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- Title
Long chain fatty acyl-CoA modulation of H<sub>2</sub>O<sub>2</sub> release at mitochondrial complex I.
- Authors
Silvia Bortolami; Evelin Comelato; Franco Zoccarato; Adolfo Alexandre; Lucia Cavallini
- Abstract
Abstract  Complex I is responsible for most of the mitochondrial H2O2 release, low during the oxidation of the NAD linked substrates and high during succinate oxidation, via reverse electron flow. This H2O2 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, 406:125â129, 2007). Long chain fatty acyl-CoAs, but not fatty acids, act as strong inhibitors of succinate dependent H2O2 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 ÎpH or Îp 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.
- Subjects
VITAMIN B complex; CARNITINE; FATTY acids; OXIDATION; FATTY-acyl-CoA
- Publication
Journal of Bioenergetics & Biomembranes, 2008, Vol 40, Issue 1, p9
- ISSN
0145-479X
- Publication type
Article
- DOI
10.1007/s10863-008-9126-1