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Chemical Compound Review

HCB     1,2,3,4,5,6-hexachlorobenzene

Synonyms: Sanocide, Anticarie, Sanocid, Amatin, Granox, ...
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Disease relevance of HEXACHLOROBENZENE

  • These findings suggest that lipid peroxidation and mitochondrial dysfunction may contribute to the hepatotoxicity seen in hexachlorobenzene-induced porphyria [1].
  • Evidence for an environmental predisposition was less clear cut, but it is interesting that members of both families used a gamma isomer of hexachlorobenzene (Nickoff) to eradicate mite infestations in their birds which might have damaged the bronchial mucosa or acted as an immunologic adjuvant in a person with underlying susceptibility to disease [2].
  • These studies demonstrate that not only are female rats far more sensitive than males to the porphyrinogenic effects of HCB but also to the hepatocarcinogenic actions, suggesting a link between these two manifestations of toxicity that may also apply to other polyhalogenated aromatics [3].
  • Pre-loading of C57BL/10ScSn mice with iron greatly sensitizes them to the induction of hepatic porphyria caused by hexachlorobenzene (HCB) (Smith and Francis, 1983) [4].
  • Under the influence of iron overload EROD was significantly depressed from HCB alone, but not the others or cytochrome P450 reductase [5].

Psychiatry related information on HEXACHLOROBENZENE


High impact information on HEXACHLOROBENZENE

  • In an antibody-dependent cell-mediated cytotoxicity test using isolated hepatocytes from normal and hexachlorobenzene-treated (porphyric) rats as targets, it was found that sera from group 1a produced high cytotoxicity against porphyric hepatocytes and low or zero cytotoxicity against normal hepatocytes (p less than 0.001) [10].
  • HCB treatments resulted in increased proliferation of normal hepatocytes, which was not observed for PECB under the same treatment regimen [11].
  • The best description of the data resulted from the model incorporating the hypothesis that PECB and HCB promoted the growth of foci via increased net growth rates of B cells [11].
  • There was a significant increase in mitochondrial lipid peroxidation in rats treated with hexachlorobenzene alone and hexachlorobenzene + Fe [1].
  • Hexachlorobenzene, benzo(a)pyrene, and beta-naphthoflavone were effective AHR agonists in the yeast system, and had EC50 values of 200, 40, and 20 nM, respectively, for beta-galactosidase activity induction [12].

Chemical compound and disease context of HEXACHLOROBENZENE


Biological context of HEXACHLOROBENZENE


Anatomical context of HEXACHLOROBENZENE

  • For example, an increase in erythrocyte protoporphyrin is a useful measurement for early detection of exposure to lead and porphyrinuria was an early manifestation of a hexachlorobenzene-induced porphyria in Turkey [21].
  • There was no major difference in the ability to hydroxylate HCB between hepatic microsomes from induced C57BL/10 mice and those from the insensitive DBA/2 strain [22].
  • Hexachlorobenzene treatment, therefore, does not affect the iron status of the mitochondria [23].
  • Hexachlorobenzene (HCB) elicits concentration-dependent and saturable type 1 binding spectra when added to oxidized (Fe3+) cytochrome P-450 (CYT P-450) in control, phenobarbital- (PB) induced, and beta-naphthoflavone- (BNF) induced male Sprague-Dawley rat liver microsomes [24].
  • 2. Hexachlorobenzene has no effect on erythrocyte porphyrin content, but produces a decrease in that of Harderian gland and an increase in the porphyrin content of the kidney and spleen, and a marked increase in the liver (1 mumol/g of tissue) [25].

Associations of HEXACHLOROBENZENE with other chemical compounds



  • The role of the Ah locus in hexachlorobenzene (HCB)-induced porphyria and the possible involvement of P-450 cytochromes P(1)450 and P(3)450 in the pathogenesis of this disease were investigated in two congenic strains of C57BL/6J mice that differ only at this locus [28].
  • The IRS-1 phosphorylation increased in HCB rats; however, it decreased in NMU-HCB vs. NMU [29].
  • IR, IGF-IR, and IRS-1 levels were higher in HCB than in controls [29].
  • In HCB exposed Lewis rats and T. spiralis infected BN rats the IL-4 mRNA expression correlated with IgE levels and T. spiralis infection, respectively, whereas the IL-4 production lacked correlation in all cases [30].
  • Hexachlorobenzene reduced the levels of IL-5, IL-10 and IFN-gamma [31].

Analytical, diagnostic and therapeutic context of HEXACHLOROBENZENE

  • A clonal growth model: time-course simulations of liver foci growth following penta- or hexachlorobenzene treatment in a medium-term bioassay [11].
  • Thus mitochondrial preparations, which were further depleted of lysosomes by Percoll-density-gradient centrifugation, contained 2.78 +/- 0.75 and 2.99 +/- 0.49 nmol of non-haem iron/mg of protein when isolated from the liver of control rats and hexachlorobenzene-treated rats respectively [23].
  • These descriptive findings are in agreement with previously reported associations between soft-tissue sarcoma and human exposure to organochlorinated compounds, as well as with animal experiments relating HCB and thyroid cancer, and add new information on the possible relation between organochlorinated compounds, and particularly HCB, and cancer [32].
  • Serum HCB was analyzed by gas chromatography coupled with electron capture detection [33].
  • No significant difference in mean breast adipose tissue levels of HCB was observed between breast cancer patients (21.0 ppb) and controls (19.1 ppb) in this large case-control study [34].


  1. Hepatic mitochondrial oxidative metabolism and lipid peroxidation in experimental hexachlorobenzene-induced porphyria with dietary carbonyl iron overload. Feldman, E.S., Bacon, B.R. Hepatology (1989) [Pubmed]
  2. Familial hypersensitivity pneumonitis. Allen, D.H., Basten, A., Williams, G.V., Woolcock, A.J. Am. J. Med. (1975) [Pubmed]
  3. Hepatocarcinogenicity of hexachlorobenzene in rats and the sex difference in hepatic iron status and development of porphyria. Smith, A.G., Francis, J.E., Dinsdale, D., Manson, M.M., Cabral, J.R. Carcinogenesis (1985) [Pubmed]
  4. Carcinogenicity of iron in conjunction with a chlorinated environmental chemical, hexachlorobenzene, in C57BL/10ScSn mice. Smith, A.G., Cabral, J.R., Carthew, P., Francis, J.E., Manson, M.M. Int. J. Cancer (1989) [Pubmed]
  5. Enhancement by iron of hepatic neoplasia in rats caused by hexachlorobenzene. Smith, A.G., Carthew, P., Francis, J.E., Cabral, J.R., Manson, M.M. Carcinogenesis (1993) [Pubmed]
  6. Developmental neurotoxicity following premating maternal exposure to hexachlorobenzene in rats. Goldey, E.S., Taylor, D.H. Neurotoxicology and teratology. (1992) [Pubmed]
  7. Effect of food deprivation on low level hexachlorobenzene exposure in rats. Villeneuve, D.C., van Logten, M.J., den Tonkelaar, E.M., Greve, P.A., Vos, J.G., Speijers, G.J., van Esch, G.J. Sci. Total Environ. (1977) [Pubmed]
  8. Dechlorination of hexachlorobenzene using ultrafine Ca-Fe composite oxides. Ma, X., Zheng, M., Liu, W., Qian, Y., Zhang, B., Liu, W. Journal of hazardous materials. (2005) [Pubmed]
  9. Levels of organochlorine contaminants in human milk in relation to the dietary habits of the mothers. Norén, K. Acta paediatrica Scandinavica. (1983) [Pubmed]
  10. Serum antibodies against porphyric hepatocytes in patients with porphyria cutanea tarda and liver disease. Baravalle, E., Prieto, J. Gastroenterology (1983) [Pubmed]
  11. A clonal growth model: time-course simulations of liver foci growth following penta- or hexachlorobenzene treatment in a medium-term bioassay. Ou, Y.C., Conolly, R.B., Thomas, R.S., Xu, Y., Andersen, M.E., Chubb, L.S., Pitot, H.C., Yang, R.S. Cancer Res. (2001) [Pubmed]
  12. Expression of the human aryl hydrocarbon receptor complex in yeast. Activation of transcription by indole compounds. Miller, C.A. J. Biol. Chem. (1997) [Pubmed]
  13. Uroporphyria produced in mice by 20-methylcholanthrene and 5-aminolaevulinic acid. Urquhart, A.J., Elder, G.H., Roberts, A.G., Lambrecht, R.W., Sinclair, P.R., Bement, W.J., Gorman, N., Sinclair, J.A. Biochem. J. (1988) [Pubmed]
  14. Bile and biliary lipid secretion in rats with hexachlorobenzene-induced porphyria. Effect of S-adenosyl-L-methionine administration. Cuomo, R., Rodino, S., Rizzoli, R., Simoni, P., Roda, E., Cantoni, L., Rizzardini, M., De Rosa, G., Le Grazie, C., Di Padova, C. J. Hepatol. (1991) [Pubmed]
  15. Search for Ha-ras codon 61 mutations in liver tumours caused by hexachlorobenzene and Aroclor 1254 in C57BL/10ScSn mice with iron overload. Rumsby, P.C., Evans, J.G., Phillimore, H.E., Carthew, P., Smith, A.G. Carcinogenesis (1992) [Pubmed]
  16. Susceptibility to infections and immune status in Inuit infants exposed to organochlorines. Dewailly, E., Ayotte, P., Bruneau, S., Gingras, S., Belles-Isles, M., Roy, R. Environ. Health Perspect. (2000) [Pubmed]
  17. The role of pentachlorophenol in causing mitochondrial derangement in hexachlorobenzene induced experimental porphyria. Masini, A., Ceccarelli-Stanzani, D., Tomasi, A., Trenti, T., Ventura, E. Biochem. Pharmacol. (1985) [Pubmed]
  18. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Peters, H.A., Gocmen, A., Cripps, D.J., Bryan, G.T., Dogramaci, I. Arch. Neurol. (1982) [Pubmed]
  19. Hexachlorobenzene, a dioxin-type compound, increases malic enzyme gene transcription through a mechanism involving the thyroid hormone response element. Loaiza-Pérez, A.I., Seisdedos, M.T., Kleiman de Pisarev, D.L., Sancovich, H.A., Randi, A.S., Ferramola de Sancovich, A.M., Santisteban, P. Endocrinology (1999) [Pubmed]
  20. Organochlorines, lead, and mercury in Akwesasne Mohawk youth. Schell, L.M., Hubicki, L.A., DeCaprio, A.P., Gallo, M.V., Ravenscroft, J., Tarbell, A., Jacobs, A., David, D., Worswick, P. Environ. Health Perspect. (2003) [Pubmed]
  21. Exposure to toxic agents: the heme biosynthetic pathway and hemoproteins as indicator. Marks, G.S. Crit. Rev. Toxicol. (1985) [Pubmed]
  22. Mechanistic studies of the inhibition of hepatic uroporphyrinogen decarboxylase in C57BL/10 mice by iron-hexachlorobenzene synergism. Smith, A.G., Francis, J.E., Kay, S.J., Greig, J.B., Stewart, F.P. Biochem. J. (1986) [Pubmed]
  23. Lysosomes, but not mitochondria, accumulate iron and porphyrins in porphyria induced by hexachlorobenzene. Tangerås, A. Biochem. J. (1986) [Pubmed]
  24. Cytochrome P-450 mediated reductive dehalogenation of the perhalogenated aromatic compound hexachlorobenzene. Takazawa, R.S., Strobel, H.W. Biochemistry (1986) [Pubmed]
  25. Porphyrins and porphyrinogen carboxy-lase in hexachlorobenzene-induced porphyria. San Martín De Viale, L.C., Ríos De Molina, M.D., De Calmanovici, R.W., Tomio, J.M. Biochem. J. (1977) [Pubmed]
  26. Detection of endocrine disrupting chemicals in samples of second trimester human amniotic fluid. Foster, W., Chan, S., Platt, L., Hughes, C. J. Clin. Endocrinol. Metab. (2000) [Pubmed]
  27. Most unwanted. Fisher, B.E. Environ. Health Perspect. (1999) [Pubmed]
  28. The role of the Ah locus in hexachlorobenzene-induced porphyria. Studies in congenic C57BL/6J mice. Hahn, M.E., Gasiewicz, T.A., Linko, P., Goldstein, J.A. Biochem. J. (1988) [Pubmed]
  29. Hexachlorobenzene is a tumor co-carcinogen and induces alterations in insulin-growth factors signaling pathway in the rat mammary gland. Randi, A.S., Cocca, C., Carbone, V., Nuñez, M., Croci, M., Gutiérrez, A., Bergoc, R., Kleiman de Pisarev, D.L. Toxicol. Sci. (2006) [Pubmed]
  30. Interleukin-10 is an unequivocal Th2 parameter in the rat, whereas interleukin-4 is not. Vandebriel, R.J., Meredith, C., Scott, M.P., van Dijk, M., van Loveren, H. Scand. J. Immunol. (2000) [Pubmed]
  31. Limited effect of selected organic pollutants on cytokine production by peripheral blood leukocytes. Devos, S., Van Den Heuvel, R., Hooghe, R., Hooghe-Peters, E.L. Eur. Cytokine Netw. (2004) [Pubmed]
  32. Risk excess of soft-tissue sarcoma and thyroid cancer in a community exposed to airborne organochlorinated compound mixtures with a high hexachlorobenzene content. Grimalt, J.O., Sunyer, J., Moreno, V., Amaral, O.C., Sala, M., Rosell, A., Anto, J.M., Albaiges, J. Int. J. Cancer (1994) [Pubmed]
  33. Evaluation of urinary porphyrin excretion in neonates born to mothers exposed to airborne hexachlorobenzene. Ozalla, D., Herrero, C., Ribas-Fitó, N., To-Figueras, J., Toll, A., Sala, M., Grimalt, J., Basagaña, X., Lecha, M., Sunyer, J. Environ. Health Perspect. (2002) [Pubmed]
  34. Environmental exposure to hexachlorobenzene (HCB) and risk of female breast cancer in Connecticut. Zheng, T., Holford, T.R., Mayne, S.T., Tessari, J., Owens, P.H., Zahm, S.H., Zhang, B., Dubrow, R., Ward, B., Carter, D., Boyle, P. Cancer Epidemiol. Biomarkers Prev. (1999) [Pubmed]
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