Assessment of 9-OH- and 7,8-diol-benzo[a]pyrene in Blood as Potent Markers of Cognitive Impairment Related to benzo[a]pyrene Exposure: An Animal Model Study

Cherif, Lynda Saber; Cao-Lei, Lei; Farinelle, Sophie; Turner, Jonathan D.; Schroeder, Henri; Grova, Nathalie

doi:10.3390/toxics9030050

Cited by 6 publications

(5 citation statements)

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“…In another study, [ 118 ] B[ a ]P (20 and 200 mg/kg/day) was repeatedly given to mice, causing a significant overexpression of cytochrome. An elevated expression of Cyp1A1 / Cyp1B1 was noted in two of the three brain regions, showing the brain’s capability to metabolize B[ a ]P alone.…”

Section: Metabolism Of B[ a ]Pmentioning

confidence: 99%

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

Bukowska

Mokra

Michałowicz

2022

IJMS

150

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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: Metabolism Of B[ a ]Pmentioning

confidence: 99%

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

Bukowska

Mokra

Michałowicz

2022

IJMS

150

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show abstract

“…The brain is one of the extrahepatic tissues that express CYP1A1 both constitutively and following induction [ 30 , 31 ]. In a recent study, exposure to B[a]P by oral gavage at 20 and 200 mg/kg for 11 consecutive days induced significant overexpression of Cyp1a1/Cyp1b1 in the frontal cortex, temporal cortex, and hippocampus regions of mouse brains [ 32 ]. The difference in the result of Cyp1b1 between the previous study and the present study might be due to the difference in exposure level.…”

Section: Discussionmentioning

confidence: 99%

Exposure to Benzo[a]pyrene Decreases Noradrenergic and Serotonergic Axons in Hippocampus of Mouse Brain

Abd El Naby,

Zong,

Fergany

et al. 2023

IJMS

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Epidemiological studies showed the association between air pollution and dementia. A soluble fraction of particulate matters including polycyclic aromatic hydrocarbons (PAHs) is suspected to be involved with the adverse effects of air pollution on the central nervous system of humans. It is also reported that exposure to benzopyrene (B[a]P), which is one of the PAHs, caused deterioration of neurobehavioral performance in workers. The present study investigated the effect of B[a]P on noradrenergic and serotonergic axons in mouse brains. In total, 48 wild-type male mice (10 weeks of age) were allocated into 4 groups and exposed to B[a]P at 0, 2.88, 8.67 or 26.00 µg/mice, which is approximately equivalent to 0.12, 0.37 and 1.12 mg/kg bw, respectively, by pharyngeal aspiration once/week for 4 weeks. The density of noradrenergic and serotonergic axons was evaluated by immunohistochemistry in the hippocampal CA1 and CA3 areas. Exposure to B[a]P at 2.88 µg/mice or more decreased the density of noradrenergic or serotonergic axons in the CA1 area and the density of noradrenergic axons in the CA3 area in the hippocampus of mice. Furthermore, exposure to B[a]P dose-dependently upregulated Tnfα at 8.67 µg/mice or more, as well as upregulating Il-1β at 26 µg/mice, Il-18 at 2.88 and 26 µg/mice and Nlrp3 at 2.88 µg/mice. The results demonstrate that exposure to B[a]P induces degeneration of noradrenergic or serotonergic axons and suggest the involvement of proinflammatory or inflammation-related genes with B[a]P-induced neurodegeneration.

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“…After oral administration of benz[ a ]anthracene (BaA), the concentration of BaA in organs of Fisher-344 rats was in the order of kidney > spleen > liver > lung > muscle > heart from high to low . Cherif et al reported that after oral exposure to B[a]P in Balb/c mice, rich B[a]P were detected in the brain . This shows that after oral administration of PAHs, they can accumulate in a variety of organs by entering the bloodstream.…”

Section: Tissue Distribution Of Pahs and The Derivatives In Vivomentioning

confidence: 99%

Influence of Exposure Pathways on Tissue Distribution and Health Impact of Polycyclic Aromatic Hydrocarbon Derivatives

et al. 2023

Environ. Health

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The oxygen (OPAHs), nitro (NPAHs), hydroxyl (OH-PAHs), and alkylated (APAHs) derivatives of polycyclic aromatic hydrocarbon (PAHs) are ubiquitous pollutants in the environment. The concentrations of NPAHs, OPAHs, OH-PAHs, and APAHs are lower than that of PAHs in the environment, but the carcinogenic abilities of the derivatives are usually 10 to 1,000-fold higher than that of parent PAHs. There are three main pathways for the exposure of polycyclic aromatic compounds to humans, including inhalation, direct contact, and ingestion. After exposure by inhalation, they are mainly distributed in the lungs, affecting lung function and causing inflammation, asthma, etc. Due to the digestive system’s strong capacity for metabolism, intake of PAHs and the derivatives is primarily distributed in the digestive system and metabolized there. And it may lead to dysplasia of these organs and even to cancer. The skin is the primary site of direct contact with PAH derivatives. PAH derivatives can enter the bloodstream through all three contact pathways, thereby accumulating in various organs. This study aimed to summarize the influence of exposure pathways on tissue distribution and the health impact of PAH derivatives to provide references for future research and evaluation on public health.

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Assessment of 9-OH- and 7,8-diol-benzo[a]pyrene in Blood as Potent Markers of Cognitive Impairment Related to benzo[a]pyrene Exposure: An Animal Model Study

Cited by 6 publications

References 50 publications

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

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

Exposure to Benzo[a]pyrene Decreases Noradrenergic and Serotonergic Axons in Hippocampus of Mouse Brain

Influence of Exposure Pathways on Tissue Distribution and Health Impact of Polycyclic Aromatic Hydrocarbon Derivatives

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