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

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.

Effects of antenatal, postpartum and post-weaning melatonin supplementation on blood pressure and renal antioxidant enzyme activities in spontaneously hypertensive rats

“…It has been reported that oral melatonin given to SHR, aged 23-25 weeks for 6 weeks, attenuated the raised blood pressure and also lowered the levels of renal TBARS compared to the untreated SHR controls [30]. Melatonin supplementation has been found to reduce the levels of markers of lipid peroxidation in subjects exposed to oxidative stress [12,13,36] but not in normal control rats [12]. The reason for the difference in the results of this study and the others is not clearly apparent.…”

Melatonin and Structurally-Related Compounds Protect Synaptosomal Membranes from Free Radical Damage

“…In the brain, melatonin prevented lipid peroxidation under various experimental conditions. Thus, this indoleamine reversed the prooxidant effects caused by the excitatory amino acid glutamate [50], kainic, quinolenic, and okadaic acids [51–53], Alzheimer amyloid peptide [54], 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine [55], homocysteine [56], and bacterial lipopolysaccharide [57]. Melatonin also reduced the severity of ischemia-reperfusion injury in brain [58].…”

Protective Effect of Melatonin Against Mitomycin C‐Induced Genotoxic Damage in Peripheral Blood of Rats

“…Melatonin, an indoleamine, directly scavenges hydroxyl radicals, singlet oxygen, and peroxynitrites [19, 55–57], increases the concentration of endogenous glutathione, and stimulates the antioxidative enzymes superoxide dismutase and glutathione peroxidase [58]. Moreover, melatonin has been shown to prevent iron-induced lipid peroxidation [59]. Thus melatonin may also prevent carcinogenesis [60].…”