Electronic Transport Chain (ETC) is a series of protein complexes and other molecules. Specifically, they transfer electrons from electron donors to electron acceptors through redox reactions and couple this electron transfer with proton transfer. There are two electron transfer pathways in ETC: complex I/III/IV with NADH as the substrate and complex II/III/IV with succinic acid as the substrate. Meanwhile, Complex I is the first enzyme in the respiratory chain. Nonetheless, it oxidizes NADH produced through the Krebs cycle in the mitochondrial matrix and reduces ubiquinone to panthenol using two electrons. Panthenol is re oxidized by the cytochrome BC1 complex and transfers electrons to reduce molecular oxygen to water in complex IV. Importantly, Complex I plays a central role in energy metabolism as it is the rate limiting step of the entire respiration process. Now, we will introduce a mitochondrial electron transport chain complex I inhibitor, Rotenone.
Rotenone is a Mitochondrial Electron Transport Chain Complex I Inhibitor for Cell Apoptosis Research.
Above all, Rotenone induces apoptosis through enhancing mitochondrial reactive oxygen species production. Particularly, MAPK, Toll-like receptor, Wnt, and Ras signaling pathways are intensively involved in the effect of rotenone on the ENS.
Next in importance, Rotenone can be used in animal modeling to construct Parkinson’s syndrome models. Additionally, Rotenone causes a significant increase in the excitatory amino acid neurotransmitters. Obviously, Rotenone causes a dose-dependent increase in α-synuclein in the substantia nigra. Furthermore, Rotenone causes a significant decrease in the number of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra, and dopamine in the striatum in rats.
All in all, Rotenone is a mitochondrial electron transport chain complex I inhibitor for cell apoptosis research.
References:
[1] Khadrawy YA, et al. Gen Physiol Biophys. 2016 Nov 30.
[2] Zhang ZN, et al. 2016 Nov 19. pii: S0006-8993(16)30776-4.