Pathways

The electron transport chain in mitochondria leads to the transport of hydrogen ions across the inner membrane of the mitochndria, and this proton gradient is eventually used in the production of ATP. Electrons travel down a chain of electron carriers in the inner mitochondrial membrane, ending with oxygen. The outer membrane of the mitochondrion is permeable to ions and other small molecules and nothing in this pathway requires a specific transporter to enter into the intermembrane space. However, the inner membrane is only permeable to water, oxygen and carbon dioxide, and all other molecules, including protons, require transport proteins. Phosphate is able to enter the mitochondrial matrix via the glucose-6-phosphate translocase, and ADP is able to enter the matrix as ATP leaves it via the ADP/ATP translocase 1 protein. Electrons donated by NADH can enter the electron transport chain as NADH dehydrogenase, known as complex I, facilitates their transfer to ubiquinone, also known as coenzyme Q10. As this occurs, the coenzyme Q10 becomes reduced to form ubiquinol, and protons are pumped from the intermembrane space to the matrix. Lower energy electrons can also be donated to complex II, which includes succinate dehydrogenase and contains FAD. These electrons move from succinic acid to the FAD in the enzyme complex, and then to coenzyme Q10, which is reduced to ubiquinol. Throughout this, succinic acid from the citric acid cycle is converted to fumaric acid, which then returns to the citric acid cycle. This step, unlike the others in the electron transport chain, does not result in any protons being pumped from the matrix to the intermembrane space. Regardless of which complex moved the electrons to coenzyme Q10, the cytochrome b-c1 complex, also known as complex III, catalyzes the movement of electrons from ubiquinol to cytochrome c, oxidizing ubiquinol to ubiquinone and reducing cytochrome c. This process also leads to the pumping of hydrogen ions into the intermembrane space. Finally, the transfer of electrons from the reduced cytochrome c is catalyzed by cytochrome c oxidase, also known as complex IV of the electron transport chain. This reaction oxidizes cytochrome c for further electron transport, and transfers the electrons to oxygen, forming molecules of water. This reaction also allows protons to be pumped across the membrane. The proton gradient that is built up through the electron transport chain allows protons to flow through the ATP synthase proteins in the mitochondrial inner membrane, providing the energy required to synthesize ATP from ADP.

The electron transport chain in mitochondria leads to the transport of hydrogen ions across the inner membrane of the mitochndria, and this proton gradient is eventually used in the production of ATP. Electrons travel down a chain of electron carriers in the inner mitochondrial membrane, ending with oxygen. The outer membrane of the mitochondrion is permeable to ions and other small molecules and nothing in this pathway requires a specific transporter to enter into the intermembrane space. However, the inner membrane is only permeable to water, oxygen and carbon dioxide, and all other molecules, including protons, require transport proteins. Phosphate is able to enter the mitochondrial matrix via the glucose-6-phosphate translocase, and ADP is able to enter the matrix as ATP leaves it via the ADP/ATP translocase 1 protein. Electrons donated by NADH can enter the electron transport chain as NADH dehydrogenase, known as complex I, facilitates their transfer to ubiquinone, also known as coenzyme Q10. As this occurs, the coenzyme Q10 becomes reduced to form ubiquinol, and protons are pumped from the intermembrane space to the matrix. Lower energy electrons can also be donated to complex II, which includes succinate dehydrogenase and contains FAD. These electrons move from succinic acid to the FAD in the enzyme complex, and then to coenzyme Q10, which is reduced to ubiquinol. Throughout this, succinic acid from the citric acid cycle is converted to fumaric acid, which then returns to the citric acid cycle. This step, unlike the others in the electron transport chain, does not result in any protons being pumped from the matrix to the intermembrane space. Regardless of which complex moved the electrons to coenzyme Q10, the cytochrome b-c1 complex, also known as complex III, catalyzes the movement of electrons from ubiquinol to cytochrome c, oxidizing ubiquinol to ubiquinone and reducing cytochrome c. This process also leads to the pumping of hydrogen ions into the intermembrane space. Finally, the transfer of electrons from the reduced cytochrome c is catalyzed by cytochrome c oxidase, also known as complex IV of the electron transport chain. This reaction oxidizes cytochrome c for further electron transport, and transfers the electrons to oxygen, forming molecules of water. This reaction also allows protons to be pumped across the membrane. The proton gradient that is built up through the electron transport chain allows protons to flow through the ATP synthase proteins in the mitochondrial inner membrane, providing the energy required to synthesize ATP from ADP.

Mitomycin is an antineoplastic that comes from cultures of Streptomyces caespitosus (antibiotic). This molecule is in the alkylating agent drug class because it inhibits DNA synthesis by cross-linking the DNA strands. Mitomycin is indicated in the treatment of malignant neoplasm of the lip, oral cavity, pharynx, digestive organs, peritoneum, breast, and urinary bladder. The guanine and cytosine content correlates with the degree of mitomycin-induced cross-linking when given to patients. At higher concentrations, cellular RNA and protein synthesis are also suppressed. Mitomycin undergoes in vivo activation by reductases, transforming into a bifunctional and trifunctional alkylating agent which binds to DNA, leading to cross-linking and inhibition of DNA synthesis. Mitomycin is cell cycle phase-nonspecific. This drug is administered as an intravenous or intravesical injection.

Mitomycin is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Mitomycin passes through the liver and is then excreted from the body mainly through the kidney.

Metabolites of Mitotane are predicted with biotransformer.

Mitoxantrone is an anthracenedione-derived chemotherapeutic agent used for the treatment of secondary (chronic) progressive, progressive relapsing, or worsening relapsing-remitting multiple sclerosis. Mitoxantrone binds to DNA, by doing this it intercalates into the acid nucleic chain through hydrogen bonding. This binding ends up causing crosslinks and strand breaks. Mitoxantrone can also interferes with ribonucleic acid (RNA) and is a potent inhibitor of topoisomerase II, the enzyme responsible for uncoiling and repairing damaged DNA. This drug has a cytocidal effect on proliferating cells and nonproliferation cells, this suggests that it is not a cell cycle-specific drug. Mitoxantrone is administered in an intravenous injection.