title: Taurine supplementation reduces oxidative stress and improves cardiovascular function in an iron-overload murine model.
abstract: BACKGROUND
  Iron overload has an increasing worldwide prevalence and is associated with significant cardiovascular morbidity and mortality. Elevated iron levels in the myocardium lead to impaired systolic and diastolic function and elevated oxidative stress. Taurine accounts for 25% to 50% of the amino acid pool in myocardium, possesses antioxidant properties, and can inhibit L-type Ca2+ channels. Thus, we hypothesized that this agent would reduce the cardiovascular effects of iron overload.
  
  
  RESULTS
  Iron-overloaded mice were generated by intraperitoneal injection of iron either chronically (5 days per week for 13 weeks) or subacutely (5 days per week for 4 weeks). Iron overload causes increased mortality, elevated oxidative stress, systolic and diastolic dysfunction, hypotension, and bradycardia. Taurine supplementation increased myocardial taurine levels by 45% and led to reductions in mortality and improved cardiac function, heart rate, and blood pressure in iron-overloaded mice. Histological examination of the myocardium revealed reduced apoptosis and interstitial fibrosis in iron-overloaded mice supplemented with taurine. Taurine mediated reduced oxidative stress in iron-overloaded mice along with attenuation of myocardial lipid peroxidation and protection of reduced glutathione level.
  
  
  CONCLUSIONS
  These results demonstrate that treatment with taurine reduces iron-mediated myocardial oxidative stress, preserves cardiovascular function, and improves survival in iron-overloaded mice. The role of taurine in protecting reduced glutathione levels provides an important mechanism by which oxidative stress-induced myocardial damage can be curtailed. Taurine, as a dietary supplement, represents a potential new therapeutic agent to reduce the cardiovascular burden from iron-overload conditions.
authors.affiliation: Department of Physiology, Toronto General Hospital, University Health Network, Heart and Stroke/Richard Lewar Centre of Excellence, University of Toronto, Toronto, Ontario, Canada.
authors.forename: Gavin Y
authors.initials: GY
authors.lastname: Oudit
authors.forename: Maria G
authors.initials: MG
authors.lastname: Trivieri
authors.forename: Neelam
authors.initials: N
authors.lastname: Khaper
authors.forename: Taneya
authors.initials: T
authors.lastname: Husain
authors.forename: Greg J
authors.initials: GJ
authors.lastname: Wilson
authors.forename: Peter
authors.initials: P
authors.lastname: Liu
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Sole
authors.forename: Peter H
authors.initials: PH
authors.lastname: Backx
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D019587:Dietary Supplements; D005978:Glutathione / Q000378:metabolism; D006331:Heart Diseases / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D006439:Hemodynamics / Q000187:drug effects; D006486:Hemosiderosis / Q000150:complications* / Q000378:metabolism; D008297:Male; D051379:Mice; D009206:Myocardium / Q000473:pathology / Q000648:ultrastructure; D018384:Oxidative Stress / Q000187:drug effects*; D013654:Taurine / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D013654:Taurine; D005978:Glutathione