Pathways

Oxiconazole is a topical antifungal agent, known as the brand name Oxistat, that is used to treat a variety of skin fungal infections such as athlete's foot, jock itch, and ringworm.It is used to treat a number of different yeasts and dermatophytes such as T. rubrum, T. mentagrophytes, T. tonsurans, T. violaceum, E. floccosum, M. canis, M. audouini, M. gypseum, C. albicans, and M. furfur. It is applied topically to the infected area where it can inhibit the target enzymes in the fungal cells by diffusing into the cell. Oxiconazole inhibits both lanosterol synthase and lanosterol 14-alpha demethylase in the endoplasmic reticulum of fungal cells. Lanosterol synthase is the enzyme that catelyzes the synthesis of lanosterol from (S)-2,3 oxidosqualene. Lanosterol 14-alpha demethylase is the enzyme that catalyzes the synthesis of 4,4'-dimethyl cholesta-8,14,24-triene-3-beta-ol from lanosterol. With both of these enzymes inhibited ergosterol synthesis cannot occur which causes a significant low concentration of ergosterol in the fungal cell. Ergosterol is essential in maintaining membrane integrity in fungi. Without ergosterol, the fungus cell cannot synthesize membranes thereby increasing fluidity and preventing growth of new cells. This causes the cell to collapse and die.

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

In the majority of organisms, fatty acid degradation occurs mostly through the beta-oxidation cycle. In plants, this cycle only happens in the peroxisome, while in mammals this cycle happens in both the peroxisomes and mitochondria. Unfortunately, traditional fatty acid oxidation does not work for branched-chain fatty acids, or fatty acids that do not have an even number of carbons, like the fatty acid phytanic acid, found in animal milk. This acid can not be oxidized through beta-oxidation, as problems arise when water is added at the branched beta-carbon. To be able to oxidize this fatty acid, the carbon is oxidized by oxygen, which removes the initial carboxyl group, which shortens the chain. Now lacking a methyl group, this chain can be beta-oxidized. Now moving to the mitochondria, there are four reactions that occur, and are repeated for each molecule of the fatty acid. Each time the cycle of these reactions is completed, the chain is relieved of two carbons, which are oxidized and are taken away by NADH and FADH2, energy carriers that collect the carbons energy. After beta-oxidation in the cycle of reactions, an acetyl-CoA unit is released and is recycled into the cycle of reactions in the mitochondria, until the chain is fully broken down into acetyl-CoA, and can enter the TCA cycle. Once in the TCA cycle, it is converted to NADH and FADH2, which in turn help move along mitochondrial ATP production. Acetyl-CoA also helps produce ketone bodies that are further converted to energy in the heart and the brain.

In the majority of organisms, fatty acid degradation occurs mostly through the beta-oxidation cycle. In plants, this cycle only happens in the peroxisome, while in mammals this cycle happens in both the peroxisomes and mitochondria. Unfortunately, traditional fatty acid oxidation does not work for branched-chain fatty acids, or fatty acids that do not have an even number of carbons, like the fatty acid phytanic acid, found in animal milk. This acid can not be oxidized through beta-oxidation, as problems arise when water is added at the branched beta-carbon. To be able to oxidize this fatty acid, the carbon is oxidized by oxygen, which removes the initial carboxyl group, which shortens the chain. Now lacking a methyl group, this chain can be beta-oxidized. Now moving to the mitochondria, there are four reactions that occur, and are repeated for each molecule of the fatty acid. Each time the cycle of these reactions is completed, the chain is relieved of two carbons, which are oxidized and are taken away by NADH and FADH2, energy carriers that collect the carbons energy. After beta-oxidation in the cycle of reactions, an acetyl-CoA unit is released and is recycled into the cycle of reactions in the mitochondria, until the chain is fully broken down into acetyl-CoA, and can enter the TCA cycle. Once in the TCA cycle, it is converted to NADH and FADH2, which in turn help move along mitochondrial ATP production. Acetyl-CoA also helps produce ketone bodies that are further converted to energy in the heart and the brain.

In the majority of organisms, fatty acid degradation occurs mostly through the beta-oxidation cycle. In plants, this cycle only happens in the peroxisome, while in mammals this cycle happens in both the peroxisomes and mitochondria. Unfortunately, traditional fatty acid oxidation does not work for branched-chain fatty acids, or fatty acids that do not have an even number of carbons, like the fatty acid phytanic acid, found in animal milk. This acid can not be oxidized through beta-oxidation, as problems arise when water is added at the branched beta-carbon. To be able to oxidize this fatty acid, the carbon is oxidized by oxygen, which removes the initial carboxyl group, which shortens the chain. Now lacking a methyl group, this chain can be beta-oxidized. Now moving to the mitochondria, there are four reactions that occur, and are repeated for each molecule of the fatty acid. Each time the cycle of these reactions is completed, the chain is relieved of two carbons, which are oxidized and are taken away by NADH and FADH2, energy carriers that collect the carbons energy. After beta-oxidation in the cycle of reactions, an acetyl-CoA unit is released and is recycled into the cycle of reactions in the mitochondria, until the chain is fully broken down into acetyl-CoA, and can enter the TCA cycle. Once in the TCA cycle, it is converted to NADH and FADH2, which in turn help move along mitochondrial ATP production. Acetyl-CoA also helps produce ketone bodies that are further converted to energy in the heart and the brain.

In the majority of organisms, fatty acid degradation occurs mostly through the beta-oxidation cycle. In plants, this cycle only happens in the peroxisome, while in mammals this cycle happens in both the peroxisomes and mitochondria. Unfortunately, traditional fatty acid oxidation does not work for branched-chain fatty acids, or fatty acids that do not have an even number of carbons, like the fatty acid phytanic acid, found in animal milk. This acid can not be oxidized through beta-oxidation, as problems arise when water is added at the branched beta-carbon. To be able to oxidize this fatty acid, the carbon is oxidized by oxygen, which removes the initial carboxyl group, which shortens the chain. Now lacking a methyl group, this chain can be beta-oxidized. Now moving to the mitochondria, there are four reactions that occur, and are repeated for each molecule of the fatty acid. Each time the cycle of these reactions is completed, the chain is relieved of two carbons, which are oxidized and are taken away by NADH and FADH2, energy carriers that collect the carbons energy. After beta-oxidation in the cycle of reactions, an acetyl-CoA unit is released and is recycled into the cycle of reactions in the mitochondria, until the chain is fully broken down into acetyl-CoA, and can enter the TCA cycle. Once in the TCA cycle, it is converted to NADH and FADH2, which in turn help move along mitochondrial ATP production. Acetyl-CoA also helps produce ketone bodies that are further converted to energy in the heart and the brain.

In the majority of organisms, fatty acid degradation occurs mostly through the beta-oxidation cycle. In plants, this cycle only happens in the peroxisome, while in mammals this cycle happens in both the peroxisomes and mitochondria. Unfortunately, traditional fatty acid oxidation does not work for branched-chain fatty acids, or fatty acids that do not have an even number of carbons, like the fatty acid phytanic acid, found in animal milk. This acid can not be oxidized through beta-oxidation, as problems arise when water is added at the branched beta-carbon. To be able to oxidize this fatty acid, the carbon is oxidized by oxygen, which removes the initial carboxyl group, which shortens the chain. Now lacking a methyl group, this chain can be beta-oxidized. Now moving to the mitochondria, there are four reactions that occur, and are repeated for each molecule of the fatty acid. Each time the cycle of these reactions is completed, the chain is relieved of two carbons, which are oxidized and are taken away by NADH and FADH2, energy carriers that collect the carbons energy. After beta-oxidation in the cycle of reactions, an acetyl-CoA unit is released and is recycled into the cycle of reactions in the mitochondria, until the chain is fully broken down into acetyl-CoA, and can enter the TCA cycle. Once in the TCA cycle, it is converted to NADH and FADH2, which in turn help move along mitochondrial ATP production. Acetyl-CoA also helps produce ketone bodies that are further converted to energy in the heart and the brain.

In the majority of organisms, fatty acid degradation occurs mostly through the beta-oxidation cycle. In plants, this cycle only happens in the peroxisome, while in mammals this cycle happens in both the peroxisomes and mitochondria. Unfortunately, traditional fatty acid oxidation does not work for branched-chain fatty acids, or fatty acids that do not have an even number of carbons, like the fatty acid phytanic acid, found in animal milk. This acid can not be oxidized through beta-oxidation, as problems arise when water is added at the branched beta-carbon. To be able to oxidize this fatty acid, the carbon is oxidized by oxygen, which removes the initial carboxyl group, which shortens the chain. Now lacking a methyl group, this chain can be beta-oxidized. Now moving to the mitochondria, there are four reactions that occur, and are repeated for each molecule of the fatty acid. Each time the cycle of these reactions is completed, the chain is relieved of two carbons, which are oxidized and are taken away by NADH and FADH2, energy carriers that collect the carbons energy. After beta-oxidation in the cycle of reactions, an acetyl-CoA unit is released and is recycled into the cycle of reactions in the mitochondria, until the chain is fully broken down into acetyl-CoA, and can enter the TCA cycle. Once in the TCA cycle, it is converted to NADH and FADH2, which in turn help move along mitochondrial ATP production. Acetyl-CoA also helps produce ketone bodies that are further converted to energy in the heart and the brain.

Oxidative phosphorylation is the concluding pathway in cellular respiration, the series of metabolic processes that convert chemical energy from glucose into adenosine triphosphate (ATP), a usable form of energy for the cell. A series of five protein complexes, each with increasing reduction potentials, located in the mitochondrial inner membrane forms the electron transport chain (ETC). Electrons are transferred from one complex to the next in a series of redox reactions which release energy used to pump protons from the mitochondrial matrix into the intermembrane space. As a result, an electrochemical gradient forms across the inner mitochondrial membrane. Complex V (ATP synthase) is the singular channel by which protons flow back into the matrix. ATP synthase uses this gradient to synthesize ATP from ADP and phosphate (Pi). Complex I is the NADH dehydrogenase complex responsible for the oxidation of NADH and the reduction of ubiquinone (coenzyme Q), transferring two electrons from NADH to the respiratory chain. Four protons are pumped into the intermembrane space as a result of this electron transfer, and a further two protons are pumped due to the reduction of ubiquinone to ubiquinol. Complex II is the succinate dehydrogenase complex responsible for the oxidation of succinate into fumarate and the reduction of ubiquinone, transferring two electrons from succinate to ubiquinone instead of directly to the ETC. No protons are pumped at this complex because succinate oxidation releases less energy than NADH oxidation. Complex III is the ubiquinol-cytochrome c oxidoreductase complex responsible for transferring electrons from ubiquinol to cytochrome c. Two protons are pumped into the intermembrane space as a result of the oxidization of one molecule of ubiquinol (a coenzyme that can carry two electrons) and the reduction of two molecules of cytochrome c (a heme protein that can carry only one electron). Complex IV is the cytochrome c oxidase complex responsible for transferring electrons to oxygen, the terminal electron acceptor, and reducing it to water. Four protons are pumped into the intermembrane space as a result of the electron transfer. In addition, the reduction of oxygen further contributes to the proton gradient due to its use of matrix protons. Complex V is the mitochondrial membrane F-Type ATP synthase which produces ATP from ADP in the presence of a proton gradient across the membrane (generated by electron transport complexes of the respiratory chain). An F-Type ATPase is composed of two domains: a catalytic core (where ATP is synthesized) and a proton channel.