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  • 1
    Electronic Resource
    Electronic Resource
    Ferrochelatase activities in patients with erythropoietic protoporphyria and their families (1996)
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 134 (1996), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary Ferrochelatase, estimated as zinc chelatase, was measured in the lymphocytes of 30 patients with erythropoietic protoporphyria (EPP), in 35 first- or second-degree relatives of patients with EPP, and in 50 healthy controls. In 30 EPP patients the zinc chelatase level (mean ± standard deviation, SD) was 0–45 ± 0·10 nmol of zinc protoporphyrin per hour per milligram of protein, in 14 EPP carriers the zinc chelatase level (mean ± SD) was 0·42 ± 0·09 and in 50 healthy controls the zinc chelatase level (mean ± SD) was 0–84 ± 0·27. All patients with EPP were also demonstrated to have an elevated protoporphyrin level in their red blood cells: the erythrocyte protoporphyrin levels were as follows EPP patients (mean ± SD) 1300 ± 758 nmol protoporphyrin/dl, EPP carriers (mean ± SD) 60 ± 24, and healthy controls (mean ± SD) 50 ± 25 (P 〈 0·001 for EPP patients compared to controls and EPP carriers).The families of 12 out of 15 EPP patients were examined with respect to the mode of inheritance of the disorder. Of 35 relatives, 14 were carriers of EPP, as characterized by reduced zinc chelatase activity in lymphocytes and by a normal protoporphyrin level in red blood cells. None of the 14 EPP carriers had presented with clinical symptoms of EPP. The mode of inheritance was autosomal dominant in seven of the 12 examined families, and autosomal recessive in two. In two families only one parent could be investigated, but we nevertheless concluded that the inheritance was autosomal dominant. Inheritance in one EPP family could not be elucidated as both parents showed normal zinc chelatase levels and did not demonstrate abnormal erythrocyte protoporphyrin levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.1996.121856.x
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  • 2
    Electronic Resource
    Electronic Resource
    Inducibility of arylhydrocarbon-hydroxylase activity in human hair follicles by topical application of liquor carbonis detergens (coal tar) (1984)
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 111 (1984), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Arylhydrocarbon-hydroxylase (AHH) is a cytochrome P-450-dependent polysubstrate mono-oxygenase which plays an important role in converting some compounds (e.g. benzo[a]pyrene) to highly reactive carcinogenic species. A simple AHH assay is described, using [3H]benzo[a]-pyrene as substrate. 7,8-Benzoflavone (10-4 M) inhibits 92% of the measured enzyme activity. Liquor carbonis detergens (which contains coal tar) induces AHH activity in human hair follicles in vivo. We suggest that using this simple assay, hair follicles would be a very suitable tissue to test whether the AHH-controlling gene is of significance in producing cancer.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2133.1984.tb04724.x
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  • 3
    Electronic Resource
    Electronic Resource
    Cytochrome P4501A1 polymorphisms in a Caucasian population with porphyria cutanea tarda (2003)
    Oxford, UK : Munksgaard International Publishers
    Experimental dermatology 12 (2003), S. 0 
    Details
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Porphyria cutanea tarda (PCT) is the most frequent porphyria in humans. The familial type is in contrast to the sporadic type due to an inherited defect of the uroporphyrinogen-III-decarboxylase (URO-D) and both types need additional porphyrinogens to lead to the clinical manifestation of the disease. Various factors such as xenobiotics (i.e. polycyclic aromatic hydrocarbons), alcohol, hormones and viral liver infections (hepatitis B and C) are known to induce porphyria. Cytochrome P450 enzymes play a crucial role in the metabolism of porphyrogens and therefore might have an important influence on the pathogenesis of hepatic porphyrias. Association of CYP1A2 polymorphisms with susceptibility to both types of PCT has already been described in Danish patients. We investigated 65 Caucasian patients with PCT in comparison to a healthy control group concerning the type of PCT and the cytochrome P4501A1 polymorphisms (m1, m2 and m4) using polymerase chain reaction (PCR) and a restriction fragment length polymorphism. We found an increased incidence of the m4 polymorphism in the familial type of PCT (odds ratio 5.5, P-value 0.01), whereas the m1 and m2 mutations were not significantly higher than in the healthy control group. These results suggest that familial PCT, in addition to the genetic mutations, might be provoked by a higher susceptibility to porphyrogens via the cytochrome P4501A1 m4 polymorphism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0906-6705.2003.00095.x
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  • 4
    Electronic Resource
    Electronic Resource
    Influence of chloroquine on the porphyrin metabolism (1985)
    Springer
    Archives of dermatological research 277 (1985), S. 114-117 
    Details
    ISSN: 1432-069X
    Keywords: Hepatic porphyria ; Chloroquine ; Hexachlorobenzene ; δ-Aminolevulinate synthase ; Cytochrome P-450
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rats were treated with the well-known porphyrogen hexachlorobenzene (HCB) to induce experimental porphyria. At the same time another group of rats was treated with chloroquine in addition to HCB. The HCB-induced increase of the urinary excretion of porphyrin precursors could thereby be reduced to normal levels and the porphyrin excretion rates were decreased significantly in comparison to those of the other group. The δ-aminolevulinate synthase in the liver of the animals was slightly increased by exclusive treatment with chloroquine, which in the HCB-treated rats chloroquine led to a dramatic decrease in the key enzyme of the porphyrin (heme)-biosynthesis. The influence of chloroquine on the HCB-induced increase of the cytochrome P-450 content and the dependent enzymatic activities were different. The 7-ethoxycumarin deethylase and the arylhydrocarbon hydroxylase activities were not influenced, whereas the increased aminopyrine-N-demethylase activity was reduced to nearly normal levels. Our findings indicate that chloroquine acts by reduction of the δ-aminolevulinate synthase activity, probably by influencing the regulation of the key enzyme of the heme biosynthesis, which is enhanced in human porphyria cutanea tarda, as well as in the HCB-induced porphyria of the rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00414107
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  • 5
    Electronic Resource
    Electronic Resource
    UVA irradiation induces collagenase in human dermal fibroblasts in vitro and in vivo (1991)
    Springer
    Archives of dermatological research 283 (1991), S. 506-511 
    Details
    ISSN: 1432-069X
    Keywords: Collagen metabolism ; Induction of collagenase mRNA ; Actinic elastosis ; UVA irradiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We report the effect of UVA irradiation on collagen metabolism of fibroblasts, including both synthesis of the collagen degrading enzyme collagenase and de novo synthesis of type I collagen as the major structural component of the dermis. For this purpose confluent fibroblast monolayers were irradiated under standardized conditions (5, 15, 35, 60 J/cm2 using UVASUN 3000, Mutzhas, Munich, FRG, and UV source Sellas sunlight type 2.001, Sellas, Gevelsberg, FRG). Subsequently, total RNA was isolated and subjected to dot blot and northern blot analysis using oligolabelled cDNA clones for human type I collagen, collagenase and Β-actin. Collagen type I and Β-actin mRNA levels remained unaltered following irradiation, suggesting that the synthetic pathway of collagen metabolism at the pretranslational level is not affected by short-term UVA irradiation. However, collagenase mRNA was found to be dose-dependently induced in fibroblasts after irradiation, thus probably contributing to the actinic damage to the dermis. These in vitro data were confirmed in vivo using in situ hybridization on frozen sections of biopsy material obtained from UVA irradiated patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00371923
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of oral thalidomide on rat liver and skin microsomal P450 isozyme activities and on urinary porphyrin excretion: interaction with oral hexachlorobenzene (1994)
    Springer
    Archives of dermatological research 286 (1994), S. 347-349 
    Details
    ISSN: 1432-069X
    Keywords: Thalidomide ; Liver ; Skin ; Cytochrome P450 ; Porphyrins ; Hexachlorobenzene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Adult female Wistar rats (n=48) divided into four groups of 12 were treated orally with 3 mg/kg per day thalidomide, a 0.05% hexachlorobenzene (HCB) — containing diet, with both drugs together and with the vehicles (controls) over periods of 10 and 60 days. The protein and P450 contents and the activities of amino-pyrine-N-demethylase (ADM) and 7-ethoxyresorufine-O-deethylase (7-ERO-D) were determined in the liver microsomes. The activity of 7-ERO-D was also determined in the skin microsomes and total porphyrins were measured in the urine of the animals. Thalidomide increased the hepatic P450 content, caused distinct changes in the activities of the hepatic and cutaneous microsomal isozymes, modified their induction by HCB and inhibited the porphyriogenic activity of HCB. These findings indicate an interaction between thalidomide and HCB with regard to their effects on the P450 isozymes and the metabolism of porphyrins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00402227
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  • 7
    Electronic Resource
    Electronic Resource
    Hexachlorbenzol (HCB)-bedingte Porphyrie der Ratte. Einfluß von HCB-Metaboliten auf die Haembiosynthese (1978)
    Springer
    Archives of dermatological research 263 (1978), S. 189-196 
    Details
    ISSN: 1432-069X
    Keywords: Porphyria ; Hexachlorobenzene (HCB) ; HCB-Metabolites (Pentachlorophenol ; Pentachlorobenzene) ; Cytochrome P-450 ; Porphyrie ; Hexachlorbenzol ; Hexachlorbenzol-Metaboliten ; Cytochrom P-450
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Weibliche Wistar-Ratten wurden mit einem 0,05% igen Futterzusatz an Hexachlorbenzol (HCB) oder den HCB-Metaboliten Pentachlorbenzol (PCB) bzw. Pentachlorphenol (PCP) behandelt. Die drei chlorierten Aromaten induzieren in ungefähr gleicher Stärke den Cytochrom P-450-Gehalt der Rattenleber, während die O-Desalkylierungsaktivität (gemessen nach Ullrich u. Weber [23]) durch PCP und PCB gering und durch HCB sehr deutlich gesteigert wird. Die Porphyrin-Ausscheidung bleibt während der gesamten Versuchsdauer (80 Tage) nach der PCP- und PCB-Verfütterung unverändert, während sich nach 60 Tagen HCB-Applikation immer eine Porphyrie nachweisen läßt. Es ist damit weitgehend ausgeschlossen, daß die HCB-Metaboliten PCB und PCP die eigentlichen Porphyrogene des HCB sind. Zusätzlich wurde durch PCP-Gabe zunächst eine Induktion des Cytochrom P-450-Systems herbeigeführt (40 Tage PCP-Vorbehandlung) und anschließend HCB appliziert. Trotz dieser Vorbehandlung führt HCB ebenso wie bei den HCB-Kontrollen erst nach 50 Tagen zur Manifestation einer Porphyrie. Es wird damit sehr unwahrscheinlich, daß die HCB-induzierte Porphyrie pathogenetisch mit der Induktion des Cytochrom P-450-Systems direkt verknüpft ist.
    Notes: Summary Female adult Wistar rats were fed with a diet containing 0.05% hexachlorobenzene (HCB) or its metabolites, pentachlorobenzene (PCB) and pentachlorphenole (PCP). These chlorinated aromatic hydrocarbons produced an increase in the liver cytochrome P-450 content in about the same degree, however, only the application of HCB showed an extremely high rise in the P-450 enzymatic activity expressed in terms of the O-dealkylation of 7-Ethoxycoumarine. No alteration was observed in the urinary porphyrin excretion in the PCB and PCP treated animals, whereas 60 days after the beginning of the HCB application a high level of porphyrins could be detected in the urine of the animals. It seems unlikely therefore that the HCB metabolites (PCB and PCP) are porphyrogenic agents. In addition, although induction of the liver cytochrome P-450 system was observed after PCP pretreatment of the rats over a period of 40 days, the consequent application of HCB did not influence the establishment of the experimental porphyria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00446440
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  • 8
    Electronic Resource
    Electronic Resource
    Influence of UVA and UVB irradiation on hepatic and cutaneous P450 isoenzymes (1996)
    Springer
    Archives of dermatological research 289 (1996), S. 46-51 
    Details
    ISSN: 1432-069X
    Keywords: Key words UVA irradiation ; UVB irradiation ; Cutaneous P450 isoenzymes ; Hepatic P450 isoenzymes ; Porphyrin metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influence of UVA and UVB irradiation of the skin for 1, 2 and 4 weeks on the activities of the hepatic and cutaneous P450 isoenzymes was investigated in female Wistar rats before and after systemic administration of hexachlorobenzene (HCB), a well-known porphyrogenic agent, which additionally induces P450 1A1 and P450 1A2 isoenzymes. UVA and UVB irradiation of the skin of the controls and HCB-treated animals did not influence porphyrin metabolism. In the nonporphyric rats hepatic EROD (P450 1A1) activity was induced by UVB, but the activity of ADM (P450 2B) and EMDM (P450 3A) was either minimally or not affected. In the HCB-treated (porphyric) rats UVA and UVB irradiation resulted in a significant depression of HCB-induced EROD in the liver and in the skin. In both the nonporphyric and the porphyric rats UVA and UVB irradiation had no effect on hepatic ADM activity. In the liver of the nonporphyric animals EMDM activity remained unchanged after UVA and UVB irradiation, whereas in the HCB-treated animals the activity of this enzyme was increased. Finally, after UVA and UVB irradiation cutaneous EMDM activity was increased in the controls, whereas the HCB-induced increase of this enzyme in porphyric animals was decreased. In addition long-term (28 days) UVB irradiation decreased hepatic GSH content significantly in normal and porphyric rats. These experimental findings cannot be directly extrapolated to humans; however, they suggest that exposure of human skin to UV radiation may result in alterations in the activity of cutaneous, hepatic and other extracutaneous P450 isoenzymes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004030050151
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  • 9
    Electronic Resource
    Electronic Resource
    Influence of chronic UV-light exposure on hepatic and cutaneous monooxygenases (1983)
    Springer
    Cellular and molecular life sciences 39 (1983), S. 385-386 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Hairless female Ng/-mice were irradiated by UV-light for 16h daily over a period of 24 weeks. Monooxygenase activities were measured in liver and skin, and an induction of the aryl-hydrocarbon hydroxylase was detected in liver by both fluorometric and radiochemical methods, whereas no induction of this enzyme could be demonstrated in the skin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01963137
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  • 10
    Electronic Resource
    Electronic Resource
    Porphyrin-untersuchungen eines gallensteines bei der erythropoetischen protoporphyrie (1976)
    Springer
    Archives of dermatological research 256 (1976), S. 283-289 
    Details
    ISSN: 1432-069X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wird eine 48jährige Frau mit dem klinischen und biochemischen Vollbild einer erythropoetischen Protoporphyrie (EPP) berichtet. Anamnestisch war seit über zehn Jahren ein Gallenstein bekannt, der operativ entfernt wurde. Im Mittel betrug der Porphyrin-Gehalt dieses Steins 22.6 mcg/g und lag damit fast 20fach über dem Gehalt anderer Cholesterinsteine. Bei der dünnschichtchromatographischen Auftrennung fanden sich in vier verschiedenen Proben außer Protoporphyrin noch 30 bis 70 % höher carboxylierte Porphyrine. Es wird diskutiert, ob es durch das kontinuierliche Überfluten der Leber mit Protoporphyrin zur Auskristallisation des Cholesterins und damit zur Gallensteinbildung kommen könnte. Die höher carboxylierten Porphyrine (mehr COOH-Gruppen als Protoporphyrin) sprechen dafür, daß nicht nur die Porphyrine aus den haemolysierten Erythrozyten im Gallenstein zu finden sind und somit auch eine hepatische Porphyrin-Stoffwechselstörung zu diskutieren wäre.
    Notes: Summary In the case of a 48 year old woman with characteristic signs of erythropoetic protoporphyria, a solitary gall-stone which had persisted over a period of 10 years was removed. Porphyrin-concentration of this gall-stone was found to be 22.6. mcg/g, which is almost twenty times the concentration of other cholestrol-stones. Besides protoporphyrin, porphyrins with a higher degree of carboxylation were discovered in four different samples by thin layer chromatography. It is postulated that the increased bile-concentration of protoporphyrin in the liver causes the cristallisation of cholestrol and the formation and growth of gall-stones. The biochemical finding of porphyrins with a higher degree of carboxylation indicates that the porphyrins of the gall-stone may not only come from hemolysed erythrocytes but possibly also from metabolites of disturbed hepatic porphyrin biosynthesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00572494
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