scholarly journals Endomorphins, endogenous opioid peptides, provide antioxidant defense in the brain against free radical-induced damage

Author(s):  
Xin Lin ◽  
Ding-Jian Yang ◽  
Wen-Qing Cai ◽  
Qian-Yu Zhao ◽  
Yan-Feng Gao ◽  
...  
1977 ◽  
Vol 130 (3) ◽  
pp. 298-304 ◽  
Author(s):  
Hans W. Kosterlitz ◽  
John Hughes

SummaryThe reasons which led to the search in the brain for substances with morphine-like actions are discussed. Two pentapeptides, methionine-enkephalin and leucine-enkephalin, were isolated. The amino acid sequence of methionine-enkephalin occurs also in the pituitary prohormone β-lipotropin, of which longer fragments (endorphins) of up to 31 amino acids exhibit strong morphine-like action.The physiological significance of these short and long opioid peptides is discussed, particularly with regard to their possible roles as neurotransmitter or neuromodulator.With regard to the mechanisms involved in the development of tolerance to and dependence on opiates, the importance of interaction between the endogenous opioid peptides and the exogenous opiate alkaloids is stressed.The possible therapeutic implications are discussed briefly.


1987 ◽  
Vol 72 (s16) ◽  
pp. 90P-91P
Author(s):  
J.R. Thornton ◽  
M.S. Losowsky

1999 ◽  
Vol 277 (6) ◽  
pp. H2442-H2450 ◽  
Author(s):  
Yasushi Takasaki ◽  
Roger A. Wolff ◽  
Grace L. Chien ◽  
Donna M. van Winkle

In rats and rabbits, endogenous opioid peptides participate in ischemic preconditioning. However, it is not known which endogenous opioid(s) can trigger cardioprotection. We examined preconditioning-induced and opioid-induced limitation of cell death in isolated, calcium-tolerant, adult rabbit cardiomyocytes. Cells were subjected to simulated ischemia by pelleting and normothermic hypoxic incubation. Preconditioning was elicited with 15 min of simulated ischemia followed by 15 min of resuspension and reoxygenation. All cells underwent 180 min of simulated ischemia. Cell death was assessed by trypan blue permeability. Morphine protected cells, as did preconditioning; naloxone blocked the preconditioning-induced protection. Exogenous Met5-enkephalin (ME) induced protection, but exogenous β-endorphin did not. ME-induced protection was blocked by the δ-selective antagonist naltrindole. Additionally, two other proenkephalin products, Leu5-enkephalin and Met5-enkephalin-Arg-Phe, provided protection equipotent to ME. These data suggest that one or more proenkephalin products interact with δ-opioid receptors to endogenously trigger opioid-mediated protection.


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