Classification Term: 667
Porphyrins (ontology term: CHEMONTID:0000212)
Compounds containing a fundamental skeleton of four pyrrole nuclei united through the alpha-positions by four methine groups to form a macrocyclic structure." []
found 39 associated metabolites at sub_class metabolite taxonomy ontology rank level.
Ancestor: Tetrapyrroles and derivatives
Child Taxonomies: There is no child term of current ontology term.
Protoporphyrin IX
Protoporphyrins are tetrapyrroles containing 4 methyl, 2 propionic, and 2 vinyl side chains. Protoporphyrin is produced by oxidation of the methylene bridge of protoporphyrinogen. Protoporphyrin IX is the only naturally occurring isomer; it is an intermediate in heme biosynthesis, combining with ferrous iron to form protoheme IX, the heme prosthetic group of hemoglobin. Protoporphyrin IX is created by the enzyme protoporphyrinogen oxidase. The enzyme ferrochelatase converts it into heme. Protoporphyrin IX naturally occurs in small amounts in feces. Protoporphyrin IX is also responsible for the brown pigment (ooporphyrin) of birds eggs. Protoporphyrin IX is used as a branch point in the biosynthetic pathway leading to heme (by insertion of iron) and chlorophylls (by insertion of Mg and further side-chain transformation). Protoporphyrin IX can be used to treat liver disorders, mainly as the sodium salt. Under certain conditions, protoporphyrin IX can act as a neurotoxin, a phototoxin, and a metabotoxin. A neurotoxin causes damage to nerve cells and nerve tissues. A phototoxin causes cell damage upon exposure to light. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of porphyrins are associated with porphyrias such as porphyria variegate, acute intermittent porphyria, and hereditary coproporphyria (HCP). In particular, it is accumulated and excreted excessively in the feces in acute intermittent porphyria, protoporphyria, and variegate porphyria. There are several types of porphyrias (most are inherited). Hepatic porphyrias are characterized by acute neurological attacks (seizures, psychosis, extreme back and abdominal pain, and an acute polyneuropathy), while the erythropoietic forms present with skin problems (usually a light-sensitive blistering rash and increased hair growth). The neurotoxicity of porphyrins may be due to their selective interactions with tubulin, which disrupt microtubule formation and cause neural malformations (PMID: 3441503). obtained by demetallation of Haemin, occurs in small amounts in faeces. Brown pigment (Ooporphyrin) of birds eggs. Isolated from Atolla wyvillei (CCD). Protoporphyrin is found in red beetroot. D011838 - Radiation-Sensitizing Agents > D017319 - Photosensitizing Agents COVID info from COVID-19 Disease Map C1420 - Photosensitizing Agent D003879 - Dermatologic Agents Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS Protoporphyrin IX is the final intermediate in the heme biosynthetic pathway. Protoporphyrin IX is the final intermediate in the heme biosynthetic pathway.
Uroporphyrinogen III
Uroporphyrinogens are porphyrinogen variants in which each pyrrole ring has one acetate side chain and one propionate side chain; it is formed by condensation 4 four molecules of porphobilinogen. 4 isomers are possible but only 2 commoly are found, types I and III. Uroporphyrinogen III is a functional intermediate in heme biosynthesis while Uroporphyrinogen I is produced in an abortive side reaction. COVID info from COVID-19 Disease Map Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS
Protoporphyrinogen IX
Protoporphyrinogen IX is an intermediate in heme biosynthesis. It is a porphyrinogen in which two pyrrole rings each have one methyl and one propionate side chain, and the other two pyrrole rings each have one methyl and one vinyl side chain. Fifteen isomers are possible but only one, type IX, occurs naturally. Protoporphyrinogen is produced by oxidative decarboxylation of coproporphyrinogen. Under certain conditions, protoporphyrinogen IX can act as a phototoxin, a neurotoxin, and a metabotoxin. A phototoxin leads to cell damage upon exposure to light. A neurotoxin causes damage to nerve cells and nerve tissues. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of porphyrins are associated with porphyrias such as porphyria variegate, acute intermittent porphyria, and hereditary coproporphyria (HCP). In particular, protoporphyrinogen IX is accumulated and excreted excessively in the feces in acute intermittent porphyria, protoporphyria, and variegate porphyria. There are several types of porphyrias (most are inherited). Hepatic porphyrias are characterized by acute neurological attacks (seizures, psychosis, extreme back and abdominal pain, and an acute polyneuropathy), while the erythropoietic forms present with skin problems (usually a light-sensitive blistering rash and increased hair growth). The neurotoxicity of porphyrins may be due to their selective interactions with tubulin, which disrupt microtubule formation and cause neural malformations (PMID: 3441503). Protoporphyrinogen IX is an intermediate in heme biosynthesis. It is a porphyrinogen in which 2 pyrrole rings each have one methyl and one propionate side chain and the other two pyrrole rings each have one methyl and one vinyl side chain. 15 isomers are possible but only one, type IX, occurs naturally. Protoporphyrinogen is produced by oxidative decarboxylation of coproporphyrinogen. [HMDB]. Protoporphyrinogen IX is found in many foods, some of which are elderberry, grapefruit, green vegetables, and pepper (c. annuum). COVID info from COVID-19 Disease Map Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS
Uroporphyrin III
Uroporphyrin is the porphyrin produced by oxidation of the methylene bridges in uroporphyrinogen. Uroporphyrins have four acetic acid and four propionic acid side chains attached to their pyrrole rings. The enzyme uroporphyrinogen I synthase catalyzes the formation of hydroxymethylbilane from four molecules of porphobilinogen. Uroporphyrinogen III cosynthase then catalyzes the conversion of hydroxymethylbilane into uroporphyrinogen III. Otherwise, hydroxymethylbilane cyclizes nonenzymatically to form uroporphyrinogen I. Uroporphyrinogen I and III yield their respective uroporphyrins via autooxidation or their respective coproporphyrinogens via decarboxylation. Excessive amounts of uroporphyrin I are excreted in congenital erythropoietic porphyria, and both uroporphyrin I and uroporphyrin III are excreted in porphyria cutanea tarda. Uroporphyrin I and III are the most common isomers. Under certain conditions, uroporphyrin III can act as a phototoxin, a neurotoxin, and a metabotoxin. A phototoxin leads to cell damage upon exposure to light. A neurotoxin causes damage to nerve cells and nerve tissues. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of porphyrins are associated with porphyrias such as porphyria variegate, acute intermittent porphyria, porphyria cutanea tarda, and hereditary coproporphyria (HCP). There are several types of porphyrias (most are inherited). Hepatic porphyrias are characterized by acute neurological attacks (seizures, psychosis, extreme back and abdominal pain, and an acute polyneuropathy), while the erythropoietic forms present with skin problems (usually a light-sensitive blistering rash and increased hair growth). The neurotoxicity of porphyrins may be due to their selective interactions with tubulin, which disrupt microtubule formation and cause neural malformations (PMID: 3441503). Occurs in urine in small amounts as by-product of haem biosynthesis, also in Rhodopseudomonas spheroides (CCD). Uroporphyrin III is found in soy bean.
Coproporphyrinogen III
Coproporphyrinogen III is a porphyrin metabolite arising from heme synthesis. Porphyrins are pigments found in both animal and plant life. Coproporphyrinogen III is a tetrapyrrole dead-end product resulting from the spontaneous oxidation of the methylene bridges of coproporphyrinogen arising from heme synthesis. It is secreted in feces and urine. Coproporphyrinogen III is biosynthesized from the tetrapyrrole hydroxymethylbilane, which is converted by the action of uroporphyrinogen III synthase to uroporphyrinogen III. Uroporphyrinogen III is subsequently converted into coproporphyrinogen III through a series of four decarboxylations. Increased levels of coproporphyrinogens can indicate congenital erythropoietic porphyria or sideroblastic anemia, which are inherited disorders. Porphyria is a pathological state characterized by abnormalities of porphyrin metabolism and results in the excretion of large quantities of porphyrins in the urine and in extreme sensitivity to light. A large number of factors are capable of increasing porphyrin excretion, owing to different and multiple causes and etiologies: (1) the main site of the chronic hepatic porphyria disease process concentrates on the liver, (2) a functional and morphologic liver injury is almost regularly associated with this chronic porphyria, and (3) the toxic form due to occupational and environmental exposure takes mainly a subclinical course. Hepatic factors include disturbance in coproporphyrinogen metabolism, which results from inhibition of coproporphyrinogen oxidase as well as from the rapid loss and diminished utilization of coproporphyrinogen in the hepatocytes. This may also explain why coproporphyrin, its autoxidation product, predominates physiologically in the urine. Decreased biliary excretion of coproporphyrin leading to a compensatory urinary excretion. Therefore, the coproporphyrin ring isomer ratio (1:III) becomes a sensitive index for impaired liver function, intrahepatic cholestasis, and disturbed activity of hepatic uroporphyrinogen decarboxylase. In itself, secondary coproporphyrinuria is not associated with porphyria symptoms of a hepatologic-gastroenterologic, neurologic, or dermatologic order, even though coproporphyrinuria can occur with such symptoms (PMID: 3327428). Under certain conditions, coproporphyrinogen III can act as a phototoxin, a neurotoxin, and a metabotoxin. A phototoxin leads to cell damage upon exposure to light. A neurotoxin causes damage to nerve cells and nerve tissues. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of porphyrins are associated with porphyrias such as porphyria variegate, acute intermittent porphyria, hereditary coproporphyria (HCP), congenital erythropoietic porphyria, and sideroblastic anemia. In particular, coproporphyrinogen III is accumulated and excreted excessively in the feces in acute intermittent porphyria, protoporphyria, and variegate porphyria. There are several types of porphyrias (most are inherited). Hepatic porphyrias are characterized by acute neurological attacks (seizures, psychosis, extreme back and abdominal pain, and an acute polyneuropathy), while the erythropoietic forms present with skin problems (usually a light-sensitive blistering rash and increased hair growth). The neurotoxicity of porphyrins may be due to their selective interactions with tubulin, which disrupt microtubule formation and cause neural malformations (PMID: 3441503). Coproporphyrinogen III oxidase is deficient in hereditary coproporphyria. These persons usually have enhanced excretion even in a subclinical state of the disease.(PubMed ID 14605502 ) [HMDB]. Coproporphyrinogen III is found in many foods, some of which are cucumber, climbing bean, horseradish, and pepper (c. frutescens). COVID info from COVID-19 Disease Map Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS
Pentaporphyrin I
Pentaporphyrin I is a porphyrin intermediate detected in liver, kidney and erythrocytes (PubMed ID 8803328 ).
Uroporphyrinogen I
Uroporphyrinogens are porphyrinogen variants in which each pyrrole ring has one acetate side chain and one propionate side chain; it is formed by condensation 4 four molecules of porphobilinogen. 4 isomers are possible but only 2 commoly are found, types I and III. Uroporphyrinogen III is a functional intermediate in heme biosynthesis while Uroporphyrinogen I is produced in an abortive side reaction. [HMDB]. Uroporphyrinogen I is found in many foods, some of which are great horned owl, nutmeg, lime, and cascade huckleberry. Uroporphyrinogens are porphyrinogen variants in which each pyrrole ring has one acetate side chain and one propionate side chain; it is formed by condensation 4 four molecules of porphobilinogen. 4 isomers are possible but only 2 commoly are found, types I and III. Uroporphyrinogen III is a functional intermediate in heme biosynthesis while Uroporphyrinogen I is produced in an abortive side reaction.
Uroporphyrin I
Uroporphyrin is the porphyrin produced by oxidation of the methylene bridges in uroporphyrinogen. Uroporphyrins have four acetic acid and four propionic acid side chains attached to their pyrrole rings. The enzyme uroporphyrinogen I synthase catalyzes the formation of hydroxymethylbilane from four molecules of porphobilinogen. Uroporphyrinogen III cosynthase then catalyzes the conversion of hydroxymethylbilane into uroporphyrinogen III. Otherwise, hydroxymethylbilane cyclizes nonenzymatically to form uroporphyrinogen I. Uroporphyrinogen I and III yield their respective uroporphyrins via autooxidation or their respective coproporphyrinogens via decarboxylation. Excessive amounts of uroporphyrin I are excreted in congenital erythropoietic porphyria, and both uroporphyrin I and uroporphyrin III are excreted in porphyria cutanea tarda. Uroporphyrin I and III are the most common isomers. Under certain conditions, uroporphyrin I can act as a phototoxin, a neurotoxin, and a metabotoxin. A phototoxin leads to cell damage upon exposure to light. A neurotoxin causes damage to nerve cells and nerve tissues. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of porphyrins are associated with porphyrias such as porphyria variegate, acute intermittent porphyria, porphyria cutanea tarda, and hereditary coproporphyria (HCP). There are several types of porphyrias (most are inherited). Hepatic porphyrias are characterized by acute neurological attacks (seizures, psychosis, extreme back and abdominal pain, and an acute polyneuropathy), while the erythropoietic forms present with skin problems (usually a light-sensitive blistering rash and increased hair growth). The neurotoxicity of porphyrins may be due to their selective interactions with tubulin, which disrupt microtubule formation and cause neural malformations (PMID: 3441503). Uroporphyrin is the porphyrin produced by oxidation of the methylene bridges in uroporphyrinogen. They have four acetic acid and four propionic acid side chains attached to the pyrrole rings. Uroporphyrinogen I and III are formed from polypyrryl methane in the presence of uroporphyrinogen III cosynthetase and uroporphyrin I synthetase, respectively. They can yield uroporphyrins by autooxidation or coproporphyrinogens by decarboxylation.Excessive amounts of uroporphyrin I are excreted in congenital erythropoietic porphyria, and both types I and III are excreted in porphyria cutanea tarda.Uroporphyrin I and III are the most common isomers. [HMDB]
Coproporphyrinogen I
Coproporphyrinogen I is a porphyrin metabolite arising from heme synthesis. Porphyrins are pigments found in both animal and plant life. Coproporphyrinogen I is a tetrapyrrole dead-end product resulting from the spontaneous oxidation of the methylene bridges of coproporphyrinogen arising from heme synthesis. It is secreted in feces and urine. Coproporphyrinogen I is biosynthesized from the tetrapyrrole hydroxymethylbilane, which is converted by the action of uroporphyrinogen synthase to uroporphyrinogen I. Uroporphyrinogen I is subsequently converted into coproporphyrinogen I through a series of four decarboxylations. Increased levels of coproporphyrinogens can indicate congenital erythropoietic porphyria or sideroblastic anemia, which are inherited disorders. Porphyria is a pathological state characterized by abnormalities of porphyrin metabolism and results in the excretion of large quantities of porphyrins in the urine and in extreme sensitivity to light. A large number of factors are capable of increasing porphyrin excretion, owing to different and multiple causes and etiologies: (1) the main site of the chronic hepatic porphyria disease process concentrates on the liver, (2) a functional and morphologic liver injury is almost regularly associated with this chronic porphyria, and (3) the toxic form due to occupational and environmental exposure takes mainly a subclinical course. Hepatic factors include disturbance in coproporphyrinogen metabolism, which results from inhibition of coproporphyrinogen oxidase as well as from the rapid loss and diminished utilization of coproporphyrinogen in the hepatocytes. This may also explain why coproporphyrin, its autoxidation product, predominates physiologically in the urine. Decreased biliary excretion of coproporphyrin leading to a compensatory urinary excretion. Therefore, the coproporphyrin ring isomer ratio becomes a sensitive index for impaired liver function, intrahepatic cholestasis, and disturbed activity of hepatic uroporphyrinogen decarboxylase. In itself, secondary coproporphyrinuria is not associated with porphyria symptoms of a hepatologic-gastroenterologic, neurologic, or dermatologic order, even though coproporphyrinuria can occur with such symptoms (PMID: 3327428). Under certain conditions, coproporphyrinogen I can act as a phototoxin, a neurotoxin, and a metabotoxin. A phototoxin leads to cell damage upon exposure to light. A neurotoxin causes damage to nerve cells and nerve tissues. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels. Chronically high levels of porphyrins are associated with porphyrias such as porphyria variegate, acute intermittent porphyria, hereditary coproporphyria (HCP), congenital erythropoietic porphyria, and sideroblastic anemia. There are several types of porphyrias (most are inherited). Hepatic porphyrias are characterized by acute neurological attacks (seizures, psychosis, extreme back and abdominal pain, and an acute polyneuropathy), while the erythropoietic forms present with skin problems (usually a light-sensitive blistering rash and increased hair growth). The neurotoxicity of porphyrins may be due to their selective interactions with tubulin, which disrupt microtubule formation and cause neural malformations (PMID: 3441503). Coproporphyrinogen I can be found in a number of food items, including cascade huckleberry, hyacinth bean, horseradish tree, and watercress. Formed by Uroporphyrinogen decarboxylase from Uroporphyrinogen I by decarboxylation of 4 acetates. [HMDB]. Coproporphyrinogen I is found in many foods, some of which are alpine sweetvetch, japanese persimmon, komatsuna, and celery leaves.
Coproporphyrin I
C36H38N4O8 (654.2689508000001)
Coproporphyrin I is a porphyrin metabolite arising from heme synthesis. Porphyrins are pigments found in both animal and plant life. Coproporphyrin I is a tetrapyrrole dead-end product from the spontaneous oxidation of the methylene bridges of coproporphynogen, arising from heme synthesis and secreted in feces and urine. Increased levels of coproporphyrins can indicate congenital erythropoietic porphyria or sideroblastic anaemia. Porphyria is a pathological state characterised by abnormalities of porphyrin metabolism and results in the excretion of large quantities of porphyrins in the urine and in extreme sensitivity to light. A large number of factors are capable of increasing porphyrin excretion, owing to different and multiple causes and etiologies: 1) the main site of the chronic hepatic porphyria disease process concentrates on the liver, 2) a functional and morphologic liver injury is almost regularly associated with this chronic porphyria, 3) the toxic form due to occupational and environmental exposure takes mainly a subclinical course. Hepatic factors includes disturbance in coproporphyrinogen metabolism, which results from inhibition of coproporphyrinogen oxidase as well as from the rapid loss from, and diminished utilization of coproporphyrinogen in the hepatocytes, which may also explain why coproporphyrin, its autoxidation product, predominates physiologically in the urine; decreased biliary excretion of coproporphyrin leading to a compensatory urinary excretion, so that the coproporphyrin ring isomer ratio (1:III) becomes a sensitive index for impaired liver function and intrahepatic cholestasis; and disturbed activity of hepatic uroporphyrinogen decarboxylase. In itself, secondary coproporphyrinuria is not associated with porphyria symptoms of a hepatologic-gastroenterologic, neurologic, or dermatologic order, even though coproporphyrinuria can occur with such symptoms. (PMID: 3327428). Coproporhyrin I is a porphyrin metabolite arising from heme synthesis. Porphyrins are pigments found in both animal and plant life.
Coproporphyrin III
C36H38N4O8 (654.2689508000001)
Coproporphyrin III is a porphyrin metabolite arising from heme synthesis. Porphyrins are pigments found in both animal and plant life. Coproporphyrin III is a tetrapyrrole dead-end product from the spontaneous oxidation of the methylene bridges of coproporphynogen, arising from heme synthesis and secreted in feces and urine. Increased levels of coproporphyrins can indicate congenital erythropoietic porphyria or sideroblastic anaemia, which are inherited disorders. Porphyria is a pathological state characterised by abnormalities of porphyrin metabolism and results in the excretion of large quantities of porphyrins in the urine and in extreme sensitivity to light. A large number of factors are capable of increasing porphyrin excretion, owing to different and multiple causes and etiologies: 1) the main site of the chronic hepatic porphyria disease process concentrates on the liver, 2) a functional and morphologic liver injury is almost regularly associated with this chronic porphyria, 3) the toxic form due to occupational and environmental exposure takes mainly a subclinical course. Hepatic factors includes disturbance in coproporphyrinogen metabolism, which results from inhibition of coproporphyrinogen oxidase as well as from the rapid loss from, and diminished utilization of coproporphyrinogen in the hepatocytes, which may also explain why coproporphyrin, its autoxidation product, predominates physiologically in the urine; decreased biliary excretion of coproporphyrin leading to a compensatory urinary excretion, so that the coproporphyrin ring isomer ratio (1:III) becomes a sensitive index for impaired liver function and intrahepatic cholestasis; and disturbed activity of hepatic uroporphyrinogen decarboxylase. In itself, secondary coproporphyrinuria is not associated with porphyria symptoms of a hepatologic-gastroenterologic, neurologic, or dermatologic order, even though coproporphyrinuria can occur with such symptoms. (PMID: 3327428). Excreted in small amounts in urine and faeces, found in blood, yeast, microorganisms etc. By-product of Haem formation in vivo, due to oxidation of the porphyrinogen (CCD) Coproporphyrin III (Zincphyrin) is a naturally occurring porphyrin derivative that is mainly found in urine[1][2].
Deuteroporphyrin IX
Deuteroporphyrin IX is a non-natural dicarboxylic porphyrin. Deuteroporphyrins are porphyrins with four methyl and two propionic acid side chains attached to the pyrrole rings. Deuteroporphyrin IX is described as a fecal porphyrin in patients with endemic chronic arsenic poisoning. (Environmental Sciences (Tokyo, Japan) (2001), 8(6), 561-570.). Excess accumulation of the biosynthetic intermediate protoporphyrin can lead to extensive tissue damage upon exposure to light since protoporpyhyrin is a potent photosensitizing agent, giving rise to membrane-destroying oxygen radicals or singlet oxygen. For instance, in the human porphyria disease porphyria variegata, a genetic deficiency in a heme biosynthetic enzyme, protoporphyrinogen oxidase, leads to protoporphyrin accumulation and lightdependent skin photosensitivity. Horseradish peroxidase (HRP) in the presence of glutathione (GSH) could oxidize the non-natural porphyrin deuteroporphyrin IX, which is closely related to protoporphyrin IX. The product is a unique green chlorin. One of the pyrrole rings had been modified by addition of an hydroxy and an oxo group, thus giving the characteristic reduced pyrrole ring of the chlorine. Of most importance for human medicine, peroxidative enzymes present in mammalian cells can also carry out these GSH-dependent oxidative conversions of protoporphyrin and deuteroporphyrin. (PMID: 10334939). Deuteroporphyrin IX is a non-natural dicarboxylic porphyrin. Deuteroporphyrins are porphyrins with four methyl and two propionic acid side chains attached to the pyrrole rings. Deuteroporphyrin IX is described as a fecal porphyrin in patients with endemic chronic arsenic poisoning. (Environmental Sciences (Tokyo, Japan) (2001), 8(6), 561-570.)
Coproporphyrin II
C36H38N4O8 (654.2689508000001)
Coproporphyrin II is a porphyrin metabolite arising from heme synthesis. Porphyrins are pigments found in both animal and plant life. This is a rare coproporphyrin isomer and it constitues only 1\\% of all coproporphyrins. This isomer appears to arise spontaneously as opposed to enzymatically. Coproporphyrin II is a tetrapyrrole dead-end product from the spontaneous oxidation of the methylene bridges of coproporphynogen, arising from heme synthesis and secreted in feces and urine. Increased levels of coproporphyrins can indicate congenital erythropoietic porphyria or sideroblastic anaemia. Porphyria is a pathological state characterised by abnormalities of porphyrin metabolism and results in the excretion of large quantities of porphyrins in the urine and in extreme sensitivity to light. A large number of factors are capable of increasing porphyrin excretion, owing to different and multiple causes and etiologies: 1) the main site of the chronic hepatic porphyria disease process concentrates on the liver, 2) a functional and morphologic liver injury is almost regularly associated with this chronic porphyria, 3) the toxic form due to occupational and environmental exposure takes mainly a subclinical course. Hepatic factors includes disturbance in coproporphyrinogen metabolism, which results from inhibition of coproporphyrinogen oxidase as well as from the rapid loss from, and diminished utilization of coproporphyrinogen in the hepatocytes, which may also explain why coproporphyrin, its autoxidation product, predominates physiologically in the urine; decreased biliary excretion of coproporphyrin leading to a compensatory urinary excretion, so that the coproporphyrin ring isomer ratio (1:III) becomes a sensitive index for impaired liver function and intrahepatic cholestasis; and disturbed activity of hepatic uroporphyrinogen decarboxylase. In itself, secondary coproporphyrinuria is not associated with porphyria symptoms of a hepatologic-gastroenterologic, neurologic, or dermatologic order, even though coproporphyrinuria can occur with such symptoms. (PMID: 3327428). Coproporhyrin II is a porphyrin metabolite arising from heme synthesis. Porphyrins are pigments found in both animal and plant life. This is a rare coproporphyrin isomer and it constitues only 1\\% of all coproporphyrins. This isomer appears to arise spontaneously as opposed to enzymatically.
Coproporphyrin IV
C36H38N4O8 (654.2689508000001)
Coproporphyrin IV is a porphyrin metabolite arising from heme synthesis. Porphyrins are pigments found in both animal and plant life. This is a rare coproporphyrin isomer and it constitues only 2\\% of all coproporphyrins. This isomer appears to arise spontaneously as opposed to enzymatically. Coproporphyrin IV is a tetrapyrrole dead-end product from the spontaneous oxidation of the methylene bridges of coproporphynogen, arising from heme synthesis and secreted in feces and urine. Increased levels of coproporphyrins can indicate congenital erythropoietic porphyria or sideroblastic anaemia. Porphyria is a pathological state characterised by abnormalities of porphyrin metabolism and results in the excretion of large quantities of porphyrins in the urine and in extreme sensitivity to light. A large number of factors are capable of increasing porphyrin excretion, owing to different and multiple causes and etiologies: 1) the main site of the chronic hepatic porphyria disease process concentrates on the liver, 2) a functional and morphologic liver injury is almost regularly associated with this chronic porphyria, 3) the toxic form due to occupational and environmental exposure takes mainly a subclinical course. Hepatic factors includes disturbance in coproporphyrinogen metabolism, which results from inhibition of coproporphyrinogen oxidase as well as from the rapid loss from, and diminished utilization of coproporphyrinogen in the hepatocytes, which may also explain why coproporphyrin, its autoxidation product, predominates physiologically in the urine; decreased biliary excretion of coproporphyrin leading to a compensatory urinary excretion, so that the coproporphyrin ring isomer ratio (1:III) becomes a sensitive index for impaired liver function and intrahepatic cholestasis; and disturbed activity of hepatic uroporphyrinogen decarboxylase. In itself, secondary coproporphyrinuria is not associated with porphyria symptoms of a hepatologic-gastroenterologic, neurologic, or dermatologic order, even though coproporphyrinuria can occur with such symptoms. (PMID: 3327428). Coproporhyrin IV is a porphyrin metabolite arising from heme synthesis. Porphyrins are pigments found in both animal and plant life. This is a rare coproporphyrin isomer and it constitues only 2\\% of all coproporphyrins. This isomer appears to arise spontaneously as opposed to enzymatically.
Hematoporphyrin IX
Iron-free derivatives of heme with 4 methyl groups, 2 hydroxyethyl groups and 2 propionic acid groups attached to the pyrrole rings. Some of these phosphosensitizing agents are used in the phototherapy of malignant neoplasms. -- Pubchem [HMDB] Iron-free derivatives of heme with 4 methyl groups, 2 hydroxyethyl groups and 2 propionic acid groups attached to the pyrrole rings. Some of these phosphosensitizing agents are used in the phototherapy of malignant neoplasms. -- Pubchem.
Harderoporphyrin
Harderoporphyrin is an intermediate in heme biosynthesis. It is formed in the conversion of coproporphyrinogen to protoporphyrinogen and excreted excessively in the feces in harderoporphyria. [HMDB] Harderoporphyrin is an intermediate in heme biosynthesis. It is formed in the conversion of coproporphyrinogen to protoporphyrinogen and excreted excessively in the feces in harderoporphyria.
Isocoproporphyrin
C36H38N4O8 (654.2689508000001)
Isocoproporphyrin is a porphyrin derivative found in the feces and in urine for patients suffering from PCT (porphyria cutanea tarda). PCT is probably the most common of the porphyrias. It manifests as vesicle formation in sun-exposed areas, particularly the dorsum of the hands, A finding that is virtually diagnostic of PCT is the presence of isocoproporphyrin in stool. A porphyrin derivative found in the feces and in urine for patients suffering from PCT (porphyria cutanea tarda). PCT is probably the most common of the porphyrias. It manifests as vesicle formation in sun-exposed areas, particularly the dorsum of the hands, A finding that is virtually diagnostic of PCT is the presence of isocoproporphyrin in stool [HMDB]
Hydroxypropionic porphyrin III
Hydroxypropionic porphyrin III is a porphyrin isolated only in patients with porphyria cutanea tarda. Porphyria cutanea tarda (PCT) is a metabolic disorder of haeme biosynthesis caused by decreased activity of uroporphyrinogen decarboxylase. Porphyria cutanea tarda is manifest by fragility, erosions, bullae, milia and scars on sun-exposed skin. Excess porphyrins in the skin interact with light of approximately 400 nm-wavelength radiant energy, forming reactive oxygen species. Porphyria cutanea tarda is categorized as familial, acquired or toxic. Factors that may induce clinical expression of PCT in susceptible individuals include alcohol, oestrogen, iron, polyhalogenated compounds and viral infections. Porphyria cutanea tarda is associated with an increased incidence of the haemochromatosis gene. Treatments for PCT include withdrawal of aggravating factors, phlebotomy and oral antimalarial medications. Porphyria cutanea tarda is associated with hepatic iron overload and responds to iron-reduction therapy. Porphyria cutanea tarda is the most common porphyria, followed by acute intermittent porphyria and erythropoietic protoporphyria. The molecular genetics of the porphyrias is very heterogenous. (PMID: 16315139, 7655298, 11105361) [HMDB] Hydroxypropionic porphyrin III is a porphyrin isolated only in patients with porphyria cutanea tarda. Porphyria cutanea tarda (PCT) is a metabolic disorder of haeme biosynthesis caused by decreased activity of uroporphyrinogen decarboxylase. Porphyria cutanea tarda is manifest by fragility, erosions, bullae, milia and scars on sun-exposed skin. Excess porphyrins in the skin interact with light of approximately 400 nm-wavelength radiant energy, forming reactive oxygen species. Porphyria cutanea tarda is categorized as familial, acquired or toxic. Factors that may induce clinical expression of PCT in susceptible individuals include alcohol, oestrogen, iron, polyhalogenated compounds and viral infections. Porphyria cutanea tarda is associated with an increased incidence of the haemochromatosis gene. Treatments for PCT include withdrawal of aggravating factors, phlebotomy and oral antimalarial medications. Porphyria cutanea tarda is associated with hepatic iron overload and responds to iron-reduction therapy. Porphyria cutanea tarda is the most common porphyria, followed by acute intermittent porphyria and erythropoietic protoporphyria. The molecular genetics of the porphyrias is very heterogenous. (PMID: 16315139, 7655298, 11105361).
Heptacarboxylporphyrin I
Heptacarboxylporphyrin I is a bile product that arises from the conversion of Heptacarboxylporphyrinogen I to Heptacarboxylporphyrin I by porphyrinogen carboxy-lyase (EC 4.1.1.37). [HMDB] Heptacarboxylporphyrin I is a bile product that arises from the conversion of Heptacarboxylporphyrinogen I to Heptacarboxylporphyrin I by porphyrinogen carboxy-lyase (EC 4.1.1.37).
Hexacarboxylporphyrin I
Hexacarboxylporphyrin I is a bile product that arises from the conversion of Hexacarboxylporphyrinogen I to Hexacarboxylporphyrin I by porphyrinogen carboxy-lyase (EC 4.1.1.37). A bile product that arises from the conversion of Hexacarboxylporphyrinogen I to Hexacarboxylporphyrin I by porphyrinogen carboxy-lyase (EC 4.1.1.37). [HMDB]
Porphinehexacarboxylic acid
Porphinehexacarboxylic acid is a porphyrinogen intermediate metabolite in the catalytic decarboxylation of the acetate groups on the rings A, B, C and D of uroporphyrinogen III to coproporphyrinogen III, a process mediated by Uroporphyrinogen decarboxylase (EC 4.1.1.37), a cytosolic haem-biosynthetic enzyme (PMID: 8424794) [HMDB] Porphinehexacarboxylic acid is a porphyrinogen intermediate metabolite in the catalytic decarboxylation of the acetate groups on the rings A, B, C and D of uroporphyrinogen III to coproporphyrinogen III, a process mediated by Uroporphyrinogen decarboxylase (EC 4.1.1.37), a cytosolic haem-biosynthetic enzyme (PMID: 8424794).
Pentacarboxylporphyrin I
C37H38N4O10 (698.2587808000001)
Pentacarboxylporphyrin I is a bile product that arises from the conversion of Pentacarboxylporphyrinogen I to Pentacarboxylporphyrin I by porphyrinogen carboxy-lyase (EC 4.1.1.37). A bile product that arises from the conversion of Pentacarboxylporphyrinogen I to Pentacarboxylporphyrin I by porphyrinogen carboxy-lyase (EC 4.1.1.37). [HMDB]
Dimethylprotoporphyrin IX dimethyl ester
The hepatic pigment accumulated as a consequence of the self-catalyzed destruction of cytochrome P-450 by norethisterone (PubMed ID 284396 ) [HMDB] The hepatic pigment accumulated as a consequence of the self-catalyzed destruction of cytochrome P-450 by norethisterone (PubMed ID 284396 ).
Pseudouroporphyrin
Porphyrins excreted in various types of porphyria (PubMed ID 5917679 ). Intermediate of haem biosynthesis (PubMed ID 1216185). Porphyrins excreted in various types of porphyria (PubMed ID 5917679 ).
Uroporphyrin II
Uroporphyrin is the porphyrin produced by oxidation of the methylene bridges in uroporphyrinogen. They have four acetic acid and four propionic acid side chains attached to the pyrrole rings. Uroporphyrinogen I and III are formed from polypyrryl methane in the presence of uroporphyrinogen III cosynthetase and uroporphyrin I synthetase, respectively. They can yield uroporphyrins by autooxidation or coproporphyrinogens by decarboxylation. Excessive amounts of uroporphyrin I are excreted in congenital erythropoietic porphyria, and both types I and III are excreted in porphyria cutanea tarda. Uroporphyrin I and III are the most common isomemrs. Uroporphyrin II is a rare isomer. Uroporphyrin is the porphyrin produced by oxidation of the methylene bridges in uroporphyrinogen. They have four acetic acid and four propionic acid side chains attached to the pyrrole rings. Uroporphyrinogen I and III are formed from polypyrryl methane in the presence of uroporphyrinogen III cosynthetase and uroporphyrin I synthetase, respectively. They can yield uroporphyrins by autooxidation or coproporphyrinogens by decarboxylation.
Uroporphyrin IV
Uroporphyrin is the porphyrin produced by oxidation of the methylene bridges in uroporphyrinogen. They have four acetic acid and four propionic acid side chains attached to the pyrrole rings. Uroporphyrinogen I and III are formed from polypyrryl methane in the presence of uroporphyrinogen III cosynthetase and uroporphyrin I synthetase, respectively. They can yield uroporphyrins by autooxidation or coproporphyrinogens by decarboxylation. Excessive amounts of uroporphyrin I are excreted in congenital erythropoietic porphyria, and both types I and III are excreted in porphyria cutanea tarda. Uroporphyrin I and III are the most common isomemrs. Uroporphyrin IV is a rare isomer; Formed together with the other Uroporphyrin isomers by the nonenzymic acid-catalysed polymerisation and oxidation of Porphobilinogen (Combined Chemical Dictionary). Uroporphyrin is the porphyrin produced by oxidation of the methylene bridges in uroporphyrinogen. They have four acetic acid and four propionic acid side chains attached to the pyrrole rings. Uroporphyrinogen I and III are formed from polypyrryl methane in the presence of uroporphyrinogen III cosynthetase and uroporphyrin I synthetase, respectively. They can yield uroporphyrins by autooxidation or coproporphyrinogens by decarboxylation.
Hexacarboxylporphyrin III
Hexacarboxylporphyrin III is a bile product that arises from the conversion of Hexacarboxylporphyrinogen III to Hexacarboxylporphyrin III by porphyrinogen carboxy-lyase (EC 4.1.1.37). A bile product that arises from the conversion of Hexacarboxylporphyrinogen III to Hexacarboxylporphyrin III by porphyrinogen carboxy-lyase (EC 4.1.1.37). [HMDB]
Heptacarboxylporphyrin III
Heptacarboxylporphyrin III is a bile product that arises from the conversion of Heptacarboxylporphyrinogen III to Heptacarboxylporphyrin III by porphyrinogen carboxy-lyase (EC 4.1.1.37). A bile product that arises from the conversion of Heptacarboxylporphyrinogen III to Heptacarboxylporphyrin III by porphyrinogen carboxy-lyase (EC 4.1.1.37). [HMDB]
Pentacarboxyl porphyrinogen III
Substrate for erythrocyte uroporphyrinogen decarboxylase in patients with porphyria cutanea tarda (PubNed ID 1610684 ) [HMDB] Substrate for erythrocyte uroporphyrinogen decarboxylase in patients with porphyria cutanea tarda (PubNed ID 1610684 ).
Harderoporphyrinogen
C35H42N4O6 (614.3104192000001)
Harderoporphyrinogen is an intermediate in the conversion of coproporphyrinogen III and protoporphyrinogen IX. An intermediate in the conversion of coproporphyrinogen III and protoporphyrinogen IX. [HMDB]
Dehydroisocoproporphyrinogen
C36H36N4O8 (652.2533016000001)
Dehydroisocoproporphyrinogen is a member of the isocoproporphyrinogen family, a group that is excreted in only trace amounts in healthy humans, but up to 36\\% of porphyrins excreted in porphyria cutanea tarda. Formed from pentacarboxyporphyrinogen by coproporphyrinogen III oxidase (Biochem J. 1991 Jan 1;273(Pt 1):246-7). A member of the isocoproporphyrinogen family, a group that is excreted in only trace amounts in healthy humans, but up to 36\\% of porphyrins excreted in porphyria cutanea tarda. Formed from pentacarboxyporphyrinogen by coproporphyrinogen III oxidase (Biochem J. 1991 Jan 1;273(Pt 1):246-7) [HMDB]
Mesoporphyrin IX
Mesoporphyrins are porphyrins with four methyl, two ethyl, and two propionic acid side chains attached to the pyrrole rings. There are fifteen isomers of mesoporphyrin. Mesoporphyrin has anti-inflammatory action. Mesoporphyrin inhibits interferon-gamma and interleukin-6 production, which is closely related to the suppression of prostaglandin E2 generation by interfering cyclooxygenase 1 and 2 enzyme activities suggesting that the inhibition of cytokine production is one of the anti-inflammatory mechanisms of mesoporphyrin. (PMID: 10446754). Mesoporphyrins are porphyrins with four methyl, two ethyl, and two propionic acid side chains attached to the pyrrole rings. There are fifteen isomers of mesoporphyrin.
Mesohydroxy uroporphyrin III
Uroporphyrin are porphyrins with four acetic acid and four propionic acid side chains attached to the pyrrole rings. [HMDB] Uroporphyrin are porphyrins with four acetic acid and four propionic acid side chains attached to the pyrrole rings.
Hydroxyacetic acid uroporphyrin III
Uroporphyrin are porphyrins with four acetic acid and four propionic acid side chains attached to the pyrrole rings. [HMDB] Uroporphyrin are porphyrins with four acetic acid and four propionic acid side chains attached to the pyrrole rings.
Peroxyacetic acid uroporphyrin III
Uroporphyrin are porphyrins with four acetic acid and four propionic acid side chains attached to the pyrrole rings. [HMDB] Uroporphyrin are porphyrins with four acetic acid and four propionic acid side chains attached to the pyrrole rings.
Inosine 2',3'-cyclic phosphate
C10H11N4O7P (330.03653460000004)
Inosine-2′,3′-cyclic phosphate is a cyclic nucleotide. A cyclic nucleotide is any nucleotide in which the phosphate group is bonded to two of the sugars hydroxyl groups, forming a cyclical or ring structure. 2,3 cyclic IMP is a substrate for 2,3-cyclic-nucleotide 3-phosphodiesterase (EC 3.1.4.37). This enzyme (also called CNP) catalyzes the chemical reaction: nucleoside 2,3-cyclic phosphate + H2O <-> nucleoside 2-phosphate. CNP is a myelin-associated enzyme that makes up 4\\% of total CNS myelin protein, and is thought to undergo significant age-associated changes. The absence of CNP causes axonal swelling and neuronal degeneration. The biological role of cyclic 2,3 monophosphates is not clear, although it is thought to have something to do with neuronal stasis or development.
Porfimer
C99H110N12O13 (1674.8314890000001)
The purified component of hematoporphyrin derivative, it consists of a mixture of oligomeric porphyrins. It is used in photodynamic therapy (hematoporphyrin photoradiation); to treat malignant lesions with visible light and experimentally as an antiviral agent. It is the first drug to be approved in the use of photodynamic therapy in the United States. [PubChem]
Chlorophyll c
C35H32N4O5 (588.2372581999999)
Chlorophyll c is widely distributed photosynthetic pigment in marine organisms, e.g. the diatom Nitzschia closteriu