Neonatal exposure to benzo[a]pyrene decreases the levels of serum testosterone and histone H3K14 acetylation of the StAR promoter in the testes of SD rats

Liang, Jiren; Zhu, Hongyan; Li, Cuizhen; Ding, Yicheng; Zhou, Zhijun; Wu, Qing

doi:10.1016/j.tox.2012.08.010

Cited by 52 publications

(17 citation statements)

References 33 publications

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“…First, we prioritized our focus on PM in this study as it is a dominant air pollutant and a long-standing pollution issue in Beijing due to re-suspended dust from traffic and construction activities resulting from Beijing’s rapid urbanization and motorization in recent decades (Wang et al, 2009a). However, we cannot exclude the possibility that other components of ambient air pollution (e.g., benzo[a]pyrene) may also contribute to histone H3 modification changes (Liang et al, 2012). Second, we utilized citywide measures of ambient PM 10 as a proxy of personal exposure to PM 10 , which potentially subjects our results to the ecological fallacy.…”

Section: Discussionmentioning

confidence: 99%

Traffic-derived particulate matter exposure and histone H3 modification: A repeated measures study

Zheng

Sanchez-Guerra

Zhang

et al. 2017

Environmental Research

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Background Airborne particulate matter (PM) may induce epigenetic changes that potentially lead to chronic diseases. Histone modifications regulate gene expression by influencing chromatin structure that can change gene expression status. We evaluated whether traffic-derived PM exposure is associated with four types of environmentally inducible global histone H3 modifications. Methods The Beijing Truck Driver Air Pollution Study included 60 truck drivers and 60 office workers examined twice, 1–2 weeks apart, for ambient PM10 (both day-of and 14-day average exposures), personal PM2.5, black carbon (BC), and elemental components (potassium, sulfur, iron, silicon, aluminum, zinc, calcium, and titanium). For both PM10 measures, we obtained hourly ambient PM10 data for the study period from the Beijing Municipal Environmental Bureau’s 27 representatively distributed monitoring stations. We then calculated a 24 h average for each examination day and a moving average of ambient PM10 measured in the 14 days prior to each examination. Examinations measured global levels of H3 lysine 9 acetylation (H3K9ac), H3 lysine 9 tri-methylation (H3K9me3), H3 lysine 27 tri-methylation (H3K27me3), and H3 lysine 36 tri-methylation (H3K36me3) in blood leukocytes collected after work. We used adjusted linear mixed-effect models to examine percent changes in histone modifications per each μg/m3 increase in PM exposure. Results In all participants each μg/m3 increase in 14-day average ambient PM10 exposure was associated with lower H3K27me3 (β=−1.1%, 95% CI: −1.6, −0.6) and H3K36me3 levels (β=−0.8%, 95% CI: −1.4, −0.1). Occupation-stratified analyses showed associations between BC and both H3K9ac and H3K36me3 that were stronger in office workers (β=4.6%, 95% CI: 0.9, 8.4; and β=4.1%, 95% CI: 1.3; 7.0 respectively) than in truck drivers (β=0.1%, 95% CI: −1.3, 1.5; and β=0.9%, 95% CI: −0.9, 2.7, respectively; both pinteraction < 0.05). Sex-stratified analyses showed associations between examination-day PM10 and H3K9ac, and between BC and H3K9me3, were stronger in women (β=10.7%, 95% CI: 5.4, 16.2; and β=7.5%, 95% CI: 1.2, 14.2, respectively) than in men (β=1.4%, 95% CI: −0.9, 3.7; and β=0.9%, 95% CI: −0.9, 2.7, respectively; both pinteraction < 0.05). We observed no associations between personal PM2.5 or elemental components and histone modifications. Conclusions Our results suggest a possible role of global histone H3 modifications in effects of traffic-derived PM exposures, particularly BC exposure. Future studies should assess the roles of these modifications in human diseases and as potential mediators of air pollution-induced disease, in particular BC exposure.

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Section: Discussionmentioning

confidence: 99%

Traffic-derived particulate matter exposure and histone H3 modification: A repeated measures study

Zheng

Sanchez-Guerra

Zhang

et al. 2017

Environmental Research

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“…In a study of neonatal rats administered B a P, the extent of acetylation of H3K14 and mRNA expression of StAR were both decreased, in correlation with a decrease in sperm count and serum testosterone levels, all changes that persisted into adulthood [68]. …”

Section: Epigenetic Effects Associated With Carcinogenic Chemicalsmentioning

confidence: 99%

Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: A systematic literature review

Chappell

Pogribny

Guyton

et al. 2016

Mutation Research/Reviews in Mutation Research

142

105

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Accumulating evidence suggests that epigenetic alterations play an important role in chemically-induced carcinogenesis. Although the epigenome and genome may be equally important in carcinogenicity, the genotoxicity of chemical agents and exposure-related transcriptomic responses have been more thoroughly studied and characterized. To better understand the evidence for epigenetic alterations of human carcinogens, and the potential association with genotoxic endpoints, we conducted a systematic review of published studies of genotoxic carcinogens that reported epigenetic endpoints. Specifically, we searched for publications reporting epigenetic effects for the 28 agents and occupations included in Monograph Volume 100F of the International Agency for the Research on Cancer (IARC) that were classified as “carcinogenic to humans” (Group 1) with strong evidence of genotoxic mechanisms of carcinogenesis. We identified a total of 158 studies that evaluated epigenetic alterations for 12 of these 28 carcinogenic agents and occupations (1,3-butadiene, 4-aminobiphenyl, aflatoxins, benzene, benzidine, benzo[a]pyrene, coke production, formaldehyde, occupational exposure as a painter, sulfur mustard, and vinyl chloride). Aberrant DNA methylation was most commonly studied, followed by altered expression of non-coding RNAs and histone changes (totaling 85, 59 and 25 studies, respectively). For 3 carcinogens (aflatoxins, benzene and benzo[a]pyrene), 10 or more studies reported epigenetic effects. However, epigenetic studies were sparse for the remaining 9 carcinogens; for 4 agents, only 1 or 2 published reports were identified. While further research is needed to better identify carcinogenesis-associated epigenetic perturbations for many potential carcinogens, published reports on specific epigenetic endpoints can be systematically identified and increasingly incorporated in cancer hazard assessments.

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“…The PAH benzo[a]pyrene (BaP), mainly sourced from wood burning, but also detected in cigarettes, has been shown to have many epigenetic-disrupting properties in a number of human and animal models (Wilson & Jones 1983, Herbstman et al 2012, Liang et al 2012, Fang et al 2013). DNA adducts involving the BaP metabolite, BaP diolepoxide (BPDE), have been identified in breast epithelial cells and human breast milk, demonstrating that BaP penetrates ductal breast epithelial cells, where most breast cancers are thought to arise (Li et al 1996, Gorlewska-Roberts et al 2002, Thompson et al 2002).…”

Section: Polycyclic Aromatic Hydrocarbonsmentioning

confidence: 99%

Endocrine disruption of the epigenome: a breast cancer link

Knower¹,

To²,

Leung³

et al. 2014

Endocrine-Related Cancer

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The heritable component of breast cancer accounts for only a small proportion of total incidences. Environmental and lifestyle factors are therefore considered to among the major influencing components increasing breast cancer risk. Endocrine-disrupting chemicals (EDCs) are ubiquitous in the environment. The estrogenic property of EDCs has thus shown many associations between ongoing exposures and the development of endocrine-related diseases, including breast cancer. The environment consists of a heterogenous population of EDCs and despite many identified modes of action, including that of altering the epigenome, drawing definitive correlations regarding breast cancer has been a point of much discussion. In this review, we describe in detail well-characterized EDCs and their actions in the environment, their ability to disrupt mammary gland formation in animal and human experimental models and their associations with exposure and breast cancer risk. We also highlight the susceptibility of early-life exposure to each EDC to mediate epigenetic alterations, and where possible describe how these epigenome changes influence breast cancer risk.

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Neonatal exposure to benzo[a]pyrene decreases the levels of serum testosterone and histone H3K14 acetylation of the StAR promoter in the testes of SD rats

Cited by 52 publications

References 33 publications

Traffic-derived particulate matter exposure and histone H3 modification: A repeated measures study

Traffic-derived particulate matter exposure and histone H3 modification: A repeated measures study

Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: A systematic literature review

Endocrine disruption of the epigenome: a breast cancer link

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