Effect of the Benzene Metabolite, Hydroquinone, on Interleukin-1 Secretion by Human Monocytes in Vitro

Carbonnelle, Pierre; Lison, Dominique; Leroy, Jacques; Lauwerys, Robert

doi:10.1006/taap.1995.1102

Cited by 12 publications

(9 citation statements)

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“…284,285 Incubation of human peripheral monocytes with 5 µM HQ resulted in substantially decreased IL-1α and -1β secretion and RNA and protein synthesis. 286 An IC 50 of 25 µM for inhibition of RNA synthesis was demonstrated for HQ in mouse peritoneal macrophages. 287 The oxidation of HQ to reactive products (i.e., semiquinone and/or BQ) either spontaneously or via metabolism within the bone marrow compartment has been postulated to represent a critical step in the mechanism of HQ (and benzene) myelotoxicity.…”

Section: Myelotoxicity and Immunotoxicitymentioning

confidence: 97%

The Toxicology of Hydroquinone — Relevance to Occupational and Environmental Exposure

DeCaprio¹

1999

Critical Reviews in Toxicology

178

128

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Hydroquinone (HQ) is a high-volume commodity chemical used as a reducing agent, antioxidant, polymerization inhibitor, and chemical intermediate. It is also used in over-the-counter (OTC) drugs as an ingredient in skin lighteners and is a natural ingredient in many plant-derived products, including vegetables, fruits, grains, coffee, tea, beer, and wine. While there are few reports of adverse health effects associated with the production and use of HQ, a great deal of research has been conducted with HQ because it is a metabolite of benzene. Physicochemical differences between HQ and benzene play a significant role in altering the pharmacokinetics of directly administered when compared with benzene-derived HQ. HQ is only weakly positive in in vivo chromosomal assays when expected human exposure routes are used. Chromosomal effects are increased significantly when parenteral or in vitro assays are used. In cancer bioassays, HQ has reproducibly produced renal adenomas in male F344 rats. The mechanism of tumorigenesis is unclear but probably involves a species-, strain-, and sex-specific interaction between renal tubule toxicity and an interaction with the chronic progressive nephropathy that is characteristic of aged male rats. Mouse liver tumors (adenomas) and mononuclear cell leukemia (female F344 rat) have also been reported following HQ exposure, but their significance is uncertain. Various tumor initiation/promotion assays with HQ have shown generally negative results. Epidemiological studies with HQ have demonstrated lower death rates and reduced cancer rates in production workers when compared with both general and employed referent populations. Parenteral administration of HQ is associated with changes in several hematopoietic and immunologic endpoints. This toxicity is more severe when combined with parenteral administration of phenol. It is likely that oxidation of HQ within the bone marrow compartment to the semiquinone or p-benzoquinone (BQ), followed by covalent macromolecular binding, is critical to these effects. Bone marrow and hematologic effects are generally not characteristic of HQ exposures in animal studies employing routes of exposure other than parenteral. Myelotoxicity is also not associated with human exposure to HQ. These differences are likely due to significant route-dependent toxicokinetic factors. Fetotoxicity (growth retardation) accompanies repeated administration of HQ at maternally toxic dose levels in animal studies. HQ exposure has not been associated with other reproductive and developmental effects using current USEPA test guidelines. The skin pigment lightening properties of HQ appear to be due to inhibition of melanocyte tyrosinase. Adverse effects associated with OTC use of HQ in FDA-regulated products have been limited to a small number of cases of exogenous ochronosis, although higher incidences of this syndrome have been reported with inappropriate use of unregulated OTC products containing higher HQ concentrations. The most serious human health effect related to HQ is p...

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Section: Myelotoxicity and Immunotoxicitymentioning

confidence: 97%

The Toxicology of Hydroquinone — Relevance to Occupational and Environmental Exposure

DeCaprio¹

1999

Critical Reviews in Toxicology

178

128

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“…In theory, measurement of IL-1a production by lipopolysaccharide-stimulated monocytes seems quite reasonable. Indeed, Carbonnelle et al (1995) found a decreased IL-1a concentration both in the culture medium of HQ-exposed human monocytes and in cell lysates. Sample conservation might have aected the IL-1a concentration.…”

Section: Discussionmentioning

confidence: 96%

“…Furthermore, MacEachern and Laskin (1992) found only a small and transient increase in IL-1 production by bone marrow leukocytes in mice receving benzene. Finally, using human monocytes exposed to HQ, Carbonnelle et al (1995) suggested that the reduction in IL-1 production seen after HQ exposure could result from a global impairment of monocyte function rather than from a speci®c eect on IL-1a. As a result, the speci®c and causal link between benzene exposure, disturbed proIL-1a processing, and anemia could be questioned.…”

Section: Discussionmentioning

confidence: 98%

Interleukin 1α and hematological examination in mechanics exposed to low benzene concentrations

Hotz¹,

Carbonnelle²,

Scheiff³

et al. 1998

International Archives of Occupational and Environmental Health

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The hypothesis of Renz and Kalf could not be confirmed. Although the low level exposure of the study population and methodological factors are possible explanations, it cannot be excluded that the hypothesis of Renz and Kalf is not generalizable to benzene-exposed humans. Presently, one cannot advise the measurement of IL-1 alpha production for biological effect monitoring of workers exposed to low concentrations of benzene.

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“…The first study that examined the role of HQ in the release of IL-1 α and IL-1 β by mononuclear phagocytes in humans was in 1995 [23]. The results of the study showed a dose-dependent reduction of IL-1 secretion by HQ that also determined the fall of total protein content.…”

Section: Introductionmentioning

confidence: 99%

Cytokine Network Involvement in Subjects Exposed to Benzene

Minciullo

Navarra

Calapai

et al. 2014

Journal of Immunology Research

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Benzene represents an ubiquitous pollutant both in the workplace and in the general environment. Health risk and stress posed by benzene have long been a concern because of the carcinogenic effects of the compound which was classified as a Group 1 carcinogen to humans and animals. There is a close correlation between leukemia, especially acute myeloid leukemia, and benzene exposure. In addition, exposure to benzene can cause harmful effects on immunological, neurological, and reproductive systems. Benzene can directly damage hematopoietic progenitor cells, which in turn could lead to apoptosis or may decrease responsiveness to cytokines and cellular adhesion molecules. Alternatively, benzene toxicity to stromal cells or mature blood cells could disrupt the regulation of hematopoiesis, including hematopoietic commitment, maturation, or mobilization, through the network of cytokines, chemokines, and adhesion molecules. Today there is mounting evidence that benzene may alter the gene expression, production, or processing of several cytokines in vitro and in vivo. The purpose of this review was to systematically analyze the published cases of cytokine effects on human benzene exposure, particularly hematotoxicity, and atopy, and on lungs.

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Effect of the Benzene Metabolite, Hydroquinone, on Interleukin-1 Secretion by Human Monocytes in Vitro

Cited by 12 publications

References 0 publications

The Toxicology of Hydroquinone — Relevance to Occupational and Environmental Exposure

The Toxicology of Hydroquinone — Relevance to Occupational and Environmental Exposure

Interleukin 1α and hematological examination in mechanics exposed to low benzene concentrations

Cytokine Network Involvement in Subjects Exposed to Benzene

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