NCBI Taxonomy: 165697
Sphingopyxis (ncbi_taxid: 165697)
found 6 associated metabolites at genus taxonomy rank level.
Ancestor: Sphingomonadaceae
Child Taxonomies: Sphingopyxis terrae, Sphingopyxis soli, Sphingopyxis lutea, Sphingopyxis flava, Sphingopyxis indica, Sphingopyxis granuli, Sphingopyxis italica, environmental samples, Sphingopyxis chilensis, Sphingopyxis macrogoltabida, Sphingopyxis yananensis, Sphingopyxis solisilvae, Sphingopyxis nepalensis, Sphingopyxis alaskensis, Sphingopyxis taejonensis, Sphingopyxis bauzanensis, Sphingopyxis ginsengisoli, Sphingopyxis panaciterrae, Sphingopyxis fribergensis, Sphingopyxis jiangsuensis, unclassified Sphingopyxis, Sphingopyxis microcysteis, Sphingopyxis witflariensis, Sphingopyxis panaciterrulae, Sphingopyxis lindanitolerans
Coproporphyrin I
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.
