| Name | uroporphyrinogen decarboxylase |
|---|---|
| Synonyms | PCT; UPD; URO D; UROD; Uroporphyrinogen III decarboxylase; Uroporphyrinogen decarboxylase; Uroporphyrinogen III decarboxylases; Uroporphyrinogen decarboxylases |
| Name | hexachlorobenzene |
|---|---|
| CAS | 1,2,3,4,5,6-hexachlorobenzene |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 12426626 | Rios de Molina MC, Mazzetti MB, Galigniana M, Aldonatti C, Tomio JM, San Martin de Viale LC: The decrease in uroporphyrinogen decarboxylase activity induced by predisposes rats to the development of porphyria and accelerates xenobiotic-triggered porphyria, regardless of hepatic damage. Braz J Med Biol Res. 2002 Nov;35(11):1273-83. We evaluated the porphyrinogenic ability of (20% in drinking water) per se, its effect on the development of sporadic porphyria cutanea tarda induced by hexachlorobenzene in female Wistar rats (170-190 g, N = 8/group), and the relationship with hepatic damage. |
2(0,0,0,2) | Details |
| 10365252 | Vilas GL, Aldonatti C, San Martin de Viale LC, Rios de Molina MC: Effect of on hexachlorobenzene porphyria. . Biochem Mol Biol Int. 1999 May;47(5):815-23. On the other hand, the second stage of uroporphyrinogen-decarboxylase activity was significantly higher in the HCB + TO group than in the HCB group. delta aminolevulic acid synthase activity was higher in the HCB group. |
2(0,0,0,2) | Details |
| 9147135 | Billi de Catabbi S, Sterin-Speziale N, Fernandez MC, Minutolo C, Aldonatti C, San Martin de Viale L: Time course of hexachlorobenzene-induced alterations of lipid metabolism and their relation to porphyria. Int J Biochem Cell Biol. 1997 Feb;29(2):335-44. Individual phospholipid content, [32P] incorporation, total lipid content, lipid peroxidation, uroporphyrinogen decarboxylase activity, its inhibitor generation and content, were the parameters measured in the liver of treated rats. |
2(0,0,0,2) | Details |
| 2273443 | Kato Y, Konishi S, Yamada S, Kimura R: Effects of -containing metabolites of hexachlorobenzene on the heme metabolic enzymes in rat liver. J Pharmacobiodyn. 1990 May;13(5):278-84. When HCB was injected once daily for 5 weeks, a marked increase in ALA synthetase activity, a significant decrease in ALA dehydratase, almost complete inhibition of uroporphyrinogen decarboxylase activity, and an increased excretion of total in the urine were shown. |
2(0,0,0,2) | Details |
| 9439724 | Franklin MR, Phillips JD, Kushner JP: Cytochrome P450 induction, uroporphyrinogen decarboxylase depression, accumulation and excretion, and gender influence in a 3-week rat model of porphyria cutanea tarda. Toxicol Appl Pharmacol. 1997 Dec;147(2):289-99. When hexachlorobenzene was substituted for Aroclor 1254 treatment in female rats, URO-D activity was 61 and 69% of normal (with and without iron loading, respectively) and liver concentrations were 96 and 25 micrograms/g, respectively. |
2(0,0,0,2) | Details |
| 498361 | Smith AG, Cabral JR, De Matteis F: A difference between two strains of rats in their liver non-haem iron content and in their response to the porphyrogenic effect of hexachlorobenzene. Chem Biol Interact. 1979 Oct;27(2-3):353-63. They also showed a greater inhibition of liver uroporphyrinogen decarboxylase [EC 4.1.1.37] activity and a marked stimulation of synthetase [EC 2.3.1.37]. |
2(0,0,0,2) | Details |
| 3327428 | Doss MO: Porphyrinurias and occupational disease. . Ann N Y Acad Sci. 1987;514:204-18. Certain foreign and environmental chemicals, such as hexachlorobenzene, polyhalogenated aromatic hydrocarbons, vinyl and dioxin, alter the heme pathway functionally. This is characterized by a simultaneous increase in hepatic and urinary uroporphyrin and heptacarboxylic porphyrins, owing to inhibition of hepatic uroporphyrinogen decarboxylase. |
2(0,0,0,2) | Details |
| 6626162 | Smith AG, Francis JE: Synergism of iron and hexachlorobenzene inhibits hepatic uroporphyrinogen decarboxylase in inbred mice. Biochem J. 1983 Sep 15;214(3):909-13. |
162(2,2,2,2) | Details |
| 2845946 | Hahn ME, Gasiewicz TA, Linko P, Goldstein JA: The role of the Ah locus in hexachlorobenzene-induced porphyria. Biochem J. 1988 Aug 15;254(1):245-54. Uroporphyrinogen decarboxylase (EC 4.1.1.37) activity was diminished by 70 and 20% in B6-Ahb B6-Ahd mice respectively after 15 weeks of treatment with HCB. |
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| 4837 | Jackson AH, Sancovich HA, Ferramola AM, Evans N, Games DE, Matlin SA, Elder GH, Smith SG: Macrocyclic intermediates in the biosynthesis of porphyrins. Philos Trans R Soc Lond B Biol Sci. 1976 Feb 5;273(924):191-206. The hepta-, hexa- and penta-carboxylic porphyrins found in the faeces of rats poisoned with hexachlorobenzene have been separated by high-pressure liquid chromatography and characterized largely by spectroscopie methods. In the poisoned rats the uroporphyrinogen decarboxylase enzyme (or group of enzymes) is probably partially inhibited and the pentacarboxylic porphyrinogen with an group on ring C accumulates. |
1(0,0,0,1) | Details |
| 2238708 | Smith AG, De Matteis F: Oxidative injury mediated by the hepatic cytochrome P-450 system in conjunction with cellular iron. Xenobiotica. 1990 Sep;20(9):865-77. Some polyhalogenated aromatic chemicals such as 2,3,7,8-tetrachloro-p-dioxin, brominated and chlorinated biphenyls, and hexachlorobenzene cause in humans, animals and hepatocyte systems a partial block in haem biosynthesis leading to accumulation and excretion of uroporphyrin, the oxidation product of the unstable biosynthetic intermediate uroporphyrinogen. 2. Besides oxidation of uroporphyrinogen to uroporphyrin, an inhibitor of uroporphyrinogen decarboxylase may also be formed. 3. |
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| 16978756 | Chaufan G, Juarez A, Basack S, Ithuralde E, Sabatini SE, Genovese G, Oneto ML, Kesten E, Rios de Molina Mdel C: Toxicity of hexachlorobenzene and its transference from microalgae (Chlorella kessleri) to crabs (Chasmagnathus granulatus). Toxicology. 2006 Oct 29;227(3):262-70. Epub 2006 Aug 18. Results demonstrated that hexachlorobenzene enters the alga, is accumulated in it, and then transferred into the crab, causing a decrease in Uroporphyrinogen decarboxylase activity in both organisms. |
87(1,1,2,2) | Details |
| 9221820 | Mylchreest E, Charbonneau M: Studies on the mechanism of uroporphyrinogen decarboxylase inhibition in hexachlorobenzene-induced porphyria in the female rat. Toxicol Appl Pharmacol. 1997 Jul;145(1):23-33. |
85(1,1,1,5) | Details |
| 3442379 | Koss G, Losekam M, Seidel J, Steinbach K, Koransky W: Inhibitory effect of tetrachloro- and other metabolites of hexachlorobenzene on hepatic uroporphyrinogen decarboxylase activity with reference to the role of Ann N Y Acad Sci. 1987;514:148-59. |
83(1,1,1,3) | Details |
| 3596737 | Cantoni L, Graziani A, Rizzardini M, Saletti MC: Porphyrinogenic effect of hexachlorobenzene and 2,3,7,8-tetrachlorodibenzo-para-dioxin: is an inhibitor involved in uroporphyrinogen decarboxylase inactivation?. IARC Sci Publ. 1986;(77):449-56. |
82(1,1,1,2) | Details |
| 7306050 | Smith AG, Francis JE: Investigations of rat liver uroporphyrinogen decarboxylase. Biochem J. 1981 Apr 1;195(1):241-50. Rapid analysis of the livers from rats made porphyric with hexachlorobenzene demonstrated that substantial quantities of the tetrapyrroles were present in vivo as the porphyrinogens (21-42%). 5. |
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| 1008488 | Doss M, Schermuly E, Koss G: Hexachlorobenzene porphyria in rats as a model for human chronic hepatic porphyrias. Ann Clin Res. 1976;8 Suppl 17:171-81. In contrast to the distribution of accumulation in the various organs, clear evidence of a uroporphyrinogen decarboxylase defect was found only in the liver. |
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| 12898129 | Mazzetti MB, Taira MC, Lelli SM, Dascal E, Basabe JC, de Viale LC: Hexachlorobenzene impairs metabolism in a rat model of porphyria cutanea tarda: a mechanistic approach. Arch Toxicol. 2004 Jan;78(1):25-33. Epub 2003 Jul 29. Loss of 60, 56, and 37%, respectively, was noted at the end of the treatment when a considerable amount of porphyrins had accumulated in the liver as a result of drastic blockage of uroporphyrinogen decarboxylase (URO-D) (95% inhibition). |
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| 7271874 | Smith AG, Francis JE: Increased inhibition of hepatic uroporphyrinogen decarboxylase by hexachlorobenzene in male rats given the oestrogenic drugs diethylstilboestrol and chlorotrianisene. Biochem Pharmacol. 1981 Jul 1;30(13):1849-53. |
81(1,1,1,1) | Details |
| 3138981 | Lambrecht RW, Sinclair PR, Bement WJ, Sinclair JF, Carpenter HM, Buhler DR, Urquhart AJ, Elder GH: Hepatic uroporphyrin accumulation and uroporphyrinogen decarboxylase activity in cultured chick-embryo hepatocytes and in Japanese quail (Coturnix coturnix japonica) and mice treated with polyhalogenated aromatic compounds. Biochem J. 1988 Jul 1;253(1):131-8. In contrast, hepatic uroporphyrin accumulation in male C57BL/6 mice treated with iron and hexachlorobenzene was accompanied by a 20-80% decrease in uroporphyrinogen decarboxylase activity, demonstrating that the assay used for uroporphyrinogen decarboxylase, using pentacarboxyporphyrinogen III as substrate, could detect decreased enzyme activity. |
41(0,1,2,6) | Details |
| 19482825 | Sopena YE, Ferramola de Sancovich AM, Sancovich HA: Hexachlorobenzene treatment on hepatic mitochondrial function parameters and intracellular coproporphyrinogen oxidase location. Int J Toxicol. 2008 Nov;27(6):455-65. After 8 weeks of treatment, rats showed high excreta and 50% inhibition of liver uroporphyrinogen decarboxylase activity. |
1(0,0,0,1) | Details |
| 7233443 | Debets FM, Reinders JH, Debets AJ, Lossbroek TG, Strik JJ, Koss G: Biotransformation and porphyringogenic action of hexachlorobenzene and its metabolites in a primary liver cell culture. Toxicology. 1981;19(3):185-96. Since none of the main HCB-metabolites could induce a pathological pattern, a reactive intermediate capable of reacting with or thiol-groups of uroporphyrinogen decarboxylase (UROG-D) is believed to be responsible for the inhibition of UROG-D. |
1(0,0,0,1) | Details |
| 8937451 | Constantin D, Francis JE, Akhtar RA, Clothier B, Smith AG: Uroporphyria induced by alone in Ahrd SWR mice. Biochem Pharmacol. 1996 Nov 8;52(9):1407-13. Despite SWR mice being AH nonresponsive, uroporphyria and decarboxylase depression after an initial iron overload and ALA for 3 weeks were greatly potentiated by a single dose (100 mg/kg) of hexachlorobenzene (a weak AH ligand). In mice, depression of hepatic uroporphyrinogen decarboxylase (UROD) leading to accumulation (uroporphyria) occurs with chlorinated ligands of the aryl hydrocarbon (AH) receptor especially after iron overload. |
1(0,0,0,1) | Details |
| 550992 | Goerz G, Vizethum W, Lissner R: [Behaviour of the hepatic (GSH) in the rat in continuous administration of hexachlorobenzene (HCB) (author's transl)]. Derm Beruf Umwelt. 1979;27(6):173-5. It is assumed that at the beginning of th HCB-feeding the microsomal mixed function monooxygenase are induced and the uroporphyrinogen decarboxylase is inhibited. |
1(0,0,0,1) | Details |
| 9777036 | Vilas GL, Ureta D, Sanchez Garcia MC, Aldonatti C, San Martin de Viale LC, Rios de Molina MC: [Effect of the in relation to the hexachlorobenzene action] . Acta Physiol Pharmacol Ther Latinoam. 1998;48(3):137-45. These results might indicate that: 1) high doses of decreases Uroporphyrinogen decarboxylase activity, masking its possible protective effect from Hexachlorobenzene's action through free radicals production and, 2) Uroporphyrinogen decarboxylase is a more sensitive parameter than conjugated dienes or malondialdehyde levels to assay the free radicals in vivo Hexachlorobenzene production. |
38(0,1,2,3) | Details |
| 3800966 | Smith AG, Francis JE, Kay SJ, Greig JB, Stewart FP: Mechanistic studies of the inhibition of hepatic uroporphyrinogen decarboxylase in C57BL/10 mice by iron-hexachlorobenzene synergism. Biochem J. 1986 Sep 15;238(3):871-8. |
32(0,1,1,2) | Details |
| 12732362 | Randi AS, Sancovich HA, Ferramola de Sancovich AM, Loaiza A, Kolliker Frers RA, Spinelli F, Kleiman de Pisarev DL: Effect of in vivo administered hexachlorobenzene on epidermal growth factor receptor levels, protein tyrosine kinase activity, and phosphotyrosine content in rat liver. Biochem Pharmacol. 2003 May 1;65(9):1495-506. To determine whether the observed alterations were correlated with a manifestation of overt toxicity, a single very low dose of HCB (1mg/kg body wt) and two much higher doses (100 and 1000 mg/kg body wt), the highest being toxicologically significant in that it reduced serum (T (4)) and inhibited uroporphyrinogen decarboxylase (URO-D) (EC 4.1.1.37) activity, were tested. |
1(0,0,0,1) | Details |
| 8347143 | van Gelder W, Siersema PD, Voogd A, de Jeu-Jaspars NC, van Eijk HG, Koster JF, de Rooy FW, Wilson JH: The effect of desferrioxamine on iron metabolism and lipid peroxidation in hepatocytes of C57BL/10 mice in experimental uroporphyria. Biochem Pharmacol. 1993 Jul 20;46(2):221-8. The effects of the iron chelator desferrioxamine (DFx) on liver iron accumulation, malondialdehyde (MDA) production, accumulation and uroporphyrinogen decarboxylase (URO-D; EC 4.1.1.37) activity were investigated over a period of 14 weeks in C57BL/10 mice, made porphyric by the administration of hexachlorobenzene (HCB) and iron-dextran (Imferon, IMF) or IMF alone. |
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| 3596736 | Elder GH, Urquhart AJ: Immunochemical studies of the uroporphyrinogen decarboxylase defect caused by hexachlorobenzene. IARC Sci Publ. 1986;(77):441-8. |
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| 3442389 | Kimbrough RD: Porphyrins and hepatotoxicity. Ann N Y Acad Sci. 1987;514:289-96. This is the "constitutional" type and is associated with a deficiency of uroporphyrinogen decarboxylase in the liver. This constitutional type must be differentiated from the "acquired" type, which occurred in hundreds of people poisoned by hexachlorobenzene in Turkey. |
1(0,0,0,1) | Details |
| 891100 | Louw M, Neethling AC, Percy VA, Carstens M, Shanley BC: Effects of hexachlorobenzene feeding and iron overload on enzymes of haem biosynthesis and cytochrome P 450 in rat liver. Clin Sci Mol Med. 1977 Aug;53(2):111-5. The effect of hexachlorobenzene feeding on liver delta-aminolaevulinate synthase, uroporphyrinogen decarboxylase and cytochrome P 450 was studied at various time-intervals in siderotic and non-siderotic rats. 2 In the non-siderotic group hexachlorobenzene feeding led to a progress decrease in liver uroporphyrinogen decarboxylase activity, accompanied by a progressive increase in delta-aminolaevulinate synthase activity. |
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| 939068 | Elder GH, Evans JO, Matlin SA: The effect of the porphyrogenic compound, hexachlorobenzene, on the activity of hepatic uroporphyrinogen decarboxylase in the rat. Clin Sci Mol Med. 1976 Jul;51(1):71-80. |
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| 4004897 | Smith AG, Francis JE, Greig JB: Continued depression of hepatic uroporphyrinogen decarboxylase activity caused by hexachlorobenzene or 2,3,7,8-tetrachlorodibenzo-p-dioxin despite regeneration after partial hepatectomy. Biochem Pharmacol. 1985 May 15;34(10):1817-20. |
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| 11378443 | Chaufan G, Rios de Molina MC, San Martin de Viale LC: How does hexachlorobenzene treatment affect liver uroporphyrinogen decarboxylase?. Int J Biochem Cell Biol. 2001 Jun;33(6):621-30. |
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| 16084099 | Cooper CL, Stob CM, Jones MA, Lash TD: Metabolism of pentacarboxylate porphyrinogens by highly purified human coproporphyrinogen oxidase: further evidence for the existence of an abnormal pathway for heme biosynthesis. Bioorg Med Chem. 2005 Nov 15;13(22):6244-51. Epub 2005 Aug 3. Although 5dab is a slightly poorer substrate than copro'gen-III, these results support the hypothesis that an abnormal route for heme biosynthesis is possible in humans suffering from PCT or related syndromes such as hexachlorobenzene poisoning. This porphyrinogen can be further metabolized by uroporphyrinogen decarboxylase to give one of the usual intermediates in heme biosynthesis. |
1(0,0,0,1) | Details |
| 2744662 | Visser O, van den Berg JW, Edixhoven-Bosdijk A, Koole-Lesuis R, Rietveld T, Wilson JH: Development of hexachlorobenzene porphyria in rats: time sequence and relationship with lipid peroxidation. Food Chem Toxicol. 1989 May;27(5):317-21. During the following weeks, liver porphyrins and malondialdehyde increased simultaneously, accompanied by a decrease in uroporphyrinogen decarboxylase activity and activity in liver, and a high excretion of porphyrins in the urine. |
1(0,0,0,1) | Details |
| 3986965 | Smith AG, Francis JE, Dinsdale D, Manson MM, Cabral JR: Hepatocarcinogenicity of hexachlorobenzene in rats and the sex difference in hepatic iron status and development of porphyria. Carcinogenesis. 1985 Apr;6(4):631-6. Females developed a massive porphyria, due to depression of uroporphyrinogen decarboxylase activity, whereas males did not. |
1(0,0,0,1) | Details |
| 15736160 | Chaufan G, Corvi MM, San Martin de Viale LC, Cardenas ML, Rios de Molina Mdel C: Abnormal kinetic behavior of uroporphyrinogen decarboxylase obtained from rats with hexachlorobenzene-induced porphyria. J Biochem Mol Toxicol. 2005;19(1):19-24. |
7(0,0,1,2) | Details |
| 2386827 | Adzharov D: [Study of the origin of urinary porphyrins in experimental hexachlorobenzene-induced porphyria ]. Biull Eksp Biol Med. 1990 Apr;109(4):355-7. The activity of the enzyme uroporphyrinogen decarboxylase was determined in the liver and the kidneys of C57BL/6 mice and Wistar albino rats with chronic hexachlorobenzene intoxication and the amount of the deposited uroporphyrin was measured in the both organs. |
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| 7159416 | Elder GH, Sheppard DM: Immunoreactive uroporphyrinogen decarboxylase is unchanged in porphyria caused by TCDD and hexachlorobenzene. Biochem Biophys Res Commun. 1982 Nov 16;109(1):113-20. |
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| 3178718 | Urquhart AJ, Elder GH, Roberts AG, Lambrecht RW, Sinclair PR, Bement WJ, Gorman N, Sinclair JA: Uroporphyria produced in mice by 20-methylcholanthrene and Biochem J. 1988 Jul 15;253(2):357-62. At 21 days, uroporphyrinogen decarboxylase (EC 4.1.1.37) activities are less than 10% of control activities. Continuous administration of ALA markedly accelerates the onset of porphyria in iron-loaded male C57BL/6 mice after a single intraperitoneal dose of hexachlorobenzene (200 mg/kg); mice given phenobarbitone and ALA do not become porphyric. |
1(0,0,0,1) | Details |
| 2173599 | Smith AG, Francis JE, Green JA, Greig JB, Wolf CR, Manson MM: Sex-linked hepatic uroporphyria and the induction of cytochromes P450IA in rats caused by hexachlorobenzene and polyhalogenated biphenyls. Biochem Pharmacol. 1990 Nov 1;40(9):2059-68. A heat-stable inhibitor (s) of liver uroporphyrinogen decarboxylase was extractable from uroporphyric livers. |
1(0,0,0,1) | Details |
| 2736716 | Stewart FP, Manson MM, Cabral JR, Smith AG: Hexachlorobenzene as a promoter of diethylnitrosamine-initiated hepatocarcinogenesis in rats and comparison with induction of porphyria. Carcinogenesis. 1989 Jul;10(7):1225-30. Inhibition of the haem biosynthesis enzyme uroporphyrinogen decarboxylase (UD) only occurred in the liver of females treated with HCB or DEN/HCB. |
1(0,0,0,1) | Details |
| 7409755 | von Tiepermann R, Koss G, Doss M: Uroporphyrinogen decarboxylase deficiency in experimental chronic hepatic porphyria. Hoppe Seylers Z Physiol Chem. 1980 Aug;361(8):1217-22. During hexachlorobenzene feeding of rats the following biochemical signs of a chronic hepatic porphyria developed: porphyrinuria with increase of uro- and hexacarboxyporphyrin, hepatic prophyrin accumulation of uro- and heptacarboxyporphyrin and a diminished activity of uroporphyrinogen decarboxylase in the liver, but nut in the red cells. |
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| 3036697 | Sweeney GD, Basford D, Krestynski F: The role of contaminants in hexachlorobenzene toxicity. IARC Sci Publ. 1986;(77):363-70. Hexachlorobenzene (HCB) is hepatotoxic, causing a porphyria with an acquired deficiency of uroporphyrinogen decarboxylase. |
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| 3442378 | Elder GH, Roberts AG, Urquhart AJ: Alterations of uroporphyrinogen decarboxylase by chlorinated organics. Ann N Y Acad Sci. 1987;514:141-7. |
1(0,0,0,1) | Details |
| 10433183 | Selden AI, Floderus Y, Bodin LS, Westberg HB, Thunell S: status in aluminum foundry workers exposed to hexachlorobenzene and octachlorostyrene. Arch Environ Health. 1999 Jul-Aug;54(4):248-53. Erythrocyte uroporphyrinogen decarboxylase activity was similar in both groups. |
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| 1850174 | Visser O, van den Berg JW, Koole-Lesuis H, Voortman G, Wilson JH: synthesis by human hepatocytes and HepG2 cells--effects of enzyme inducers and Toxicology. 1991 Mar 25;67(1):75-83. After treatment with hexachlorobenzene, 3-methylcholanthrene, phenobarbital or was the predominating accumulating in presence of |
0(0,0,0,0) | Details |
| 3966921 | Alleman MA, Koster JF, Wilson JH, Edixhoven-Bosdijk A, Slee RG, Kroos MJ, von Eijk HG: The involvement of iron and lipid peroxidation in the pathogenesis of HCB induced porphyria. Biochem Pharmacol. 1985 Jan 15;34(2):161-6. Hexachlorobenzene (HCB) induces a porphyria characterized by a diminished activity of the enzyme uroporphyrinogen decarboxylase (URO-D), presumably due to inactivation by reactive metabolites of HCB. |
6(0,0,1,1) | Details |
| 3236339 | Rizzardini M, Graziani A, Carugo C, Cantoni L: Investigations on the role of free radical processes in hexachlorobenzene-induced porphyria in mice. J Biochem Toxicol. 1988 Spring;3:33-45. |
0(0,0,0,0) | Details |
| 3271868 | Smith AG, Francis JE, Bird I: Distinction between octachlorostyrene and hexachlorobenzene in their potentials to induce ethoxyphenoxazone deethylase and cause porphyria in rats and mice. J Biochem Toxicol. 1986 Mar;1(1):105-17. |
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| 2263875 | Cantoni L, Budillon G, Cuomo R, Rodino S, Le Grazie C, Di Padova C, Rizzardini M: Protective effect of in hepatic uroporphyria. Scand J Gastroenterol. 1990 Oct;25(10):1034-40. The potential use of as therapy for human porphyria cutanea tarda was investigated in an experimental model of hepatic porphyria--that is, chronic treatment of female rats with 0.2% hexachlorobenzene (HCB) in the diet. |
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| 3813879 | Kondo M, Shimizu Y: The effects of and hexachlorobenzene on the activities of hepatic synthetase, delta-aminolevulinate dehydratase, and uroporphyrinogen decarboxylase in male rats. Arch Toxicol. 1986 Oct;59(3):141-5. |
6(0,0,1,1) | Details |
| 1959868 | Siersema PD, van Helvoirt RP, Ketelaars DA, Cleton MI, de Bruijn WC, Wilson JH, van Eijk HG: and uroporphyrin in hepatocytes of inbred mice in experimental porphyria: a biochemical and morphological study. Hepatology. 1991 Dec;14(6):1179-88. Hexachlorobenzene-induced porphyria is iron dependent and characterized by the decreased activity of uroporphyrinogen decarboxylase and the accumulation of porphyrins in the liver. |
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| 3442377 | Cantoni L, Rizzardini M, Graziani A, Carugo C, Garattini S: Effects of chlorinated organics on intermediates in the heme pathway and on uroporphyrinogen decarboxylase. Ann N Y Acad Sci. 1987;514:128-40. |
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| 3596742 | Adjarov DG, Elder GH: Accumulation of uroporphyrin does not provoke further inhibition of liver uroporphyrinogen decarboxylase activity in hexachlorobenzene-induced porphyria. IARC Sci Publ. 1986;(77):467-9. The inhibition of uroporphyrinogen decarboxylase (Uro-D) is the basic pathogenetic mechanism in porphyria caused by hexachlorobenzene (HCB). |
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| 20099833 | Smith AG, Elder GH: Complex Gene-Chemical Interactions: Hepatic Uroporphyria As a Paradigm. Chem Res Toxicol. 2010 Jan 25. Association studies of uroporphyria induced by TCDD or hexachlorobenzene with DNA markers in mouse intercrosses have shown the participation of other, unknown, genetic factors in addition to the strong influence of the Ahr gene. The human disease, porphyria cutanea tarda (PCT), is a skin disease caused by the photosensitizing action of porphyrins arising secondary to the decreased activity of an enzyme of heme biosynthesis, uroporphyrinogen decarboxylase (UROD), in the liver. |
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| 3675556 | Smith AG, Francis JE: Chemically-induced formation of an inhibitor of hepatic uroporphyrinogen decarboxylase in inbred mice with iron overload. Biochem J. 1987 Aug 15;246(1):221-6. |
3(0,0,0,3) | Details |
| 10567850 | Fernandez-Tome MC, Billi de Catabbi SC, Aldonatti C, San Martin de Viale LC, Sterin-Speziale NB: metabolism and lipid peroxidation in rat kidney hexachlorobenzene-induced porphyria: A compartmentalized study of biochemical pathogenic mechanisms. Kidney Blood Press Res. 2000;23(1):20-6. For this purpose, conjugated diene and malondialdehyde levels, as lipid peroxidation parameters, and accumulation, uroporphyrinogen decarboxylase activity, and its inhibitor formation, as measures of heme metabolism, were determined in renal cortex, medulla, and papilla. |
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| 7394329 | Smith AG, Francis JE: Relative abilities on a molar basis of hexafluoro-, hexachloro- and hexabromobenzenes to decrease liver uroporphyrinogen decarboxylase activity and cause porphyria in female rats. Res Commun Chem Pathol Pharmacol. 1980 May;28(2):377-84. However, depression of decarboxylase activity and increase in levels were Cl greater than Br greater than F, (hexachlorobenzene and hexabromobenzene increased porphyrins by 513- and 17-fold respectively) suggesting that at its site of action in the liver hexabromobenzene may be more porphyrogenic than the analogue. |
2(0,0,0,2) | Details |
| 3513989 | Sweeney GD: Porphyria cutanea tarda, or the uroporphyrinogen decarboxylase deficiency diseases. Clin Biochem. 1986 Feb;19(1):3-15. Its usage now is usually restricted to disorders associated with a deficiency of uroporphyrinogen decarboxylase (UROD), for which the term "UROD-deficiency" may be more appropriate. |
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| 11083027 | De Catabbi SCB, Aldonatti C, de Viale LC: metabolism after discontinued hexachlorobenzene administration in rats: possible irreversible changes and biomarker for hexachlorobenzene persistence. Comp Biochem Physiol C Toxicol Pharmacol. 2000 Sep;127(2):165-75. Hepatic uroporphyrinogen decarboxylase activity, its inhibitor formation, content and composition were studied in Wistar rats treated with the fungicide for 1, 2, 3, or 4 weeks and then withdrawn for a 20-week period. |
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