroxyl radicals revealed patterns of antioxidant consumption and lipid hydroperoxide formation similar to those described previously for human extravascular fluids and isolated lipoproteins, respectively. In particular, rates of TG-OOH formation in lymph and chylomicrons were very low to undetectable as long as ascorbate and/or ubiquinols were present, but subsequently proceeded in a chain reaction despite the presence of alpha-tocopherol. These studies demonstrate that rat intestine and mesenteric lymph possess efficient antioxidant defenses against preformed lipid hydroperoxides and (peroxyl) radical mediated lipid oxidation. We conclude that dietary lipid hydroperoxides or postprandial oxidation of lipids are not likely to contribute to these particular forms of oxidized lipids in circulation and aortic tissue.
authors.affiliation: Biochemistry Group, The Heart Research Institute, Camperdown, New South Wales, Australia.
authors.forename: D
authors.initials: D
authors.lastname: Mohr
authors.forename: Y
authors.initials: Y
authors.lastname: Umeda
authors.forename: T G
authors.initials: TG
authors.lastname: Redgrave
authors.forename: R
authors.initials: R
authors.lastname: Stocker
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000032:analysis* / Q000378:metabolism; D002914:Chylomicrons / Q000378:metabolism*; D003314:Corn Oil / Q000008:administration & dosage / Q000737:chemistry / Q000378:metabolism*; D004041:Dietary Fats / Q000032:analysis / Q000378:metabolism*; D006801:Humans; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000502:physiology*; D007421:Intestine, Small / Q000502:physiology*; D007700:Kinetics; D008043:Linseed Oil / Q000008:administration & dosage / Q000737:chemistry / Q000378:metabolism*; D008054:Lipid Peroxides / Q000378:metabolism*; D008196:Lymph / Q000502:physiology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D000975:Antioxidants; D002914:Chylomicrons; D004041:Dietary Fats; D008054:Lipid Peroxides; D008043:Linseed Oil; D003314:Corn Oil