Mediation effect of AhR expression between polycyclic aromatic hydrocarbons exposure and oxidative DNA damage among Chinese occupational workers

Li, Yanli; Zhang, Hongjie; Zhang, Huitao; Niu, Yingying; Fu, Ye; Nie, Jing; Yang, Aimin; Zhao, Jianping; Yang, Jin

doi:10.1016/j.envpol.2018.09.014

Cited by 35 publications

(15 citation statements)

References 31 publications

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“…In turn, the PAH-activated (ligand-bound) AHR moves to the cell nucleus to alter transcription of catabolic pathway genes including the cytochromes CYP1A1 and CYP1B1. The multifunctional AHR protein is also a xenobiotic barrier against PAH in gut (Liu et al 2018); prenatally, placental AHR and CYP1A1 proteins are elevated by maternal smoking (Huuskonen et al 2008). Some AHR products are are fully detoxified, while others are carcinogenic.…”

Section: Smoke and Cooking: Detoxification By Ahr-cyp And N-acetyltramentioning

confidence: 99%

“…The TCAF proteins (TRPM8 channel-associated factors) detect coldness by their binding to the ion channel receptor TRPM8 (Gkika et al 2015). TRPM8 is the only receptor that responds to moderate cold, and is expressed in somatosensory neurons and airway epithelial cells (Bautista et al 2007;Knowlton et al 2013;Liu et al 2018). The TCAF genes have multiple copies in modern and archaic humans, while Neandertals and Denisovans had but one (Dennis et al 2017).…”

Section: Thermosensitivity and Expansion To Colder Climesmentioning

confidence: 99%

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The Exposome in Human Evolution: From Dust to Diesel

Trumble¹,

Finch²

2019

The Quarterly Review of Biology

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Global exposures to air pollution and cigarette smoke are novel in human evolutionary history and are associated with about 16 million premature deaths per year. We investigate the history of the human exposome for relationships between novel environmental toxins and genetic changes during human evolution in six phases. Phase I: With increased walking on savannas, early human ancestors inhaled crustal dust, fecal aerosols, and spores; carrion scavenging introduced new infectious pathogens. Phase II: Domestic fire exposed early Homo to novel toxins from smoke and cooking. Phases III and IV: Neolithic to preindustrial Homo sapiens incurred infectious pathogens from domestic animals and dense communities with limited sanitation. Phase V: Industrialization introduced novel toxins from fossil fuels, industrial chemicals, and tobacco at the same time infectious pathogens were diminishing. Thereby, pathogen-driven causes of mortality were replaced by chronic diseases driven by sterile inflammogens, exogenous and endogenous. Phase VI: Considers future health during global warming with increased air pollution and infections. We hypothesize that adaptation to some ancient toxins persists in genetic variations associated with inflammation and longevity.

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Section: Smoke and Cooking: Detoxification By Ahr-cyp And N-acetyltramentioning

confidence: 99%

Section: Thermosensitivity and Expansion To Colder Climesmentioning

confidence: 99%

The Exposome in Human Evolution: From Dust to Diesel

Trumble¹,

Finch²

2019

The Quarterly Review of Biology

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“…A number of studies have indicated that PAH metabolites may lead to oxidative stress and inflammation [ 8 , 9 , 10 , 11 , 36 ]. Several studies have shown that PAHs are ligands of aryl hydrocarbon receptors (AhR), and are able to activate these receptors [ 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

“…The International Agency for Research on Cancer (IARC) classified BaP as carcinogenic to humans (Group 1) [ 6 ] and classified naphthalene as possibly carcinogenic to humans (Group 2B). Although many PAHs, including fluorene and phenanthrene, are undetermined due to a lack of investigations, exposure to PAHs brings out many other potentially harmful effects on human health [ 7 ], including oxidative stress [ 8 , 9 ], inflammation [ 10 , 11 ], cardiovascular disease [ 12 , 13 ], respiratory disease [ 14 ], and poor fetal development [ 15 ]. A cross-sectional study revealed that PAH metabolites, such as 2-hydroxyfluorene, 3-hydroxyfluorene, and 3-hydroxyphenanthrene, have a possible effect on rheumatoid arthritis [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Clinical Relevance of Urine Flow Rate and Exposure to Polycyclic Aromatic Hydrocarbons

Jeng

Huang

Wang

et al. 2021

IJERPH

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Background: Polycyclic aromatic hydrocarbon (PAH) metabolites have received increasing attention because several of these organic substances are highly carcinogenic or mutagenic. Exposure to PAHs is associated with many harmful health effects; however, we are not aware of any study that has explored the exposure to PAHs and urinary conditions in the general population. The present work aimed to investigate the correlation among PAH and urine flow rate (UFR). Method: Cross-sectional data from the National Health and Nutrition Examination Survey (NHANES) 2009–2012 were used in our study. A total of 4172 participants and a total of nine PAH metabolites were examined. The UFR was measured as the amount of urine excreted in a period of time (mL/h). Several covariates were adjusted in linear regression models. Result: After adjusting for variables, the PAH metabolites in urine showed a significant correlation with UFR. Dose-dependent associations between PAH metabolites in the urine and UFR were also found. Higher quartiles of PAH metabolites in urine exhibited higher regression coefficients. Conclusion: Our study highlighted that PAH metabolites in urine had a strong association with decreased UFR in the US adult population. These findings support the possibility that PAH exposure is related to bladder dysfunction. Further prospective studies are warranted.

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“…We can't get answer here whether IS directly leads to DNA damage through AhR, or indirectly through inflammation or oxidative stress. But the first case is reasonable since it has been well-proved that activation of AhR could directly cause DNA damage in other settings (28,29).…”

Section: Gene Namementioning

confidence: 99%

Transcriptome Profiling Reveals Indoxyl Sulfate Should Be Culpable of Impaired T Cell Function in Chronic Kidney Disease

et al. 2020

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Introduction: Chronic inflammation and immune system dysfunction have been evaluated as major factors in the pathogenesis of chronic kidney disease (CKD), contributing to the high mortality rates observed in these populations. Uremic toxins seem to be the potential "missing link." Indoxyl sulfate (IS) is one of the protein-bound renal toxins. It participates in multiple pathologies of CKD complications, yet its effect on immune cell has not been studied. This study aimed to explore the genome-wide expression profile in human peripheral blood T cells under stimulation by IS. Methods: In this study, we employed RNA-sequencing transcriptome profiling to identify differentially expressed genes (DEGs) responding to IS stimulation in human peripheral T cells in vitro. Flow cytometry and western blot were used to verify the discovery in RNA-sequencing analysis. Results: Our results yielded a total of 5129 DEGs that were at least twofold up-regulated or down-regulated significantly by IS stimulation and half of them were concentration-specific. Analysis of T cell functional markers revealed a quite different transcription profile under various IS concentration. Transcription factors analysis showed the similar pattern. Aryl hydrocarbon receptor (AhR) target genes CYP1A1, CYP1B1, NQO1, and AhRR were up-regulated by IS stimulation. Pro-inflammatory genes TNF-α and IFN-γ were up-regulated as verified by flow cytometry analysis. DNA damage was induced by IS stimulation as confirmed by elevated protein level of p-ATM, p-ATR, p-BRCA1, and p-p53 in T cells. Conclusion: The toxicity of IS to T cells could be an important source of chronic inflammation in CKD patients. As an endogenous ligand of AhR, IS may influence multiple biological functions of T cells including inflammatory response and cell cycle regulation. Further researches are required to promulgate the underling mechanism and explore effective method of reserving T cell function in CKD.

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Mediation effect of AhR expression between polycyclic aromatic hydrocarbons exposure and oxidative DNA damage among Chinese occupational workers

Cited by 35 publications

References 31 publications

The Exposome in Human Evolution: From Dust to Diesel

The Exposome in Human Evolution: From Dust to Diesel

Clinical Relevance of Urine Flow Rate and Exposure to Polycyclic Aromatic Hydrocarbons

Transcriptome Profiling Reveals Indoxyl Sulfate Should Be Culpable of Impaired T Cell Function in Chronic Kidney Disease

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