N-acetyldopamine inhibits rat brain lipid peroxidation induced by lipopolysaccharide.
The effects of N-acetyldopamine, a sepiapterin reductase inhibitor, on lipopolysaccharide-induced lipid peroxidation were examined in rat brain homogenates in vitro. Lipid peroxidation in the form of malondialdehyde (MDA) was evaluated by the measurement of thiobarbituric acid (TBA) reactive substances. N-Acetyldopamine inhibited the formation of MDA in a concentration-dependent manner. The effect was similar to that of N-acetylserotonin, but stronger than that of the endogenous antioxidant agent, melatonin. Possible clinical applications of N-acetyldopamine and its derivatives are discussed.
Oxenkrug
Gregory F
GF
Melatonin Clinic and Pineal Research Laboratory, Department of Psychiatry, Caritas St. Elizabeth's Medical Center/Tufts University School of Medicine, Boston, Massachusetts 02135, USA. goxenkrug@tufts-nemc.org
Requintina
Pura J
PJ
D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects*; D004298:Dopamine / Q000031:analogs & derivatives* / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D016166:Free Radical Scavengers / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008550:Melatonin / Q000494:pharmacology; D009419:Nerve Tissue Proteins / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D011916:Rats, Inbred F344; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D016166:Free Radical Scavengers; D008070:Lipopolysaccharides; D009419:Nerve Tissue Proteins; D017392:Thiobarbituric Acid Reactive Substances; C006374:N-acetyldopamine; D008550:Melatonin; D004298:Dopamine