Long chain fatty acyl-CoA modulation of H2O2 release at mitochondrial complex I

Complex I is responsible for most of the mitochondrial H 2 O 2 release, low during the oxidation of the NAD linked substrates and high during succinate oxidation, via reverse electron flow. This H 2 O 2 production appear physiological since it occurs at submillimolar concentrations of succinate also...

Full description

Saved in:
Bibliographic Details
Published in:Journal of bioenergetics and biomembranes 2008-02, Vol.40 (1), p.9-18
Main Authors: Bortolami, Silvia, Comelato, Evelin, Zoccarato, Franco, Alexandre, Adolfo, Cavallini, Lucia
Format: Article
Language:English
Subjects:
Animal Anatomy
Animal Biochemistry
Biochemistry
Bioenergetics
Bioorganic Chemistry
Chemistry
Chemistry and Materials Science
Fatty acids
Histology
Hydrogen peroxide
Membranes
Mitochondria
Morphology
Organic Chemistry
Oxidation
Substrates
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Complex I is responsible for most of the mitochondrial H 2 O 2 release, low during the oxidation of the NAD linked substrates and high during succinate oxidation, via reverse electron flow. This H 2 O 2 production appear physiological since it occurs at submillimolar concentrations of succinate also in the presence of NAD substrates in heart (present work) and rat brain mitochondria (Zoccarato et al., Biochem J , 406:125–129, 2007). Long chain fatty acyl-CoAs, but not fatty acids, act as strong inhibitors of succinate dependent H 2 O 2 release. The inhibitory effect of acyl-CoAs is independent of their oxidation, being relieved by carnitine and unaffected or potentiated by malonyl-CoA. The inhibition appears to depend on the unbound form since the acyl-CoA effect decreases at BSA concentrations higher than 2 mg/ml; it is not dependent on ΔpH or Δ p and could depend on the inhibition of reverse electron transfer at complex I, since palmitoyl-CoA inhibits the succinate dependent NAD(P) or acetoacetate reduction.
ISSN:0145-479X
1573-6881
DOI:10.1007/s10863-008-9126-1