Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:1.3.5.1 (
succinate dehydrogenase
)
8,177
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Lipid peroxidation in brain mitochondria was induced by NADH in the presence of ADP and
FeCl3
. A novel quinone compound, idebenone, inhibited this peroxidation and the inhibition was markedly enhanced by succinate, a substrate of mitochondrial respiration. The concentration of succinate required to exert the maximal effect was 1.5 mM. The concentration of idebenone giving 50% inhibition (IC50) was 0.5 and 84 microM in the presence and absence of succinate, respectively, indicating that succinate enhances the inhibition by 170-fold. Moreover, the inhibitory effect of idebenone in the presence of succinate was abolished by adding thenoyltrifluoroacetate (TTFA), an inhibitor of
complex II
in the mitochondrial respiratory chain. These results indicate that idebenone is changed through
complex II
to its reduced form, which protects mitochondria against lipid peroxidation.
...
PMID:Inhibition of lipid peroxidation by idebenone in brain mitochondria in the presence of succinate. 276 44
The activity of
succinic dehydrogenase
, myosin ATPase, as well as lactic dehydrogenase (LDG) spectrum and cross-section area of different type of muscle fibers have been studied for 3 weeks after denervation (control) and after denervation and intraperitoneal injection of 10(-6) M
FeCl3
. Intraperitoneal injection of
FeCl3
prevented the development of denervation phenomena (increase in cross-section area of muscle fibers, changes in LDG spectrum).
...
PMID:[Effect of trivalent iron on denervated skeletal muscles]. 294 27
Lipid peroxidation in rat brain mitochondria was induced by NADH in the presence of ADP and
FeCl3
. CV-2619 inhibited the lipid peroxidation in a concentration-dependent manner; the concentration giving 50% inhibition (IC50) was 84 microM. In addition, the inhibitory effect of CV-2619 was strongly enhanced by adding substrates of mitochondrial respiration; when succinate, glutamate, or succinate plus glutamate was added, the IC50 of CV-2619 was changed to 1.1, 10, or 0.5 microM, respectively. Metabolites of CV-2619 also inhibited the lipid peroxidation. The inhibitory effect of CV-2619 on mitochondrial lipid peroxidation disappeared when TTFA, an inhibitor of
complex II
in mitochondrial respiratory chain, was added. The results indicate that in mitochondria CV-2619 is changed to its reduced form which inhibits lipid peroxidation.
...
PMID:Inhibition of lipid peroxidation by a novel compound (CV-2619) in brain mitochondria and mode of action of the inhibition. 651 32
