Carcinogenic activity of hexacholorobenzene in hamsters

Cabral, J. R. P.; Shubik, Philippe; Mollner, Teresa J.; Raitano, F.

doi:10.1038/269510a0

Cited by 105 publications

(25 citation statements)

References 7 publications

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“…Increased levels of hexachlorobenzene as well as octachlorostyrene were found in blood plasma of foundry workers several years after the end of exposure to the by-products of HCE in aluminum degassing . Hexachlorobenzene induces liver cancer in rodents [Cabral and Shubik, 1986], and one case of hepatocellular carcinoma has been described in an aluminum foundry worker with this particular exposure [Seldén et al, 1989].…”

Section: Liver Cancermentioning

confidence: 99%

Cancer morbidity in workers at aluminum foundries and secondary aluminum smelters

1997

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Section: Liver Cancermentioning

confidence: 99%

Cancer morbidity in workers at aluminum foundries and secondary aluminum smelters

1997

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“…, 1979). In the latter study, higher doses of 0.01% or 0.02% gave 10% and 16% incidences of liver tumours, respectively, whereas in rats and hamsters such levels of HCB produced significantly higher incidences (>85%) (Cabral et al, 1977;Smith et al, 1985; Ertiirk et al, 1986). The demonstration that, in mice, iron overload could enhance the induction of tumours as well as that of porphyria would be an important step in establishing the role of iron in some carcinogenic processes.…”

mentioning

confidence: 92%

Carcinogenicity of iron in conjunction with a chlorinated environmental chemical, hexachlorobenzene, in c57bl/10scsn mice

Smith¹,

Cabral²,

Carthew³

et al. 1989

Intl Journal of Cancer

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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). HCB will also cause liver tumours in experimental animals. Elevated liver iron stores are implicated in the development of some human liver cancers. To determine whether iron overload will potentiate the hepatocarcinogenicity of HCB, male C57BL/10ScSn mice received a single dose of iron-dextran complex or the dextran carrier and were then fed HCB in the diet (0.01%) for up to 18 months. A very clear potentiation by iron of liver tumour incidence occurred. Of the mice which received HCB, but no iron, for 12 months a low incidence of liver hyperplastic nodules was observed, whereas preadministration of iron increased the incidence. After 18 months, all surviving mice initially given iron followed by HCB developed advanced hepatic nodules and 90% had hepatocellular carcinomas. No tumours were seen in animals that only received HCB. Nodules were not seen in iron-dosed mice receiving control diet, but another novel observation was that these animals developed porphyria by 6 months. Although iron enhanced tumour formation in the presence of HCB, the foci, nodules and carcinomas formed all excluded iron. Preliminary studies with the DBA/2 strain suggested that these mice were considerably less susceptible to potentiation by iron.

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“…Laboratory animal studies revealed that chronic exposure to HCB could induce livercell tumors in rats and mice (27)(28)(29), renal adenomas in rats (30), and liver-cell tumors, haemangioendotheliomas, and thyroid adenomas in hamsters (31). HCB acts as a promoter of cancer in several studies (32,33).…”

Section: General Toxicity Ofhcbmentioning

confidence: 99%

The role of the immune system in hexachlorobenzene-induced toxicity.

Michielsen

Loveren

Vos

1999

Environ Health Perspect

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Hexachlorobenzene (HCB) is a persistent environmental pollutant. The toxicity of HCB has been extensively studied after an accidental human poisoning in Turkey and more recently it has been shown that HCB has immunotoxic properties in laboratory animals and probably also in man. Oral exposure of rats to HCB showed stimulatory effects on spleen and lymph node weights and histology, increased serum IgM levels, and an enhancement of several parameters of immune function. Moreover, more recent studies indicate that HCB-induced effects in the rat may be related to autoimmunity. In Wistar rats exposed to HCB, IgM antibodies against several autoantigens were elevated; in the Lewis rat, HCB differently modulated two experimental models of autoimmune disease. Oral exposure of rats to HCB induces skin and lung pathology in the rat. Recently several studies have been conducted to investigate whether these skin and lung lesions can be related to HCB-induced immunomodulation, and these studies will be discussed in this review. HCB-induced skin and lung lesions probably have a different etiology; pronounced strain differences and correlation of skin lesions with immune parameters suggest a specific involvement of the immune system in HCB-induced skin lesions. The induction of lung lesions by HCB was thymus independent. Thymus-dependent T cells were not likely to be required for the induction of skin lesions, although T cells enhanced the rate of induction and the progression of the skin lesions. No deposition of autoantibodies was observed in nonlesional or lesional skin of HCB-treated rats. Therefore, we concluded that it is unlikely that the mechanism by which most allergic or autoimmunogenic chemicals work, i.e., by binding to macromolecules of the body and subsequent T-and B-cell activation, is involved in the HCB-induced immunopathology in the rat. Such a thymus-independent immunopathology is remarkable, as HCB strongly modulates T-cell-mediated immune parameters. This points at a very complex mechanism and possible involvement of multiple factors in the immunopathology of HCB.

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Carcinogenic activity of hexacholorobenzene in hamsters

Cited by 105 publications

References 7 publications

Cancer morbidity in workers at aluminum foundries and secondary aluminum smelters

Cancer morbidity in workers at aluminum foundries and secondary aluminum smelters

Carcinogenicity of iron in conjunction with a chlorinated environmental chemical, hexachlorobenzene, in c57bl/10scsn mice

The role of the immune system in hexachlorobenzene-induced toxicity.

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