title: Oxy free radical system in heart failure and therapeutic role of oral vitamin E.
abstract: Twenty patients of heart failure and ten matched healthy controls were included in the trial. Out of these 20 patients of heart failure, 12 patients were also studied prospectively. Plasma levels of superoxide anion and malonyldialdehyde were increased while the levels of superoxide dismutase, catalase and glutathione reductase were decreased in patients of heart failure as compared to control subjects. The alteration in oxidative stress and antioxidant system did not correlate with the age and sex of patients or the etiology of heart failure. With the increasing severity of heart failure the malonyldialdehyde and superoxide anion increased significantly and catalase, glutathione reductase and superoxide dismutase levels decreased. The group of heart failure patients with ejection fraction < 40% (n = 7) exhibited significantly higher levels of malonyldialdehyde than those with an ejection fraction > 40% (n = 13). The superoxide anion and malonyldialdehyde levels were significantly higher in patients of heart failure in the pre-treatment state as compared to those in post-treatment state. Conversely catalase, glutathione reductase and superoxide dismutase were higher in the post-treatment period as compared to their values before treatment. The addition of vitamin E in doses of 400 mg once a day orally for 4 weeks significantly reduced the malonyldialdehyde and superoxide anion levels and produced an elevation of the antioxidant enzymes. Thus, there is an apparent normalisation of the indices of oxidative stress following treatment of heart failure and a markedly improved response on vitamin E supplementation which may be more beneficial.
authors.affiliation: Division of Clinical and Experimental Medicine, Central Drug Research Institute, Lucknow, India.
authors.forename: A
authors.initials: A
authors.lastname: Ghatak
authors.forename: M J
authors.initials: MJ
authors.lastname: Brar
authors.forename: A
authors.initials: A
authors.lastname: Agarwal
authors.forename: N
authors.initials: N
authors.lastname: Goel
authors.forename: A K
authors.initials: AK
authors.lastname: Rastogi
authors.forename: A K
authors.initials: AK
authors.lastname: Vaish
authors.forename: A R
authors.initials: AR
authors.lastname: Sircar
authors.forename: M
authors.initials: M
authors.lastname: Chandra
mesh_terms: D000284:Administration, Oral; D000328:Adult; D002374:Catalase / Q000032:analysis / Q000378:metabolism*; D004311:Double-Blind Method; D005260:Female; D005980:Glutathione Reductase / Q000032:analysis / Q000378:metabolism*; D006333:Heart Failure / Q000175:diagnosis / Q000188:drug therapy* / Q000201:enzymology*; D006801:Humans; D008297:Male; D008315:Malondialdehyde / Q000032:analysis / Q000378:metabolism*; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D011446:Prospective Studies; D013482:Superoxide Dismutase / Q000032:analysis / Q000378:metabolism*; D013481:Superoxides / Q000032:analysis / Q000378:metabolism*; D016896:Treatment Outcome; D014810:Vitamin E / Q000008:administration & dosage / Q000627:therapeutic use*
chemical_list: D013481:Superoxides; D014810:Vitamin E; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase