Influence of culture conditions on the DNA-damaging effect of benzene and its metabolites in human peripheral blood mononuclear cells

Fabiani, Roberto; Bartolomeo, Angelo De; Rosignoli, Patrizia; Scamosci, Michela; Lepore, Luca; Morozzi, Guido

doi:10.1002/1098-2280(2001)37:1<1::aid-em1000>3.0.co;2-1

Cited by 26 publications

(23 citation statements)

References 26 publications

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“…In a previous study, we found that incubating human peripheral blood mononuclear cells (PBMCs) with BQ in a simple phosphate buffer or RPMI 1640 cell culture medium resulted in relatively weak genotoxic activity [Fabiani et al, 2001]. However, we found that the presence of fetal calf serum (FCS) in the incubation medium increased the genotoxic activity of BQ by 7-10 fold [Fabiani et al, 2001].…”

Section: Introductionmentioning

confidence: 99%

Involvement of oxygen free radicals in the serum‐mediated increase of benzoquinone genotoxicity

Fabiani

Bartolomeo

Morozzi

2005

Environ and Mol Mutagen

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The genotoxicity of benzoquinone (BQ), a toxic benzene metabolite, is greatly enhanced by the presence of fetal calf serum (FCS) in the incubation medium. The FCS effect is abolished by heat denaturation of serum proteins and is slightly decreased by dialysis. In the present study, we have further investigated the serum effect on BQ genotoxicity by measuring DNA damage produced in peripheral blood mononuclear cells (PBMCs) using the Comet assay. We have also evaluated the effect of human serum and rat liver post-mitochondrial fraction (S9) on the DNA damage produced by BQ. Both human serum and a rat liver S9 enhanced the genotoxicity of BQ in a manner similar to FCS. Gel filtration experiments showed that all the enhancing activity of the serum eluted with the high molecular weight fractions, suggesting that low molecular weight serum constituents do not play an important role in modulating genotoxicity. The genotoxicity-enhancing activity of serum was inhibited by the iron chelator deferoxamine and by superoxide dismutase and catalase. Incubating PBMCs with BQ in the presence of FCS also resulted in the accumulation of intracellular peroxides as demonstrated by loading the cells with 2',7'-dichlorofluorescin diacetate and analyzing for peroxide formation by flow cytometry. These results indicate that oxygen free radicals are involved in the enhancement of BQ-induced DNA damage by serum. We hypothesize that enzyme activities that reduce BQ by transferring single electrons could be the source of the oxygen free radicals.

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Section: Introductionmentioning

confidence: 99%

Involvement of oxygen free radicals in the serum‐mediated increase of benzoquinone genotoxicity

Fabiani

Bartolomeo

Morozzi

2005

Environ and Mol Mutagen

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“…The length and DNA content are directly proportional to the degree of DNA damage. Therefore, the single-cell DNA breakage can be quantitative analysed, reflecting the results of genetic toxicity due to low-dose or minor damage (Fabiani et al 2001;Deng et al 2005;Yang and Zheng 2006). In this study, comet assay was used to determine DNA damage on rat liver cells due to organic extract in soil.…”

Section: Discussionmentioning

confidence: 99%

Hepatotoxicity and nephrotoxicity of organic contaminants in wastewater-irrigated soil

Gao

Liu

Guan

et al. 2014

Environ Sci Pollut Res

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The objective of this study is to investigate the hepatotoxicity and nephrotoxicity of organic contaminants in wastewater-irrigated soil using in vivo and in vitro experiments on mice and rat. Soil samples were collected from a wastewater-irrigated area and groundwater-irrigated area, i.e. clean water-irrigated area as control group. The organic contaminants were extracted using an ultrasonic oscillator. In vivo experiment was performed by contamination of hepatocytes of rat using the organic extract, and comet assay was used to analyse the DNA damage of hepatocytes. For in vitro experiment, mice were first gavaged with extracts, and then the indicators for kidney functions, liver functions and oxidative damage of tissues were investigated. The result shows, for in vitro experiments, compared with clean water-irrigated area groups, the average DNA tailing length for the wastewater-irrigated area group is larger, and for the wastewater-irrigated area groups with extract concentration 0.6 g/ml and 0.9 g/ml, the tailing rate increases significantly (P < 0.05). For in vivo experiments, the change of weight across each group shows no significant difference (P < 0.05). Compared with clean water-irrigated groups, the liver indices have decreased for all groups of the wastewater-irrigated area, while both kidney and liver indices decreased for wastewater-irrigated area high-dose group (P < 0.05 or P < 0.01). The total proteins for wastewater-irrigated low-dose group and Gamma-glutamyl transpeptidase, creatinine for high-dose group all increased (P < 0.01). Compared with the reagent control group, total superoxide dismutase activity of liver for wastewater-irrigated groups and glutathione peroxidase activity for high-dose group, malondialdehyde content all decreased (P < 0.05 or P < 0.01); glutathione peroxidase activity of kidney tissue for wastewater-irrigated high-dose group decreased (P < 0.01). The result shows that the joint toxicity in extracts of wastewater-irrigated soil is able to cause DNA damage of hepatocytes in rats, changes of liver functions in mice and lead to oxidative damage of liver and kidney.

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“…Some studies on human lymphocytes indicated that hydroquinone was clastogenic and produces micronuclei, 44,45 while others showed neither clastogenic effects nor micronuclei induction 46,47 . Culture conditions markedly affect the outcome of studies on the DNA‐damaging effects of hydroquinone 48 …”

Section: In Vitro and In Vivo Animal Studiesmentioning

confidence: 99%

“…46,47 Culture conditions markedly affect the outcome of studies on the DNA-damaging effects of hydroquinone. 48 By contrast, oral ingestion or systemic injections of hydroquinone into animals have failed to induce malignancies or marrow toxicity. 29,42,49 These results suggest that hydroquinone in vivo is metabolized by various tissues, including the liver, into nontoxic by-products.…”

Section: In Vitro and In Vivo Animal Studiesmentioning

confidence: 99%

The safety of hydroquinone

Grimes

Jp³

2006

Acad Dermatol Venereol

157

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Hydroquinone is one of the most effective molecules for the treatment of hyperpigmentary disorders, with over 40 years of efficacy and safety data. Concerns over its safety have been raised because of the fact that it is a derivative of benzene and because of the long-term side-effects observed with cosmetic products containing high concentrations of hydroquinone. However, despite 40-50 years use of hydroquinone for medical conditions, there has not been a single documented case of either a cutaneous or internal malignancy associated with this drug. This article reviews the evidence for the safety of hydroquinone in the treatment of hyperpigmentation conditions.

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Influence of culture conditions on the DNA-damaging effect of benzene and its metabolites in human peripheral blood mononuclear cells

Cited by 26 publications

References 26 publications

Involvement of oxygen free radicals in the serum‐mediated increase of benzoquinone genotoxicity

Involvement of oxygen free radicals in the serum‐mediated increase of benzoquinone genotoxicity

Hepatotoxicity and nephrotoxicity of organic contaminants in wastewater-irrigated soil

The safety of hydroquinone

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