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Protective effects of endomorphins, endogenous opioid peptides in the brain, on human low density lipoprotein oxidation
Author(s) -
Lin Xin,
Xue LiYing,
Wang Rui,
Zhao QianYu,
Chen Qiang
Publication year - 2006
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2006.05150.x
Subject(s) - chemistry , oxidative stress , tbars , lipid peroxidation , oxidative phosphorylation , low density lipoprotein , antioxidant , biochemistry , pharmacology , cholesterol , medicine
Neurodegenerative disorders are associated with oxidative stress. Low density lipoprotein (LDL) exists in the brain and is especially sensitive to oxidative damage. Oxidative modification of LDL has been implicated in the pathogenesis of neurodegenerative diseases. Therefore, protecting LDL from oxidation may be essential in the brain. The antioxidative effects of endomorphin 1 (EM1) and endomorphin 2 (EM2), endogenous opioid peptides in the brain, on LDL oxidation has been investigated in vitro . The peroxidation was initiated by either copper ions or a water‐soluble initiator 2,2′‐azobis(2‐amidinopropane hydrochloride) (AAPH). Oxidation of the LDL lipid moiety was monitored by measuring conjugated dienes, thiobarbituric acid reactive substances, and the relative electrophoretic mobility. Low density lipoprotein oxidative modifications were assessed by evaluating apoB carbonylation and fragmentation. Endomorphins markedly and in a concentration‐dependent manner inhibited Cu 2+ and AAPH induced the oxidation of LDL, due to the free radical scavenging effects of endomorphins. In all assay systems, EM1 was more potent than EM2 and l ‐glutathione, a major intracellular water‐soluble antioxidant. We propose that endomorphins provide protection against free radical‐induced neurodegenerative disorders.