Mitochondrial electron transport chain
Template:Infobox metabolic pathway
The Mitochondrial Electron Transport Chain (ETC) is a series of complexes that transfer electrons from electron donors to electron acceptors via redox reactions, and couples this electron transfer with the transfer of protons (H+ ions) across the mitochondrial membrane. This process is vital for the production of adenosine triphosphate (ATP), the cell's main energy-carrying molecule. The ETC is located in the inner membrane of the mitochondrion and is the final stage of cellular respiration.
Components[edit | edit source]
The mitochondrial electron transport chain comprises four main complexes, each with specific components and functions:
- Complex I (NADH:ubiquinone oxidoreductase): This complex, also known as NADH dehydrogenase, accepts electrons from NADH, which is generated from the Krebs cycle. It transfers these electrons to ubiquinone (coenzyme Q), coupled with the transfer of protons across the mitochondrial membrane.
- Complex II (succinate dehydrogenase): Unlike Complex I, Complex II directly receives electrons from succinate, another product of the Krebs cycle. It also contributes to the reduction of ubiquinone.
- Complex III (cytochrome bc1 complex): This complex facilitates the transfer of electrons from reduced ubiquinone to cytochrome c, another electron carrier. This step is also coupled with proton transfer.
- Complex IV (cytochrome c oxidase): The final complex in the chain, Complex IV, transfers electrons from cytochrome c to molecular oxygen, reducing it to water. This complex is crucial for maintaining the proton gradient across the mitochondrial membrane by further pumping protons.
Function[edit | edit source]
The primary function of the mitochondrial electron transport chain is to create a proton gradient across the mitochondrial inner membrane. The energy stored in this gradient is used by ATP synthase to synthesize ATP from ADP and inorganic phosphate. This process is known as oxidative phosphorylation.
Regulation[edit | edit source]
The activity of the ETC is tightly regulated to meet cellular energy demands and to prevent excessive production of reactive oxygen species (ROS), which can be harmful to cells. Regulation occurs through various mechanisms including substrate availability, post-translational modifications of ETC components, and the presence of inhibitors and uncouplers.
Clinical significance[edit | edit source]
Dysfunction in the electron transport chain can lead to a variety of mitochondrial diseases, which can affect multiple systems of the body. These diseases are often severe and can include symptoms such as muscle weakness, neurological disorders, and organ failure.
See also[edit | edit source]
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Contributors: Prab R. Tumpati, MD