The protection of long chain polyunsaturated fatty acids by melatonin during nonenzymatic lipid peroxidation of rat liver microsomes

2002 ◽  
Vol 32 (3) ◽  
pp. 129-134 ◽  
Author(s):  
P. Leaden ◽  
J. Barrionuevo ◽  
A. Catalá
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Rat Liver ◽  
Liver Microsomes ◽  
Rat Liver Microsomes ◽  
Long Chain

scholarly journals Effects of CoA and acyl-CoA on Ca2+-permeability of endoplasmic-reticulum membranes from rat liver

1995 ◽  
Vol 306 (3) ◽  
pp. 703-708 ◽  
Author(s):  
G T Rich ◽  
J G Comerford ◽  
S Graham ◽  
A P Dawson
Keyword(s):  
Fatty Acids ◽  
Membrane Fusion ◽  
Rat Liver ◽  
Liver Microsomes ◽  
Rat Liver Microsomes ◽  
Short Term ◽  
Esterified Fatty Acids ◽  
Chain Acyl ◽  
Microsomal Membranes ◽  
Long Chain

We have studied the effects of CoA and palmitoyl-CoA on Ca2+ movements and GTP-dependent vesicle fusion in rat liver microsomes. (1) Inhibition of membrane fusion by CoA depends on esterification of CoA to long-chain acyl-CoA using endogenous non-esterified fatty acids. (2) Binding of long-chain acyl-CoA to microsomal membranes is inhibited by BSA, which also relieves inhibition of membrane fusion. (3) Under conditions where acyl-CoA binding is inhibited, CoA causes increased Ca2+ accumulation, apparently by decreasing the Ca2+ leak rate. (4) Conversely, palmitoyl-CoA, in the presence of BSA, causes Ca2+ efflux. (5) The decrease in Ca(2+)-permeability caused by CoA does not depend on the presence of ATP or GTP, and is irreversible in the short term. (6) Using 14C-labelled CoA we show that CoA derivatives can be formed from endogenous components of microsomal membranes in the absence of ATP. (7) The results are interpreted in terms of a Ca(2+)-permeability which is controlled by CoA and/or long-chain acyl-CoA esters.

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