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Manfred O. Doss - One of the best experts on this subject based on the ideXlab platform.
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Studies on Coproporphyrin isomers in urine and feces in the porphyrias.
Clinica Chimica Acta, 1999Co-Authors: A Kühnel, Karl Jacob, U Gross, Manfred O. DossAbstract:Abstract The urinary and fecal distribution and the relative proportions of the four Coproporphyrin (copro) isomers I–IV were analysed in 20 healthy subjects and in patients suffering from one of the seven common types of hepatic or erythropoietic hereditary porphyrias. The ratios of copro isomers I–IV were analyzed by ion-pair high-performance liquid chromatography (HPLC). Observations showed significantly increased proportions of fecal copro isomer I and decreased proportions of copro isomers III, II and IV in erythropoietic porphyrias. In acute hepatic porphyrias the excretion of fecal copro isomer III is dominant (isomer III=58.4±24.0%; x ±S.D.) and significantly higher (P x ±S.D.) and chronic hepatic porphyrias (isomer III=25.8±7.6%; x ±S.D.). The increased proportions of fecal copro isomer III proved to be important for the diagnosis of hereditary coproporphyria and porphyria variegata independent of the clinical phase existing. These last two acute hepatic porphyrias also showed markedly elevated percentages of the fecal atypical isomers II and IV. In urine significantly decreased proportions of copro isomer I in acute hepatic porphyrias (isomer I=12.3±6.0%; x ±S.D.) could be observed as compared with non-acute porphyrias (isomer I=53.7±15.2%; x ±S.D.). Conversely, the proportion of urinary copro isomer III was significantly higher in acute hepatic porphyrias (isomer III=81.4±6.4%; x ±S.D.). As expected, the greatest amounts of urinary copro isomer I were found in congenital erythropoietic porphyria (isomer I=92.0±3.3; x ±S.D.) and protoporphyria with hepatobiliary complications (isomer I=81.3±10.7; x ±S.D.). The atypical urinary copro isomers II and IV were detected in all types of porphyrias ranging from 0.1 to 11.5%. The combined amounts of copro isomers II and IV show a significantly decreased percentage in congenital erythropoietic porphyria as compared with all other types of hereditary porphyrias. In conclusion, we demonstrate that the characteristic pattern of the copro isomer constellations I–IV in the various types of porphyrias are of differential diagnostic importance. The inversion of the I to III ratio in feces in hereditary coproporphyria and porphyria variegata allows the recognition of gene carriers.
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investigations on the formation of urinary Coproporphyrin isomers i iv in 5 aminolevulinic acid dehydratase deficiency porphyria acute lead intoxication and after oral 5 aminolevulinic acid loading
Clinical Biochemistry, 1999Co-Authors: Karl Jacob, Emil Egeler, Ulrich Gros, Manfred O. DossAbstract:Abstract Objectives: Investigation of the metabolism of the four urinary Coproporphyrin isomers I–IV in the extremely rare 5-aminolevulinic acid dehydratase (ALAD) deficiency porphyria (syn.: Doss porphyria), in acute lead intoxication, and after oral 5-aminolevulinic acid (ALA) loading. Design and methods: We analyzed the excretion of total urinary Coproporphyrins and the composition of the respective isomers I–IV with ion-pair HPLC methods in these conditions. Results: The concentration of total Coproporphyrins was about 30-fold increased in patients with ALAD deficiency porphyria and acute lead intoxication as compared with controls. In addition, the proportion of Coproporphyrin III as well as that of the atypical isomers II and IV were significantly elevated at the expense of isomer I. After oral ALA administration to normal volunteers, a 10- to 15-fold increase in the maximal concentration of total urinary Coproporphyrins was observed within 12 to 24 h. Urinary levels were back to normal after another 24 h. The excretion pattern of the individual urinary Coproporphyrin isomers I–IV after ALA ingestion revealed a dynamic process: initially isomer III was preferentially formed, followed by a 3-fold increase of isomers II and IV via non-enzymatic rearrangement of isomer III, and finally normalization of all four isomers occurred within 48 h. Conclusions: These results demonstrate that oral ALA loading can be used as an in vivo model to study the metabolism of the four urinary Coproporphyrin isomers I–IV especially in ALAD deficiency porphyria and in acute lead poisoning.
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Excretion pattern of faecal Coproporphyrin isomers I-IV in human porphyrias.
Clinical Chemistry and Laboratory Medicine, 1995Co-Authors: Karl Jacob, Manfred O. DossAbstract:The relative proportions of the four Coproporphyrin isomers I- IV were analysed in faeces of 20 healthy subjects and 60 patients suffering from one of the seven common types of hepatic or erythropoietic hereditary porphyrias. A newly developed, reliable method for sample preparation was applied, using reversed-phase thin-layer chromatography for the isolation of naturally occurring Coproporphyrin free carboxylic acids. Accurate separation and quantitation of the individual isomers I-IV were achieved with the help of ion-pair high-performance liquid chromatography. The four Coproporphyrin isomers I-IV were positively identified by on-line scanning of their fluorescence spectra in the emission and excitation modes. Recovery rates with this new analytical procedure were between 90 and 100%, and coefficients of variation varied between 0.8 and 5.7% (N = 7). Diagnostically important findings were greatly increased proportions of isomer I and decreased proportions of isomers III, II and IV in erythropoietic porphyrias, such as congenital erythropoietic porphyria and protoporphyria. Significantly increased proportions of isomers III, II and IV, on the other hand, were observed in acute hepatic porphyrias, e. g. acute intermittent porphyria and porphobilinogen synthase deficiency porphyria, as compared with porphyria cutanea tarda (p < 0.005 and p < 0.03, respectively). Inversion of the faecal Coproporphyrin III to I ratios and markedly elevated percentages of the atypical isomers II and IV were important diagnostic markers for variegate porphyria and hereditary coproporphyria. The highest proportions of isomer III were found in hereditary coproporphyria, where the amount of the isomers II and IV exceeded that of isomer I. Asymptomatic carriers of the relevant gene defect in families with hereditary coproporphyria could be detected by an increased faecal Coproporphyrin III to I ratio. Our results clearly demonstrate the potential of faecal Coproporphyrin I-IV isomer ratios for the diagnosis and differential diagnosis of hereditary porphyrias.
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Excretion Pattern of Faecal Coproporphyrin Isomers I—IV in Human Porphyrias1)
1995Co-Authors: Eur J Clin, Karl Jacob, Chem Clin Biochem, Manfred O. DossAbstract:Summary: The relative proportions of the four Coproporphyrin isomers I—IV were analysed in faeces of 20 healthy subjects and 60 patients suffering from one of the seven common types of hepatic or erythropoietic hereditary porphyrias. A newly developed, reliable method for sample preparation was applied, using reversed-phase thin-layer chromatography for the isolation of naturally occurring Coproporphyrin free carboxylic acids. Accurate separa-tion and quantitation of the individual isomers I—IV were achieved with the help of ion-pair high-performance liquid chromatography. The four Coproporphyrin isomers I—IV were positively identified by on-line scanning of their fluorescence spectra in the emission and excitation modes. Recovery rates with this new analytical procedure were between 90 and 100%, and coefficients of variation varied between 0.8 and 5.7 % (N = 7). Diagnostically important findings were greatly increased proportions of isomer I and decreased proportions of isomers III, II and IV in erythropoietic porphyrias, such as congenital erythropoietic porphyria and protoporphyria. Significantly increased proportions of isomers III, II and IV, on the other hand, were observed in acute hepatic porphyrias, e. g. acute intermittent porphyria and porphobilinogen synthase deficiency porphyria, as compared with porphyria cutanea tarda (p < 0.005 and p < 0.03, respectively). Inversion of the faecal Coproporphyrin to I ratios and markedly elevated percentages of the atypical isomers II and IV were important diagnostic markers for variegate porphyria and hereditary coproporphyria. The highes
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composition of urinary Coproporphyrin isomers i iv in human porphyrias
Clinical Chemistry and Laboratory Medicine, 1993Co-Authors: Karl Jacob, Manfred O. DossAbstract:The urinary distribution and relative proportions of the four Coproporphyrin isomers I-IV were investigated in 50 patients suffering from hepatic and erythropoietic types of hereditary porphyrias. A highly efficient sample preparation method was applied to isolate urinary Coproporphyrins, the isomer ratios of which were quantitated by isocratic ion-pair high-performance liquid chromatography. Results showed a significant decrease (p < 0.001) of the proportion of Coproporphyrin I in acute hepatic porphyria (acute intermittent porphyria, hereditary coproporphyria, variegate porphyria, porphobilinogen synthase deficiency porphyria) as compared with chronic hepatic porphyria (porphyria cutanea tarda, chronic hepatic porphyria type B and C) (13.2 +/- 5.3%, mean +/- S.D., vs. 31.4 +/- 11.5%). Conversely, the proportion of isomer III was significantly higher (p < 0.001) in acute hepatic porphyria than in chronic hepatic porphyria (80.9 +/- 5.2% vs. 62.2 +/- 10.9%). As expected, the highest level of Coproporphyrin I (90.0 +/- 1.9%) was found in congenital erythropoietic porphyria. The atypical Coproporphyrins II and IV were detected in all types of porphyria analysed and ranged from 0.2 to 9.0%; no significant differences were seen between acute and chronic hepatic porphyrias. The diagnostic importance of the isomer ratios of Coproporphyrins I and III has been confirmed in our study, while the significance of the atypical Coproporphyrin isomers II and IV is still unclear at present.
Karl Jacob - One of the best experts on this subject based on the ideXlab platform.
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molecular immunological enzymatic and biochemical studies of Coproporphyrinogen oxidase deficiency in a family with hereditary coproporphyria
Cellular and Molecular Biology, 2002Co-Authors: Udo Groß, U Meissauer, Alexandra Kühnel, Jean-charles Deybach, Yves Nordmann, Pavel Martásek, Karl Jacob, Mirko DossAbstract:: A 27-year-old woman who had recurrent pain in renal bed since 1998 with increasing character, was stationary admitted. The patient showed dark urine, complained of hair loss and took since 1994 a hormonal oral contraceptive. No photosensitivity was observed. Determinations of urinary porphyrin metabolites in 1998 revealed a porphyria cutanea tarda like excretion pattern with elevations of uro- (1767 nmol/24 hr, normal <29 nmol/24 hr) and heptacarboxyporphyrin (568 nmol/24 hr; normal <4 nmol/24 hr). Follow-up studies in feces showed the characteristics of a hereditary coproporphyria with dominance of Coproporphyrin isomer III (total= 1470 nmol/g, isomer III= 93%), (normal: <37 nmol/g, isomer III = 25-35%). The excretion of porphyrin precursors (delta-aminolevulinic acid and porphobilinogen) was increased by taking an ethinylestradiol-cyproteronacetate-preparation, but acute and/or chronic manifestations were not observed. Coproporphyrinogen oxidase activity was decreased to 35% in the patient (normal=138+/-21 pkat/g protein; x+/-s), whereas the activity of red cell uroporphyrinogen decarboxylase was normal. Her mother and both sisters could be verified as heterozygous gene carriers of hereditary coproporphyria by their urinary and fecal excretion parameters and because of reduced Coproporphyrinogen oxidase activity up to 50%. The father was normal with respect to his genotype. Molecular analysis revealed a hitherto unknown mutation with the transversion of a cytosine to thymine at nucleotide position 854 in exon 4 of the Coproporphyrinogen oxidase gene. The gene defect was confirmed by DGGE in the mother and her three daughters. The investigation of the immunological nature of the defective Coproporphyrinogen oxidase gene from the whole family revealed decreased concentrations of Coproporphyrinogen oxidase protein in the patient, her mother and her two sisters.
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Studies on Coproporphyrin isomers in urine and feces in the porphyrias.
Clinica Chimica Acta, 1999Co-Authors: A Kühnel, Karl Jacob, U Gross, Manfred O. DossAbstract:Abstract The urinary and fecal distribution and the relative proportions of the four Coproporphyrin (copro) isomers I–IV were analysed in 20 healthy subjects and in patients suffering from one of the seven common types of hepatic or erythropoietic hereditary porphyrias. The ratios of copro isomers I–IV were analyzed by ion-pair high-performance liquid chromatography (HPLC). Observations showed significantly increased proportions of fecal copro isomer I and decreased proportions of copro isomers III, II and IV in erythropoietic porphyrias. In acute hepatic porphyrias the excretion of fecal copro isomer III is dominant (isomer III=58.4±24.0%; x ±S.D.) and significantly higher (P x ±S.D.) and chronic hepatic porphyrias (isomer III=25.8±7.6%; x ±S.D.). The increased proportions of fecal copro isomer III proved to be important for the diagnosis of hereditary coproporphyria and porphyria variegata independent of the clinical phase existing. These last two acute hepatic porphyrias also showed markedly elevated percentages of the fecal atypical isomers II and IV. In urine significantly decreased proportions of copro isomer I in acute hepatic porphyrias (isomer I=12.3±6.0%; x ±S.D.) could be observed as compared with non-acute porphyrias (isomer I=53.7±15.2%; x ±S.D.). Conversely, the proportion of urinary copro isomer III was significantly higher in acute hepatic porphyrias (isomer III=81.4±6.4%; x ±S.D.). As expected, the greatest amounts of urinary copro isomer I were found in congenital erythropoietic porphyria (isomer I=92.0±3.3; x ±S.D.) and protoporphyria with hepatobiliary complications (isomer I=81.3±10.7; x ±S.D.). The atypical urinary copro isomers II and IV were detected in all types of porphyrias ranging from 0.1 to 11.5%. The combined amounts of copro isomers II and IV show a significantly decreased percentage in congenital erythropoietic porphyria as compared with all other types of hereditary porphyrias. In conclusion, we demonstrate that the characteristic pattern of the copro isomer constellations I–IV in the various types of porphyrias are of differential diagnostic importance. The inversion of the I to III ratio in feces in hereditary coproporphyria and porphyria variegata allows the recognition of gene carriers.
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investigations on the formation of urinary Coproporphyrin isomers i iv in 5 aminolevulinic acid dehydratase deficiency porphyria acute lead intoxication and after oral 5 aminolevulinic acid loading
Clinical Biochemistry, 1999Co-Authors: Karl Jacob, Emil Egeler, Ulrich Gros, Manfred O. DossAbstract:Abstract Objectives: Investigation of the metabolism of the four urinary Coproporphyrin isomers I–IV in the extremely rare 5-aminolevulinic acid dehydratase (ALAD) deficiency porphyria (syn.: Doss porphyria), in acute lead intoxication, and after oral 5-aminolevulinic acid (ALA) loading. Design and methods: We analyzed the excretion of total urinary Coproporphyrins and the composition of the respective isomers I–IV with ion-pair HPLC methods in these conditions. Results: The concentration of total Coproporphyrins was about 30-fold increased in patients with ALAD deficiency porphyria and acute lead intoxication as compared with controls. In addition, the proportion of Coproporphyrin III as well as that of the atypical isomers II and IV were significantly elevated at the expense of isomer I. After oral ALA administration to normal volunteers, a 10- to 15-fold increase in the maximal concentration of total urinary Coproporphyrins was observed within 12 to 24 h. Urinary levels were back to normal after another 24 h. The excretion pattern of the individual urinary Coproporphyrin isomers I–IV after ALA ingestion revealed a dynamic process: initially isomer III was preferentially formed, followed by a 3-fold increase of isomers II and IV via non-enzymatic rearrangement of isomer III, and finally normalization of all four isomers occurred within 48 h. Conclusions: These results demonstrate that oral ALA loading can be used as an in vivo model to study the metabolism of the four urinary Coproporphyrin isomers I–IV especially in ALAD deficiency porphyria and in acute lead poisoning.
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Excretion pattern of faecal Coproporphyrin isomers I-IV in human porphyrias.
Clinical Chemistry and Laboratory Medicine, 1995Co-Authors: Karl Jacob, Manfred O. DossAbstract:The relative proportions of the four Coproporphyrin isomers I- IV were analysed in faeces of 20 healthy subjects and 60 patients suffering from one of the seven common types of hepatic or erythropoietic hereditary porphyrias. A newly developed, reliable method for sample preparation was applied, using reversed-phase thin-layer chromatography for the isolation of naturally occurring Coproporphyrin free carboxylic acids. Accurate separation and quantitation of the individual isomers I-IV were achieved with the help of ion-pair high-performance liquid chromatography. The four Coproporphyrin isomers I-IV were positively identified by on-line scanning of their fluorescence spectra in the emission and excitation modes. Recovery rates with this new analytical procedure were between 90 and 100%, and coefficients of variation varied between 0.8 and 5.7% (N = 7). Diagnostically important findings were greatly increased proportions of isomer I and decreased proportions of isomers III, II and IV in erythropoietic porphyrias, such as congenital erythropoietic porphyria and protoporphyria. Significantly increased proportions of isomers III, II and IV, on the other hand, were observed in acute hepatic porphyrias, e. g. acute intermittent porphyria and porphobilinogen synthase deficiency porphyria, as compared with porphyria cutanea tarda (p < 0.005 and p < 0.03, respectively). Inversion of the faecal Coproporphyrin III to I ratios and markedly elevated percentages of the atypical isomers II and IV were important diagnostic markers for variegate porphyria and hereditary coproporphyria. The highest proportions of isomer III were found in hereditary coproporphyria, where the amount of the isomers II and IV exceeded that of isomer I. Asymptomatic carriers of the relevant gene defect in families with hereditary coproporphyria could be detected by an increased faecal Coproporphyrin III to I ratio. Our results clearly demonstrate the potential of faecal Coproporphyrin I-IV isomer ratios for the diagnosis and differential diagnosis of hereditary porphyrias.
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Excretion Pattern of Faecal Coproporphyrin Isomers I—IV in Human Porphyrias1)
1995Co-Authors: Eur J Clin, Karl Jacob, Chem Clin Biochem, Manfred O. DossAbstract:Summary: The relative proportions of the four Coproporphyrin isomers I—IV were analysed in faeces of 20 healthy subjects and 60 patients suffering from one of the seven common types of hepatic or erythropoietic hereditary porphyrias. A newly developed, reliable method for sample preparation was applied, using reversed-phase thin-layer chromatography for the isolation of naturally occurring Coproporphyrin free carboxylic acids. Accurate separa-tion and quantitation of the individual isomers I—IV were achieved with the help of ion-pair high-performance liquid chromatography. The four Coproporphyrin isomers I—IV were positively identified by on-line scanning of their fluorescence spectra in the emission and excitation modes. Recovery rates with this new analytical procedure were between 90 and 100%, and coefficients of variation varied between 0.8 and 5.7 % (N = 7). Diagnostically important findings were greatly increased proportions of isomer I and decreased proportions of isomers III, II and IV in erythropoietic porphyrias, such as congenital erythropoietic porphyria and protoporphyria. Significantly increased proportions of isomers III, II and IV, on the other hand, were observed in acute hepatic porphyrias, e. g. acute intermittent porphyria and porphobilinogen synthase deficiency porphyria, as compared with porphyria cutanea tarda (p < 0.005 and p < 0.03, respectively). Inversion of the faecal Coproporphyrin to I ratios and markedly elevated percentages of the atypical isomers II and IV were important diagnostic markers for variegate porphyria and hereditary coproporphyria. The highes
Vincenzo Penteriani - One of the best experts on this subject based on the ideXlab platform.
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feather content of porphyrins in eurasian eagle owl bubo bubo fledglings depends on body condition and breeding site quality
Integrative Zoology, 2018Co-Authors: Ismael Galvan, Rui Lourenco, Pablo R. Camarero, Maria Del Mar Delgado, Rafael Mateo, Vincenzo PenterianiAbstract:: Porphyrins are pigments produced in most animal cells during the synthesis of heme, but their importance for external coloration is unclear. Owls (Order Strigiformes) are among the few animals that accumulate porphyrins in the integument, where it could serve as a means of signaling. Here we hypothesized that the porphyrin content of feathers may depend on body condition and breeding site quality in Eurasian eagle owl (Bubo bubo) fledglings and, thus, constitute amplifiers of the quality of the area where they are born. Using high-performance liquid chromatography, we found 2 porphyrins (protoporphyrin IX and Coproporphyrin III) in the body feathers of 19 eagle owl fledglings from 7 breeding territories. Coproporphyrin III, but not protoporphyrin IX feather concentration, was positively associated with the body mass of fledglings and with the quality of the breeding sites where they were reared with respect to food quality and availability. As Coproporphyrin III is produced under oxidative stress, we suggest that good breeding sites may lead to fledglings in good condition. This, in turn, may make fledglings induce a certain level of free radical and Coproporphyrin III production to signal to conspecifics their site-mediated capacity to cope with oxidative stress. This is the first time that porphyrin content in the integument has been found to be related to individual quality, opening a new scenario for studying evolution of animal coloration.
Thomas J Beatty - One of the best experts on this subject based on the ideXlab platform.
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porphyrin excretion resulting from mutation of a gene encoding a class i fructose 1 6 bisphosphate aldolase in rhodobacter capsulatus
Frontiers in Microbiology, 2019Co-Authors: Hao Ding, Rafael G. Saer, Thomas J BeattyAbstract:This paper describes a mutant (called SB1707) of the Rhodobacter capsulatus wild type strain SB1003 in which a transposon-disrupted rcc01707 gene resulted in a ~25-fold increase in the accumulation of Coproporphyrin III in the medium of phototrophic (anaerobic) cultures grown in a yeast extract/peptone medium. There was little or no stimulation of pigment accumulation in aerobic cultures. Therefore, this effect of rcc01707 mutation appears to be specific for the anaerobic Coproporphyrinogen III oxidase HemN as opposed to the aerobic enzyme HemF. The protein encoded by rcc01707 is homologous to Class I fructose 1,6-bisphosphate aldolases, which catalyze a glycolytic reaction that converts fructose 1, 6-bisphosphate to dihydroxyacetone phosphate and glyceraldehyde 3-phosphate, precursors of pyruvate. There were significant differences in Coproporphyrin III accumulation using defined media with individual organic acids and sugars as the sole carbon source: pyruvate, succinate and glutamate stimulated accumulation the most, whereas glucose suppressed Coproporphyrin III accumulation to 10% of that of succinate. However, although quantitatively lesser, similar effects of carbon source on the amount of accumulated pigment in the culture medium were seen in a wild type control. Therefore, this mutation appears to exaggerate effects also seen in the wild type strain. It is possible that mutation of rcc01707 causes a metabolic bottleneck or imbalance that was not rectified during growth on the several carbon sources tested. However, we speculate that, analogous to other fructose 1,6-bisphosphate aldolases, the rcc01707 gene product has a "moonlighting" activity that in this case is needed for the maximal expression of the hemN gene. Indeed, it was found that the rcc01707 gene is needed for maximal expression of a hemN promoter-lacZ reporter. With the decrease in hemN expression due to the absence of the rcc01707 gene product, Coproporphyrinogen III accumulates and is released from the cell, yielding the spontaneous oxidation product Coproporphyrin III.
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Data_Sheet_1_Porphyrin Excretion Resulting From Mutation of a Gene Encoding a Class I Fructose 1,6-Bisphosphate Aldolase in Rhodobacter capsulatus.PDF
2019Co-Authors: Hao Ding, Rafael G. Saer, Thomas J BeattyAbstract:This paper describes a mutant (called SB1707) of the Rhodobacter capsulatus wild type strain SB1003 in which a transposon-disrupted rcc01707 gene resulted in a ∼25-fold increase in the accumulation of Coproporphyrin III in the medium of phototrophic (anaerobic) cultures grown in a yeast extract/peptone medium. There was little or no stimulation of pigment accumulation in aerobic cultures. Therefore, this effect of rcc01707 mutation appears to be specific for the anaerobic Coproporphyrinogen III oxidase HemN as opposed to the aerobic enzyme HemF. The protein encoded by rcc01707 is homologous to Class I fructose 1,6-bisphosphate aldolases, which catalyze a glycolytic reaction that converts fructose 1, 6-bisphosphate to dihydroxyacetone phosphate and glyceraldehyde 3-phosphate, precursors of pyruvate. There were significant differences in Coproporphyrin III accumulation using defined media with individual organic acids and sugars as the sole carbon source: pyruvate, succinate and glutamate stimulated accumulation the most, whereas glucose suppressed Coproporphyrin III accumulation to 10% of that of succinate. However, although quantitatively lesser, similar effects of carbon source on the amount of accumulated pigment in the culture medium were seen in a wild type control. Therefore, this mutation appears to exaggerate effects also seen in the wild type strain. It is possible that mutation of rcc01707 causes a metabolic bottleneck or imbalance that was not rectified during growth on the several carbon sources tested. However, we speculate that, analogous to other fructose 1,6-bisphosphate aldolases, the rcc01707 gene product has a “moonlighting” activity that in this case is needed for the maximal expression of the hemN gene. Indeed, it was found that the rcc01707 gene is needed for maximal expression of a hemN promoter-lacZ reporter. With the decrease in hemN expression due to the absence of the rcc01707 gene product, Coproporphyrinogen III accumulates and is released from the cell, yielding the spontaneous oxidation product Coproporphyrin III.
Rafael Mateo - One of the best experts on this subject based on the ideXlab platform.
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feather content of porphyrins in eurasian eagle owl bubo bubo fledglings depends on body condition and breeding site quality
Integrative Zoology, 2018Co-Authors: Ismael Galvan, Rui Lourenco, Pablo R. Camarero, Maria Del Mar Delgado, Rafael Mateo, Vincenzo PenterianiAbstract:: Porphyrins are pigments produced in most animal cells during the synthesis of heme, but their importance for external coloration is unclear. Owls (Order Strigiformes) are among the few animals that accumulate porphyrins in the integument, where it could serve as a means of signaling. Here we hypothesized that the porphyrin content of feathers may depend on body condition and breeding site quality in Eurasian eagle owl (Bubo bubo) fledglings and, thus, constitute amplifiers of the quality of the area where they are born. Using high-performance liquid chromatography, we found 2 porphyrins (protoporphyrin IX and Coproporphyrin III) in the body feathers of 19 eagle owl fledglings from 7 breeding territories. Coproporphyrin III, but not protoporphyrin IX feather concentration, was positively associated with the body mass of fledglings and with the quality of the breeding sites where they were reared with respect to food quality and availability. As Coproporphyrin III is produced under oxidative stress, we suggest that good breeding sites may lead to fledglings in good condition. This, in turn, may make fledglings induce a certain level of free radical and Coproporphyrin III production to signal to conspecifics their site-mediated capacity to cope with oxidative stress. This is the first time that porphyrin content in the integument has been found to be related to individual quality, opening a new scenario for studying evolution of animal coloration.
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altered porphyrin excretion and histopathology of greylag geese anser anser exposed to soil contaminated with lead and arsenic in the guadalquivir marshes southwestern spain
Environmental Toxicology and Chemistry, 2006Co-Authors: Rafael Mateo, Mark A Taggart, Andy J Green, C Cristofol, Antoni Ramis, H Lefranc, Jordi Figuerola, Andrew A MehargAbstract:Greylag geese (Anser anser) in the Guadalquivir Marshes (southwestern Spain) can be exposed to sources of inorganic pollution such as heavy metals and arsenic from mining activities or Pb shot used for hunting. We have sampled 270 fecal excreta in different areas of the marshes in 2001 to 2002 to evaluate the exposure to Pb, Zn, Cu, Mn, and As and to determine its relationship with soil ingestion and with the excretion of porphyrins and biliverdin as biomarkers. These effects and the histopathology of liver, kidney, and pancreas were also studied in 50 geese shot in 2002 to 2004. None of the geese had ingested Pb shot in the gizzard. This contrasts with earlier samplings before the ban of Pb shot for waterfowl hunting in 2001 and the removal of Pb shot in points of the Donana National Park (Spain) in 1999 to 2000. The highest exposure through direct soil ingestion to Pb and other studied elements was observed in samples from Entremuros, the area of the Donana Natural Park affected by the Aznalcollar mine spill in 1998. Birds from Entremuros also more frequently showed mononuclear infiltrates in liver and kidney than birds from the unaffected areas, although other more specific lesions of Pb or Zn poisoning were not observed. The excretion of Coproporphyrins, especially of the isomer I, was positively related to the fecal As concentration, and the ratio of Coproporphyrin III/I was positively related to fecal Pb concentration. Biliary protoporphyrin IX concentration was also slightly related to hepatic Pb concentration. This study reflects biological effects on terrestrial animals by the mining pollution in Donana that can be monitored with the simple noninvasive sampling of feces.