Get access

Melatonin reduces protein and lipid oxidative damage induced by homocysteine in rat brain homogenates

Authors

  • Santiago Ortega-Gutiérrez,

    1. Department of Pharmacology and Physiology, University of Zaragoza, Zaragoza, Spain
    2. Department of Neurology and Internal Medicine, Medical College of Wisconsin and Zablocki Veterans Affairs Medical Center, WI
    Search for more papers by this author
  • Lorena Fuentes-Broto,

    1. Department of Pharmacology and Physiology, University of Zaragoza, Zaragoza, Spain
    Search for more papers by this author
  • Joaquín J. García,

    Corresponding author
    1. Department of Pharmacology and Physiology, University of Zaragoza, Zaragoza, Spain
    2. Department of Cellular and Structural Biology, University of Texas, Health Science Center at San Antonio, TX
    • Department of Pharmacology and Physiology, University of Zaragoza, Domingo Miral s/n 50009, Zaragoza, Spain.
    Search for more papers by this author
  • Marta López-Vicente,

    1. Department of Pharmacology and Physiology, University of Zaragoza, Zaragoza, Spain
    2. Department of Neurology and Internal Medicine, Medical College of Wisconsin and Zablocki Veterans Affairs Medical Center, WI
    Search for more papers by this author
  • Enrique Martínez-Ballarín,

    1. Department of Pharmacology and Physiology, University of Zaragoza, Zaragoza, Spain
    Search for more papers by this author
  • Francisco Javier Miana-Mena,

    1. Department of Pharmacology and Physiology, University of Zaragoza, Zaragoza, Spain
    Search for more papers by this author
  • Sergio Millán-Plano,

    1. Department of Pharmacology and Physiology, University of Zaragoza, Zaragoza, Spain
    Search for more papers by this author
  • Russel J. Reiter

    1. Department of Cellular and Structural Biology, University of Texas, Health Science Center at San Antonio, TX
    Search for more papers by this author

Abstract

Numerous data indicate that hyperhomocysteinemia is a risk factor for cardio- and cerebrovascular diseases. At least in part, homocysteine (HCY) impairs cerebrovascular function because it generates large numbers of free radicals. Since melatonin is a well-known antioxidant, which reduces oxidative stress and decreases HCY concentrations in plasma, the aim of this study was to investigate the effect of melatonin in preventing HCY-induced protein and lipid oxidation in rat brain homogenates. Brain homogenates were obtained from Sprague–Dawley rats and were incubated with or without HCY (0.01–5 mM) or melatonin (0.01–3 mM). Carbonyl content of proteins, and malondialdehyde (MDA) and 4-hydroxyalkenals (4-HDA) concentrations in the brain homogenates were used as an index of protein and lipid oxidation, respectively. Under the experimental conditions used, the addition of HCY (0.01–5 mM) to the homogenates enhanced carbonyl protein and MDA+4-HDA formation. Melatonin reduced, in a concentration-dependent manner, protein and lipid oxidation due to HCY in the brain homogenates. These data suggest that preserving proteins from oxidative insults is an additional mechanism by which melatonin may act as an agent in potentially decreasing cardiovascular and cerebrovascular diseases related to hyperhomocysteinemia. J. Cell. Biochem. 102: 729–735, 2007. © 2007 Wiley-Liss, Inc.

Get access to the full text of this article

Ancillary