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At least 19 recordsLinked to original sources
PubMed1977

Production of copper coproporphyrin III by Bacillus cereus. II. Regulation of the biosynthesis of coproporphyrin III and its copper complex by oxygen and heavy metal ions.

The effects of oxygen and heavy metal ions on the production of copper coproporphyrin III were studied in Bacillus cereus strain 2. The formation of copper coproporphyrin III was found to be maximum when the cells were cultivated in G-medium at a low level of oxygen supply, but it was suppressed at extremely low oxygen supply levels. When the cells were cultured in metal-free G-medium, neither metal-coproporphyrin III nor coproporphyrin III was formed. In the presence of copper in the medium (400-100 micrometers), the formation of coproporphyrin III copper salt was maximum, but the addition of various heavy metal ions other than copper to the copper-free medium resulted in the formation of neither coproporphyrin III nor its metal chelates. Copper ions appear to be specifically required for coproporphyrin III formation.

Bacillus cereus↗
PubMed1976

Coproporphyrin isomers in Dubin-Johnson syndrome.

To shed light on the nature of abnormal porphyrin metabolism in Dubin-Johnson syndrome (DJS), coproporphyrin isomer distribution in urine and bile was investigated in carriers and patients with DJS selected from among the families in the cluster area of the syndrome in Japan. Urinary total coproporphyrin content in patients with DJS exceeded that of normal controls (P less than 0.01). However, the increase in urinary excretion of total coproporphyrin was of a much lesser degree compared to a remarkable increase in urinary total coproporphyrin reported for erythropoietic porphyria in which a deficiency of uroporphyrinogen III cosynthetase had been demonstrated. Urinary total coproporphyrin content in carriers was significantly smaller than that of normal controls (P less than 0.05). This paradoxical decrease of urinary total coproporphyrin concentration in DJS carriers was observed in consequence of a decrease in coproporphyrin III excretion without concomitant increase in type I isomer. Administration of griseofulvin, in the dose which had been shown to precipitate attacks of acute porphyria in susceptible subjects, to carriers and patients with DJS did not elicit clinical signs suggestive of porphyria, and urinary total coproporphyrin concentration and the percentage of coproporphyrin I remained unchanged. These results were interpreted to demonstrate an aspect of DJS that was not consistent with the hypothesis that a partial defect in uroporphyrinogen III cosynthetase of the liver might be the cause of DJS. Coproporphyrin in the bile of DJS patients was preponderantly type I.

Bile↗
PubMed1982

Urinary coproporphyrin excretion in Rotor's syndrome: a family study.

A family of seven is described in which a teenage boy and two siblings were found to have Rotor's syndrome. Total urinary coproporphyrin excretion was found to be significantly elevated in the patients with Rotor's syndrome (mean 59 . 0 mumol/mol creatinine), when compared with control subjects (mean 16 . 3 mumol/mol creatinine) (p less than 0 . 005). Similarly, urinary excretion of both coproporphyrin isomer I and coproporphyrin isomer III was greater in the subjects with Rotor's syndrome than in controls (p less than 0 . 005). Coproporphyrin I comprised 60 . 2% of total urinary coproporphyrin excretion in the subjects with Rotor's syndrome, compared with 38 . 6% in the controls, but the difference was not significant. In the parents and clinically unaffected siblings neither total urinary coproporphyrin excretion (13 . 3 and 19 . 3 mumol/mol creatinine respectively) nor percentage coproporphyrin I excretion (36 . 8 and 30 . 4%) differed from controls. Thus, although we have confirmed the previous finding of increased urinary coproporphyrin excretion in subjects with Rotor's syndrome, we have not found the previously noted intermediate increase in coproporphyrin I excretion amongst phenotypically normal relatives of subjects with this autosomal recessive disorder.

Adolescent↗
PubMed2004

Rapid and simultaneous determination of coproporphyrin and protoporphyrin in feces by derivative matrix isopotential synchronous fluorescence spectrometry.

BACKGROUND: Measurement of fecal porphyrins is important in the diagnosis of porphyria, but conventional methods to measure them have drawbacks. We explored the use of derivative matrix isopotential synchronous fluorescence (MISF) spectrometry for the measurement of coproporphyrin and protoporphyrin. METHODS: The MISF scanning route was selected based on information from the three-dimensional fluorescence spectrum, which was a combination of the contour line of protoporphyrin via a detection point of coproporphyrin and that of coproporphyrin via a detection point of protoporphyrin. Derivative technique eliminated the constant interfering signals. MISF was used to measure porphyrins in stools from 2 pregnant women and 20 healthy volunteers. RESULTS: The coproporphyrin and protoporphyrin spectra were resolved with almost no mutual interference. The amplitudes of the derivative peaks were linearly related to the concentrations of coproporphyrin up to 310 nmol/L and protoporphyrin up to 590 nmol/L. The detection limits for coproporphyrin and protoporphyrin were 1.2 and 1.7 nmol/L, respectively. The within-run imprecision (CV; n = 6) was 2.2% at 175 nmol/L for coproporphyrin and 2.3% at 500 nmol/L for protoporphyrin. Bland-Altman analysis indicated no significant differences between the proposed MISF method and conventional spectrophotometry or fluorimetry. Mean (SD) recoveries of porphyrins added to fecal samples were of 98 (7)% for coproporphyrin and 102 (4)% for protoporphyrin. CONCLUSIONS: This technique provides spectral resolution of coproporphyrin and protoporphyrin, obviating the need for chromatographic separation, and measurements can be made in a single scanning. The method also appears suitable for routine testing of large numbers of samples.

Coproporphyrins↗
PubMed1988

[Renal and enteral elimination of coproporphyrin isomers in Rotor's syndrome. A family study].

Urinary and fecal total, isomer I, and isomer III coproporphyrin excretion of a Rotor's syndrome patient and his family were determined. The propositus showed increased urinary total coproporphyrin excretion (248 micrograms/24 h) and a shift of the coproporphyrin isomer I/III relation (70%/30%). The propositus's father and two siblings also had elevated renal excretion of coproporphyrin I. Total coproporphyrin excretion was enhanced only in the propositus's father and one sibling, while being normal in another sibling. All family members that could be investigated showed considerably decreased fecal porphyrin excretion. In Rotor's syndrome porphyrin excretion is mainly renal. The coproporphyrin isomer I/III relation is shifted towards isomer I. Phenotypically normal relatives with normal bilirubin plasma levels may have alterations in both their renal and enteral coproporphyrin excretion.

Adult↗
PubMed1999

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.

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.

Administration, Oral↗