Impact of benzo[a]pyrene with other pollutants induce the molecular alternation in the biological system: Existence, detection, and remediation methods

Saravanakumar, Kandasamy; SivaSantosh, Sugavaneswaran; Sathiyaseelan, Anbazhagan; Sankaranarayanan, A.; Naveen, Kumar Vishven; Zhang, Xin; Jamla, Monica; Vijayasarathy, S; Priya, V. Vishnu; MubarakAli, D.; Wang, Myeong‐Hyeon

doi:10.1016/j.envpol.2022.119207

Cited by 29 publications

(20 citation statements)

References 215 publications

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“…The exposure to B[ a ]P in recent times is more common than ever before. Sources of B[ a ]P emissions are mostly anthropogenic, and to a lower extent natural, including wildfires and volcanic eruptions [ 3 ].…”

Section: General Informationmentioning

confidence: 99%

Benzo[a]pyrene—Environmental Occurrence, Human Exposure, and Mechanisms of Toxicity

Bukowska

Mokra

Michałowicz

2022

IJMS

156

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Benzo[a]pyrene (B[a]P) is the main representative of polycyclic aromatic hydrocarbons (PAHs), and has been repeatedly found in the air, surface water, soil, and sediments. It is present in cigarette smoke as well as in food products, especially when smoked and grilled. Human exposure to B[a]P is therefore common. Research shows growing evidence concerning toxic effects induced by this substance. This xenobiotic is metabolized by cytochrome P450 (CYP P450) to carcinogenic metabolite: 7β,8α-dihydroxy-9α,10α-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE), which creates DNA adducts, causing mutations and malignant transformations. Moreover, B[a]P is epigenotoxic, neurotoxic, and teratogenic, and exhibits pro-oxidative potential and causes impairment of animals’ fertility. CYP P450 is strongly involved in B[a]P metabolism, and it is simultaneously expressed as a result of the association of B[a]P with aromatic hydrocarbon receptor (AhR), playing an essential role in the cancerogenic potential of various xenobiotics. In turn, polymorphism of CYP P450 genes determines the sensitivity of the organism to B[a]P. It was also observed that B[a]P facilitates the multiplication of viruses, which may be an additional problem with the widespread COVID-19 pandemic. Based on publications mainly from 2017 to 2022, this paper presents the occurrence of B[a]P in various environmental compartments and human surroundings, shows the exposure of humans to this substance, and describes the mechanisms of its toxicity.

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Section: General Informationmentioning

confidence: 99%

Benzo[a]pyrene—Environmental Occurrence, Human Exposure, and Mechanisms of Toxicity

Bukowska

Mokra

Michałowicz

2022

IJMS

156

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“…Taking BaP as an example, the metabolism and transformation products of BaP also had a relatively high probability of potential environmental (phytotoxicity) and human health (neurotoxicity, immunotoxicity, developmental toxicity, carcinogenicity, and endocrine disruption effect) risks. BaP derivatives were the same as BaP in terms of carcinogenic effects [ 64 ]. The high lipophilicity of PAHs increases their bioavailability in organisms, further increasing their carcinogenic risk [ 73 ].…”

Section: Resultsmentioning

confidence: 99%

“…The environmental impact and toxicological effects of PAHs and their derivatives, including neurotoxicity, oxidative stress, immunotoxicity, and genetic toxicity as well as reproductive and endocrine disruption effects have been confirmed [ 64 ]. In order to comprehensively and systematically measure the potential toxicity risk of PAHs and their derivatives, this paper intends to construct a set of priority-control evaluation systems based on the risk entropy method to evaluate the potential ecological risk of biodegradation and transformation behavior of PAHs in natural scenarios, and then prioritize the risks of different metabolic and transformation pathways.…”

Section: Methodsmentioning

confidence: 99%

Potential Toxicity Risk Assessment and Priority Control Strategy for PAHs Metabolism and Transformation Behaviors in the Environment

Zhao

Zhou

Zhao

et al. 2022

IJERPH

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In this study, 16 PAHs were selected as the priority control pollutants to summarize their environmental metabolism and transformation processes, including photolysis, plant degradation, bacterial degradation, fungal degradation, microalgae degradation, and human metabolic transformation. Meanwhile, a total of 473 PAHs by-products generated during their transformation and degradation in different environmental media were considered. Then, a comprehensive system was established for evaluating the PAHs by-products’ neurotoxicity, immunotoxicity, phytotoxicity, developmental toxicity, genotoxicity, carcinogenicity, and endocrine-disrupting effect through molecular docking, molecular dynamics simulation, 3D-QSAR model, TOPKAT method, and VEGA platform. Finally, the potential environmental risk (phytotoxicity) and human health risks (neurotoxicity, immunotoxicity, genotoxicity, carcinogenicity, developmental toxicity, and endocrine-disrupting toxicity) during PAHs metabolism and transformation were comprehensively evaluated. Among the 473 PAH’s metabolized and transformed products, all PAHs by-products excluding ACY, CHR, and DahA had higher neurotoxicity, 152 PAHs by-products had higher immunotoxicity, and 222 PAHs by-products had higher phytotoxicity than their precursors during biological metabolism and environmental transformation. Based on the TOPKAT model, 152 PAH by-products possessed potential developmental toxicity, and 138 PAH by-products had higher genotoxicity than their precursors. VEGA predicted that 247 kinds of PAH derivatives had carcinogenic activity, and only the natural transformation products of ACY did not have carcinogenicity. In addition to ACY, 15 PAHs produced 123 endocrine-disrupting substances during metabolism and transformation. Finally, the potential environmental and human health risks of PAHs metabolism and transformation products were evaluated using metabolic and transformation pathway probability and degree of toxic risk as indicators. Accordingly, the priority control strategy for PAHs was constructed based on the risk entropy method by screening the priority control pathways. This paper assesses the potential human health and environmental risks of PAHs in different environmental media with the help of models and toxicological modules for the toxicity prediction of PAHs by-products, and thus designs a risk priority control evaluation system for PAHs.

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“…Cigarette smoke is the leading cause of the lung cancerrelated death, accounting for more than 87% (14, 36). Cigarette smoke and environmental pollutants contains high level of Bap, which is a member of the polycyclic aromatic hydrocarbon (PAH) family (6,(37)(38)(39). Accumulating evidence indicates that Bap exposure contributes to inducing cancer stem cell (CSC)like property (40), immune destruction (36) and cell malignant transformation (6,39).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of RNF182 mediated by Bap promotes non-small cell lung cancer progression

et al. 2023

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IntroductionUbiquitylation that mediated by ubiquitin ligases plays multiple roles not only in proteasome-mediated protein degradation but also in various cellular process including DNA repair, signal transduction and endocytosis. RING finger (RNF) proteins form the majority of these ubiquitin ligases. Recent studies have demonstrated the important roles of RNF finger proteins in tumorigenesis and tumor progression. Benzo[a]pyrene (BaP) is one of the most common environmental carcinogens causing lung cancer. The molecular mechanism of Bap carcinogenesis remains elusive. Considering the critical roles of RNF proteins in tumorigenesis and tumor progression, we speculate on whether Bap regulates RNF proteins resulting in carcinogenesis.MethodsWe used GEO analysis to identify the potential RING finger protein family member that contributes to Bap-induced NSCLC. We next used RT-qPCR, Western blot and ChIP assay to investigate the potential mechanism of Bap inhibits RNF182. BGS analyses were used to analyze the methylation level of RNF182.ResultsHere we reported that the carcinogen Bap suppresses the expression of ring finger protein 182 (RNF182) in non-small cell lung cancer (NSCLC) cells, which is mediated by abnormal hypermethylation in an AhR independent way and transcriptional regulation in an AhR dependent way. Furthermore, RNF182 exhibits low expression and hypermethylation in tumor tissues. RNF182 also significantly suppresses cell proliferation and induces cell cycle arrest in NSCLC cell lines.ConclusionThese results demonstrated that Bap inhibits RNF182 expression to promote lung cancer tumorigenesis through activating AhR and promoting abnormal methylation.

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Impact of benzo[a]pyrene with other pollutants induce the molecular alternation in the biological system: Existence, detection, and remediation methods

Cited by 29 publications

References 215 publications

Benzo[a]pyrene—Environmental Occurrence, Human Exposure, and Mechanisms of Toxicity

Benzo[a]pyrene—Environmental Occurrence, Human Exposure, and Mechanisms of Toxicity

Potential Toxicity Risk Assessment and Priority Control Strategy for PAHs Metabolism and Transformation Behaviors in the Environment

Inhibition of RNF182 mediated by Bap promotes non-small cell lung cancer progression

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