Abstract
Oxidative damage is implicated in several pathologies including cardiovascular disease. As a model system to study the response of cells to oxidative insults, homocysteine toxicity was examined since it is an independent risk factor for atherosclerotic disease. The levels of malondialdehyde and 4-hydroxyalkenals were assayed as an index of oxidatively damaged lipid. In in vitro experiments, the increase of lipid peroxidation products induced by homocysteine were concentration- and time-dependent. To study the protective effect of melatonin on homocystine induced lipid peroxidation, brain homogenates were treated with different concentrations of melatonin. The accumulation of malondialdehyde and 4-hydroxyalkenals induced by homocysteine was significantly reduced by melatonin in a concentration-dependent manner. Additionally, a melatonin concentration of 1.5 mM reduced the levels of oxidatively damaged lipid products below those measured in control homogenates (no homocysteine, no melatonin). These data suggest that melatonin, an endogenous antioxidant may have a role in protecting cells from oxidative damage due to homocysteine and they support the idea that pharmacological concentrations could be used as a therapeutic agent in reducing cardiovascular disease where homocysteine may be a causative or contributing agent.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 32-37 |
| Number of pages | 6 |
| Journal | Pharmacology and Toxicology |
| Volume | 90 |
| Issue number | 1 |
| DOIs | |
| State | Published - 2002 |
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ASJC Scopus subject areas
- Pharmacology
- Toxicology
- Health, Toxicology and Mutagenesis
Cite this
Inhibitory effect of melatonin on homocysteine-induced lipid peroxidation in rat brain homogenates. / Osuna, Carmen; Reiter, Russel J; García, Joaquin J.; Karbownik, Malgorzata; Tan, Dun Xian; Calvo, Juan R.; Manchester, Lucien C.
In: Pharmacology and Toxicology, Vol. 90, No. 1, 2002, p. 32-37.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Inhibitory effect of melatonin on homocysteine-induced lipid peroxidation in rat brain homogenates
AU - Osuna, Carmen
AU - Reiter, Russel J
AU - García, Joaquin J.
AU - Karbownik, Malgorzata
AU - Tan, Dun Xian
AU - Calvo, Juan R.
AU - Manchester, Lucien C.
PY - 2002
Y1 - 2002
N2 - Oxidative damage is implicated in several pathologies including cardiovascular disease. As a model system to study the response of cells to oxidative insults, homocysteine toxicity was examined since it is an independent risk factor for atherosclerotic disease. The levels of malondialdehyde and 4-hydroxyalkenals were assayed as an index of oxidatively damaged lipid. In in vitro experiments, the increase of lipid peroxidation products induced by homocysteine were concentration- and time-dependent. To study the protective effect of melatonin on homocystine induced lipid peroxidation, brain homogenates were treated with different concentrations of melatonin. The accumulation of malondialdehyde and 4-hydroxyalkenals induced by homocysteine was significantly reduced by melatonin in a concentration-dependent manner. Additionally, a melatonin concentration of 1.5 mM reduced the levels of oxidatively damaged lipid products below those measured in control homogenates (no homocysteine, no melatonin). These data suggest that melatonin, an endogenous antioxidant may have a role in protecting cells from oxidative damage due to homocysteine and they support the idea that pharmacological concentrations could be used as a therapeutic agent in reducing cardiovascular disease where homocysteine may be a causative or contributing agent.
AB - Oxidative damage is implicated in several pathologies including cardiovascular disease. As a model system to study the response of cells to oxidative insults, homocysteine toxicity was examined since it is an independent risk factor for atherosclerotic disease. The levels of malondialdehyde and 4-hydroxyalkenals were assayed as an index of oxidatively damaged lipid. In in vitro experiments, the increase of lipid peroxidation products induced by homocysteine were concentration- and time-dependent. To study the protective effect of melatonin on homocystine induced lipid peroxidation, brain homogenates were treated with different concentrations of melatonin. The accumulation of malondialdehyde and 4-hydroxyalkenals induced by homocysteine was significantly reduced by melatonin in a concentration-dependent manner. Additionally, a melatonin concentration of 1.5 mM reduced the levels of oxidatively damaged lipid products below those measured in control homogenates (no homocysteine, no melatonin). These data suggest that melatonin, an endogenous antioxidant may have a role in protecting cells from oxidative damage due to homocysteine and they support the idea that pharmacological concentrations could be used as a therapeutic agent in reducing cardiovascular disease where homocysteine may be a causative or contributing agent.
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UR - http://www.scopus.com/inward/citedby.url?scp=0036178331&partnerID=8YFLogxK
U2 - 10.1034/j.1600-0773.2002.900107.x
DO - 10.1034/j.1600-0773.2002.900107.x
M3 - Article
VL - 90
SP - 32
EP - 37
JO - Basic and Clinical Pharmacology and Toxicology
JF - Basic and Clinical Pharmacology and Toxicology
SN - 1742-7835
IS - 1
ER -