AI Article Synopsis
- Hyperhomocysteinemia is linked to increased risk of heart and brain diseases due to its ability to generate free radicals that harm blood vessel function.
- This study examines how melatonin, known for its antioxidant properties, can help prevent the oxidative damage caused by homocysteine in rat brain tissues.
- Results showed that while homocysteine increased protein and lipid oxidation, melatonin effectively reduced this damage, suggesting it may help lower risks associated with hyperhomocysteinemia.
Article 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.
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| http://dx.doi.org/10.1002/jcb.21327 | DOI Listing |
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