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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↗
PubMed1976

Multicompartment analysis of 14C-labelled coproporphyrin and uroporphyrin kinetics in human beings.

14C-labelled coproporphyrin I and III and uroporphyrin I were injected intravenously into healthy human subjects. Two experiments were performed with each porphyrin. Counting of blood, urine and faeces was made as a function of time. The coproporphyrin data were simulated by means of an analogy computer by using a four-compartment model with a delay pool. The physiological counterparts to the compartments were considered to be liver, blood and gut. From the blood radioactivity disappearance curve of uroporphyrin three exponential components could be worked out. The least square method was used for the solution of the plasma and urine radioactivity curves. A three-compartment model was constructed to illustrate the kinetics of uroporphyrin I. Coproporphyrin I and III behaved essentially similarly, whilst the kinetic behaviour of uroporphyrin I was completely different from that of coproporphyrins. A rapid hepatic uptake, preferential faecal excretion and a significant enterohepatic circulation were features of coproporphyrin kinetics. Over 70 per cent of the tracer activity of uroporphyrin I was found to accumulate to a rather large pool (volume 16--28 times the plasma volume) from where the back flow to plasma was rather slow. Practically all the uroporphyrin was excreted via urine.

Adult↗
PubMed1991

[Determination of coproporphyrin in urine].

Methods for urinary coproporphyrin measurements are analyzed. Data obtained by two methods, spectrophotometry and fluorescent method, are presented, the advantages and shortcomings of both are discussed. The authors recommend the fluorescent technique as a universal rapid method for wide medical practice. The problem of the units of coproporphyrin measurement is also discussed. The authors suggest replacing measurements per g of creatinine or daily portion by estimation of the coproporphyrin index in the morning portion of the urine. Study of the effects of various factors (climatic conditions, nutrition, patient's age and sex) on normal coproporphyrin excretion from the body has demonstrated that these factors do not noticeably influence porphyrin metabolism; for normal subjects the coproporphyrin index varies from 30 to 110 micrograms/day.

Adult↗
PubMed1978

Copper coproporphyrin excretion in familial coproporphyria.

Analysis of stool specimens from a patient with familial coproporphyria by high-performance liquid chromatography revealed that 112 microgram per gram of dry feces (14% of the total porphyrin present) was copper coproporphyrin. Examination of stool specimens from other patients with this disease confirmed the presence of significant amounts of both copper coproporphyrin and coproporphyrin. Further investigation showed that the copper coproporphyrin was probably formed by a nonenzymic incorporation of copper by the coproporphyrin in either the bile or feces.

Adolescent↗
PubMed1991

Isolation and characterization of zinc coproporphyrin I: a major fluorescent component in meconium.

We isolated a substance from an organic extract of meconium (in neutral pH) that exhibited a porphyrin-like fluorescence peak at 580 nm on excitation at 405 nm and deduced its structure. Spectrometric data suggest that the substance is not free coproporphyrin I or free coproporphyrin III, but is a chelate of coproporphyrin I with Zn2+. We also detected a chelate of coproporphyrin III with Zn2+ by HPLC. These substances may be useful as new indicators of the presence of meconium.

Amniotic Fluid↗
PubMed1991

Characterization of a coproporphyrin-protein complex from Rhodobacter capsulatus.

Rhodobacter capsulatus strain AJB530 excretes large amounts of coproporphyrin into the culture supernatant. The coproporphyrin was precipitable with ammonium sulfate, suggesting that it was part of a macromolecular complex. Analysis of an ammonium sulfate fraction indicated that the coproporphyrin was bound to a 66-kDa protein with a pI' of 4.0. The same protein was found in the culture supernatant of the bch+ strain PAS100.

Bacterial Proteins↗
PubMed1991

Application of ion-pair high-performance liquid chromatography to detection of the atypical coproporphyrin isomers II and IV in human faeces.

A highly selective and sensitive method has been developed for the detection of small amounts of the atypical isomers II and IV of coproporphyrin in human faeces. This method combines liquid-liquid extraction and solid-phase sampling techniques using talc and C18-modified silica gel as the sorbents. Simultaneous separation of the four coproporphyrin isomers I-IV was achieved by isocratic ion-pair high-performance liquid chromatography. Stool samples of healthy subjects (n = 12) contained 1.1 +/- 0.4% (mean +/- S.D.) isomer II and 2.2 +/- 0.9% isomer IV of total coproporphyrins. A somewhat higher content of isomer II (2.7%) and isomer IV (5.4%) was found in faeces of a patient suffering from porphyria variegata.

Chromatography, High Pressure Liquid↗
PubMed1978

The effects of water restriction and water loading on urinary excretion of lead, delta-aminolevulinic acid and coproporphyrin.

Alterations in daily urinary excretion of lead, delta-aminolevulinic acid (ALA), coproporphyrin, creatinine and total solutes following water restriction and water loading were examined in nine lead workers. Excretion of lead, ALA and total solutes was significantly decreased when urinary volume was reduced, showing that these values are dependent on urinary volume: conversely, excretion of coproporphyrin and creatinine was independent of urinary volume. Excretion of lead and total solutes was also dependent on creatinine excretion. The renal excretory mechanism of lead, ALA and coproporphyrin is discussed in the light of these findings.

Adult↗
PubMed1976

[Study of the mechanism of the effect of extracellular pH on the synthesis of the oxidative complex (cytochrome a+a3) of Bacillus coagulans: relationship to the "glucose effect" and role of excreted coproporphyrin III (author's transl)].

During the "respiratory adaptation" of Bacillus coagulans, it was possible to dissociate the kinetics of cytochrome a and a3 synthesis with carbon monoxide. The synthesis of cytochrome a3 is preferentially repressed when the pH of the incubation medium is pH 6.5 instead of pH 5.5. However, though the total synthesis of tetrapyrrole compounds is the same at both pH values, the excretion of coproporphyrin III is much increased at pH 6.5. Bacillus coagulans, sensitive to the "glucose effect", shows the "pH effect" only in the presence of high glucose concentrations. The repression of the oxidase complex synthesis by a slight increase of the extracellular pH appears directly related to the increase of the extracellular coproporphyrin III.

Aerobiosis↗
PubMed1978

A mutant of Escherichia coli which accumulates large amounts of coproporphyrin.

A mutant of Escherichia coli which accumulates a large amount of coproporphyrin, presumably because of a block in heme biosynthesis, has been isolated after nitrosoguanidine mutagenesis. On rich media, the mutant forms colonies which give bright orange fluorescence when illuminated with ultraviolet light. The mutant appears to be similar to a Salmonella typhimurium mutant, deficient in uroporphyrinogen III cosynthase, described by Sasarman and Desrochers ((1976) J. Bacteriol. 128, 717--721). A striking property of the mutant is that coproporphyrin is retained within the cells in rich media but is almost totally excreted out of cells in minimal glucose medium.

Coproporphyrins↗
PubMed1991

The isomer ratios of urinary coproporphyrins I--IV are pH-dependent.

The percentage of porphyrinogens as related to total porphyrin excretion was determined in the urine of healthy subjects. Acidic urines (pH 5.0 to 5.9) contained 62.9 +/- 10.7% (means +/- s, N = 11) porphyrinogens, whereas in neutral urines (pH 6.0 to 7.2) a somewhat lower percentage (51.2 +/- 15.3%, N = 11) was detected. However, there was no significant difference between the mean porphyrinogen contents of acidic and neutral urines. Evidence was found for a previously unreported pH-dependent influence on the isomer ratios of urinary coproporphyrins I and III. Acidic urines (N = 18) from healthy subjects showed significantly higher percentages of isomer I (27.1 +/- 6.4%), isomer II (2.7 +/- 1.1%), and isomer IV (5.0 +/- 1.3%) as compared to respective values from neutral urines (22.2 +/- 5.1% isomer I, 0.6 +/- 0.6% isomer II, and 1.5 +/- 1.3% isomer IV; N = 16, p less than 0.001). Conversely, the percentage of isomer III was markedly lower in acidic urines than in neutral urines (65.1 +/- 7.9% vs. 75.9 +/- 5.4%; p less than 0.001). The same relationship was confirmed in an individual subject by analysis of a series of urines (N = 13) with pH values ranging from 5.4 to 7.3. These results point to the possibility that the atypical coproporphyrin isomers II and IV are predominantly formed by an increased isomerization rate of coproporphyrinogens under acidic intravesical conditions.

Chromatography, High Pressure Liquid↗
PubMed1992

Fecal coproporphyrin isomers in hereditary coproporphyria.

To see whether the fecal coproporphyrin III:coproporphyrin I (CIII:CI) ratio (determined by HPLC) would be suitable for screening patients at risk of hereditary coproporphyria (HC), we compared such ratios with the lymphocyte coproporphyrinogen oxidase (EC 1.3.3.3) activities (COOX) in 38 subjects from one large family and two smaller families with HC. The CIII:CI ratio was normal (less than 1.3) in adults with normal COOX (greater than 180 nmol/g of protein per hour) and high (greater than 2) in those with low COOX. Results were difficult to interpret in six of 10 children, who had borderline or low COOX but normal fecal CIII:CI ratios. Five subjects with low COOX and abnormal fecal CIII:CI ratios had normal fecal total porphyrin, indicating that the latter investigation alone is inadequate for family studies. The sample for determining the fecal CIII:CI ratio is easier to obtain and the assay is technically less demanding than COOX. We found the fecal CIII:CI ratio suitable for investigation of adults in a family study, but its usefulness in children needs to be established.

Adolescent↗
PubMed1977

Compensation by zinc chelation for fluorescent background in determining coproporphyrin and uroporphyrin in urine.

An improved method for separation and fluorescent analysis of coproporphyrin and uroporphyrin in urine was presented by Sobel, Cano, and Thiers [Clin. Chem. 20, 1397 (1974)]. Accurate determination of porphyrin concentrations by this method is impeded by the fluorescent background in urine samples, which varies from one specimen to another. By use of a straightforward procedure, zinc may be incorporated into coproporphyrin and uroporphyrin. Measurement of the difference in the fluorescent emission intensity at 650 nm for the porphyrin solutions before and after zinc incorporation compensates for fluorescent background and gives a more accurate determination.

Aged↗
PubMed1979

Uroporphyrin- and coproporphyrin I-accumulating mutant of Escherichia coli K12.

A new type of haem-deficient mutant was isolated in Escherichia coli K12 by neomycin selection. The mutant was deficient in uroporphyrinogen III cosynthase activity as indicated by the accumulation of uroporphyrin I and coproporphyrin. The mapping of the corresponding hemD gene by P1-mediated transduction showed that the new gene was located between ilv and cya, at min 83 on the chromosomal map of Escherichia coli K12.

Chromosome Mapping↗
PubMed1976

Effect of a short, heavy exposure to lead dust upon blood lead level, erythrocyte delta-aminolevulinic acid dehydratase activity and urinary excretion of lead delta-aminolevulinic acid coproporphyrin. Results of a 6-month follow-up of two male subjects.

During 1 h two healthy volunteers, not earlier exposed occupationally to lead, inhaled about 100 mg of lead as a mixture of lead oxides and lead sulfate. Maximum blood lead (PbB) concentrations of about 0.5 mg/1 and minimum blood cell delta-aminolevulinic acid dehydratase activities (ALAD) (6% of the preexposure values) were observed within 38 h after exposure. PbB and ALAD returned to preexposure levels after about 300 and 150 days. A highly significant correlation between ALAD and PbB was seen even at lead levels in the range 0.1-0.2 mg/1. Delta-aminolevulinic acid, coproporphyrin and lead in the urine (ALAU, CPU, and PbU, respectively) increased. The peak levels occurred after about 15 h for ALAU and CPU and after about 24 h for PbU. There was a very good correlation between log PbU and lin PbB. ALAU increased already at PbB levels of about 0.3 mg/1.

Adult↗
PubMed1992

Determining zinc coproporphyrin in maternal plasma--a new method for diagnosing amniotic fluid embolism.

We measured the concentration of zinc coproporphyrin I (ZnCP-I), a characteristic component of meconium, in maternal plasma by fluorometry after HPLC. We obtained plasma samples from 89 women: 35 at weeks 10-40 of normal pregnancy, 41 shortly after normal delivery, 4 from patients with amniotic fluid embolism (AFE), and 9 from non-AFE patients with intra- or postpartum shock caused by genital bleeding. The plasma ZnCP-I concentration was 97 (SD 83, range 38-240) nmol/L in the AFE patients, 11 (SD 9.2) nmol/L in the non-AFE patients, 12 (SD 7.9) nmol/L during normal pregnancy, and 26 (SD 10) nmol/L shortly after normal delivery. We suggest that measuring ZnCP-I in maternal plasma by fluorometry on HPLC is a rapid, noninvasive, and sensitive method for diagnosing AFE and propose 35 nmol/L as the cutoff value for the ZnCP-I concentration in maternal plasma for the diagnosis of AFE.

Adult↗