title: [In vitro oxidation of low density lipoproteins in patients after ischemic stroke].
abstract: The aim of this work was the evaluation of low density lipoprotein (LDL) susceptibility to oxidation in the survivors of ischaemic stroke. The investigations were performed in 65 individuals at least three months after the onset of acute symptoms. In 24 patients stroke was caused by alterations in main cerebral arteries, in 19 by considerable narrowing of carotid artery, in 15 by alterations in small cerebral arteries with often accompanying hypertension and/or diabetes (lacunar stroke) and in 7 by embolism of cardiac origin in individuals with cardiac arrhythmia and coronary artery disease. The control group comprised 25 age matched persons without pathological symptoms. Plasma lipids and apolipoprotein B levels were determined as well as two antioxidants: alpha-tocopherol level and superoxide dismutase activity. The evaluation of lipid peroxidation was performed by determining thiobarbituric acid reacting substances (TBARS) and lipid peroxides (LPO) increase after 5 hours oxidation of isolated LDL in vitro in the presence of copper ions. The level of IgG directed against modified LDL was also evaluated. In the patients decreased HDL cholesterol level was observed as well as increased apolipoprotein B. In the group of thrombotic strokes high triglycerides were observed. alpha-tocopherol level was decreased in the group of cerebral strokes. The amounts of oxidation products did not differ between the whole group of patients after stroke and the controls. A significant increase concerned only the group of lacunar strokes. The evaluation of LDL susceptibility to oxidation in patients after stroke by measuring absorption at 234 nm and determining the time period necessary to the onset of intensive LDL oxidation will be the subject of a separate publication.
authors.forename: H
authors.initials: H
authors.lastname: Wehr
authors.forename: D
authors.initials: D
authors.lastname: Ryglewicz
authors.forename: M
authors.initials: M
authors.lastname: Rodo
authors.forename: M
authors.initials: M
authors.lastname: Poźniak
authors.forename: M
authors.initials: M
authors.lastname: Swiderska
authors.forename: B
authors.initials: B
authors.lastname: Panczenko
authors.forename: A
authors.initials: A
authors.lastname: Stajniak
mesh_terms: D000208:Acute Disease; D000368:Aged; D000975:Antioxidants / Q000378:metabolism; D001055:Apolipoproteins B / Q000097:blood; D002545:Brain Ischemia / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D002536:Cerebral Arteries / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications; D007074:Immunoglobulin G / Q000276:immunology; D066298:In Vitro Techniques; D015227:Lipid Peroxidation / Q000502:physiology; D008054:Lipid Peroxides / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood / Q000276:immunology / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D013482:Superoxide Dismutase / Q000378:metabolism; D014280:Triglycerides / Q000097:blood; D014810:Vitamin E / Q000097:blood
chemical_list: D000975:Antioxidants; D001055:Apolipoproteins B; D007074:Immunoglobulin G; D008054:Lipid Peroxides; D008077:Lipoproteins, LDL; D014280:Triglycerides; D014810:Vitamin E; D013482:Superoxide Dismutase