Gene expression in benzene-exposed workers by microarray analysis of peripheral mononuclear blood cells: Induction and silencing of CYP4F3A and regulation of DNA-dependent protein kinase catalytic subunit in DNA double strand break repair

Bi, Yang; Li, Yuhong; Kong, Mengmeng; Xiao, Xiao; Zhao, Zhiwei; He, Xiaoqing; Ma, Qiang

doi:10.1016/j.cbi.2009.12.024

Cited by 22 publications

(19 citation statements)

References 10 publications

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“…Spontaneous recombination in response to DNA damage occurs due to lesions that do not block the replication fork, but instead leave potential recombinogenic substrates such as single-stranded gaps in DNA sequences [28,29,51,52] . Double strand breaks are caused by environmental carcinogen exposure (such as exposure to certain benzene-derived products) [54][55][56] and replication stress [31,32] . This type of DNA damage is repaired through (1) HR recombination (as described above) or (2) non-homologous end-joining (NHEJ).…”

Section: Types Of Dna Lesions and Their Repair Mechanismsmentioning

confidence: 99%

DNA damage and breast cancer

Davis

Lin

2011

WJCO

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Cancer is intimately related to the accumulation of DNA damage, and repair failures (including mutation prone repair and hyperactive repair systems). This article relates current clinical categories for breast cancer and their common DNA damage repair defects. Information is included on the potential for accumulation of DNA damage in the breast tissue of a woman during her lifetime and the role of DNA damage in breast cancer development. We then cover endogenous and exogenous sources of DNA damage, types of DNA damage repair and basic signal transduction pathways for three gene products involved in the DNA damage response system; namely BRCA1, BRIT1 and PARP-1. These genes are often considered tumor suppressors because of their roles in DNA damage response and some are under clinical investigation as likely sources for effective new drugs to treat breast cancers. Finally we discuss some of the problems of DNA damage repair systems in cancer and the conundrum of hyper-active repair systems which can introduce mutations and confer a survival advantage to certain types of cancer cells.

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Section: Types Of Dna Lesions and Their Repair Mechanismsmentioning

confidence: 99%

DNA damage and breast cancer

Davis

Lin

2011

WJCO

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“…We have previously found that the expressions of CYP4F3A and DNA-PKcs were elevated in workers diagnosed with benzene poisoning by microarray analysis of peripheral mononuclear blood cells. In K562 and HL-60 cells, CYP4F3A and DNA-PKcs were shown to be induced by benzene metabolites at both protein and mRNA levels [24]–[27]. CYP4f3A encodes the leukotriene B 4 ω-hydroxylase in human polymorphonuclear leukocytes.…”

Section: Introductionmentioning

confidence: 99%

Comparison of Toxicity of Benzene Metabolite Hydroquinone in Hematopoietic Stem Cells Derived from Murine Embryonic Yolk Sac and Adult Bone Marrow

et al. 2013

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Benzene is an occupational toxicant and an environmental pollutant that potentially causes hematotoxicity and leukemia in exposed populations. Epidemiological studies suggest an association between an increased incidence of childhood leukemia and benzene exposure during the early stages of pregnancy. However, experimental evidence supporting the association is lacking at the present time. It is believed that benzene and its metabolites target hematopoietic stem cells (HSCs) to cause toxicity and cancer in the hematopoietic system. In the current study, we compared the effects of hydroquinone (HQ), a major metabolite of benzene in humans and animals, on mouse embryonic yolk sac hematopoietic stem cells (YS-HSCs) and adult bone marrow hematopoietic stem cells (BM-HSCs). YS-HSCs and BM-HSCs were isolated and enriched, and were exposed to HQ at increasing concentrations. HQ reduced the proliferation and the differentiation and colony formation, but increased the apoptosis of both YS-HSCs and BM-HSCs. However, the cytotoxic and apoptotic effects of HQ were more apparent and reduction of colony formation by HQ was more severe in YS-HSCs than in BM-HSCs. Differences in gene expression profiles were observed in HQ-treated YS-HSCs and BM-HSCs. Cyp4f18 was induced by HQ both in YS-HSCs and BM-HSCs, whereas DNA-PKcs was induced in BM-HSCs only. The results revealed differential effects of benzene metabolites on embryonic and adult HSCs. The study established an experimental system for comparison of the hematopoietic toxicity and leukemogenicity of benzene and metabolites during mouse embryonic development and adulthood.

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“…Albeit we did not correlate humans and animal exposures, it is conceivable suppose that, in this study, mice were subjected to low levels of HQ, as defined by their air concentrations in the exposure chamber (0.044 ppm). Our subsequent studies reinforced such point of view, by observations that relevant biochemical and biological end-points described in the literature to in vivo BZ or HQ exposure, as number of circulating leukocytes and DNA alterations (Bi et al, 2010, McGrgeor, 2007, were not affected by the experimental intoxication procedure here employed.…”

Section: Effects Of In Vivo Hq Exposure On Adhesion Molecules Expressionmentioning

confidence: 54%

“…is also achieved as a component of tobacco, and high concentrations are released during smoking . In addition, HQ is a relevant BZ endogenous metabolite and it has been clearly demonstrated that HQ is a key determinant for immune suppression and leukemias development in human exposed to BZ (Badham et al, 2010;Bi et al, 2010;Atkinson, 2009). These effects have been partially associated to DNA lesions, as HQ exposure causes oxidative DNA damage in a variety of cells, including circulating leukocytes and lung tissue (Melikian et al, 2008;Várkonyi et al, 2006;Leanderson, 1993).…”

Section: Discussionmentioning

confidence: 99%

Efeitos da exposição in vivo à hidroquinona sobre funções do tecido traqueal e de macrófagos alveolares de camundongos

Shimada¹

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Gene expression in benzene-exposed workers by microarray analysis of peripheral mononuclear blood cells: Induction and silencing of CYP4F3A and regulation of DNA-dependent protein kinase catalytic subunit in DNA double strand break repair

Cited by 22 publications

References 10 publications

DNA damage and breast cancer

DNA damage and breast cancer

Comparison of Toxicity of Benzene Metabolite Hydroquinone in Hematopoietic Stem Cells Derived from Murine Embryonic Yolk Sac and Adult Bone Marrow

Efeitos da exposição in vivo à hidroquinona sobre funções do tecido traqueal e de macrófagos alveolares de camundongos

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