Parental exposure to benzo(a)pyrene in the peripubertal period impacts reproductive aspects of the F1 generation in rats

Jorge, Bárbara Campos; Reis, Ana Carolina Casali; Stein, Júlia; Balin, Paola da Silva; Sterde, Érika Tissiana; Barbosa, Mariana Gazoli; Aquino, Ariana Musa de; Kassuya, Cândida Aparecida Leite; Arena, Arielle Cristina

doi:10.1016/j.reprotox.2021.01.011

Cited by 17 publications

(5 citation statements)

References 54 publications

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“…A very interesting study was conducted by Jorge et al [ 158 ], who assessed how peripubertal exposure to B[ a ]P in male rats could cause reproductive disorders in the offspring. B[ a ]P was given orally to male rats in the postnatal period 23–53 days at environmentally relevant doses (0, 0.1, 1, or 10 µg/kg/day).…”

Section: Adverse Effects Observed In In Vitro and In Vivo Studiesmentioning

confidence: 99%

“…Females showed changes in estrus cycles and some fertility parameters, as well as histological changes in the ovaries and uterus. B[ a ]P changed the reproductive parameters of the F1 generation, which suggested that the peripubertal exposure of the F0 generation to this compound caused permanent modifications in the reproduction of these animals [ 158 ].…”

Section: Adverse Effects Observed In In Vitro and In Vivo Studiesmentioning

confidence: 99%

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

Bukowska

Mokra

Michałowicz

2022

IJMS

187

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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: Adverse Effects Observed In In Vitro and In Vivo Studiesmentioning

confidence: 99%

Section: Adverse Effects Observed In In Vitro and In Vivo Studiesmentioning

confidence: 99%

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

Bukowska

Mokra

Michałowicz

2022

IJMS

187

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“…BaP is toxic to the reproductive system [64,65]. Recent studies have shown that taurine (2-aminoethanesulfonic acid), an organic chemical compound from the group of biogenic amino acids, ameliorated toxic reactions in the epididymis and testes of rats exposed to BaP.…”

Section: Taurinementioning

confidence: 99%

Molecular Mechanisms of Action of Selected Substances Involved in the Reduction of Benzo[a]pyrene-Induced Oxidative Stress

Bukowska

Duchnowicz

2022

Molecules

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Benzo[a]pyrene (BaP) is a polycyclic aromatic hydrocarbon (PAH) primarily formed by burning of fossil fuels, wood and other organic materials. BaP as group I carcinogen shows mutagenic and carcinogenic effects. One of the important mechanisms of action of (BaP) is its free radical activity, the effect of which is the induction of oxidative stress in cells. BaP induces oxidative stress through the production of reactive oxygen species (ROS), disturbances of the activity of antioxidant enzymes, and the reduction of the level of non-enzymatic antioxidants as well as of cytokine production. Chemical compounds, such as vitamin E, curcumin, quercetin, catechin, cyanidin, kuromanin, berberine, resveratrol, baicalein, myricetin, catechin hydrate, hesperetin, rhaponticin, as well as taurine, atorvastatin, diallyl sulfide, and those contained in green and white tea, lower the oxidative stress induced by BaP. They regulate the expression of genes involved in oxidative stress and inflammation, and therefore can reduce the level of ROS. These substances remove ROS and reduce the level of lipid and protein peroxidation, reduce formation of adducts with DNA, increase the level of enzymatic and non-enzymatic antioxidants and reduce the level of pro-inflammatory cytokines. BaP can undergo chemical modification in the living cells, which results in more reactive metabolites formation. Some of protective substances have the ability to reduce BaP metabolism, and in particular reduce the induction of cytochrome (CYP P450), which reduces the formation of oxidative metabolites, and therefore decreases ROS production. The aim of this review is to discuss the oxidative properties of BaP, and describe protective activities of selected chemicals against BaP activity based on of the latest publications.

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“…This PAH has been categorized by the International Agency for Research on Cancer (IARC) as a human group 1 carcinogen because of its mutagenic and carcinogenic effects in animal models and its association with the development of several types of human cancer, including lung, breast, and liver [38,39]. In addition to sufficient evidence of carcinogenicity in humans, the neurotoxicity, epigenotoxicity, alteration of various metabolic pathways, and reproductive toxicity of B[a]P have been demonstrated experimentally [31,35,[38][39][40][41][42]. The molecular mechanisms associated with B[a]P toxicity involve the creation of stable and depurinating DNA adducts, repetitive redox cycling that generates reactive oxygen species (ROS), radical-cation mechanism, mechanism via formation of ortho-quinone, and interaction with the aryl hydrocarbon (AhR) receptor, among others [39,43].…”

Section: Introductionmentioning

confidence: 99%

Exposure to Benzo(a)pyrene Enhances Acetaminophen-Induced Liver Injury in Mice at Non-Hepatotoxic Doses

Montero-Pérez,

Olivero-Verbel

2024

Sci. Pharm.

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Acetaminophen (APAP) is a widely used analgesic, especially for children. Its primary mechanism involves inhibiting cyclooxygenase enzymes and activating the endocannabinoid and TRPV1 systems. Though its toxicity is low, it can harm the liver in a dose-dependent manner. Low APAP doses can also increase pollutant-induced liver damage. Little is known about interactions between APAP and benzo[a]pyrene (B[a]P). This study aimed to assess if co-exposure to non-hepatotoxic doses of B[a]P and APAP causes liver injury in mice, exploring the underlying mechanisms. Female ICR mice received 50 mg/kg B[a]P or a vehicle for three days, followed by 200 mg/kg APAP or a vehicle. Liver injury was assessed through histopathological examination, serum transaminase activity, and gene expression analysis. In the B[a]P/APAP group, several histology changes were observed, including ballooning injury, steatosis, necrosis, inflammation, and apoptosis. Transaminase levels correlated with histopathological scores, and there was an increase in hepatic cytochrome P450 family 1 subfamily a member 1 (Cyp1a1) mRNA levels and a decrease in aryl hydrocarbon receptor (Ahr), cytochrome P450 family 2 subfamily e polypeptide 1 (Cyp2e1), superoxide dismutase 1 (Sod1), peroxisome proliferator activated receptor gamma (Ppar-γ), and caspase 3 (Casp3). This suggests that prior exposure to B[a]P makes mice more susceptible to APAP-induced liver injury, involving changes in gene expression related to metabolism, redox balance, and cell proliferation. Therefore, using therapeutic APAP doses after exposure to B[a]P could lead to liver injury.

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Parental exposure to benzo(a)pyrene in the peripubertal period impacts reproductive aspects of the F1 generation in rats

Cited by 17 publications

References 54 publications

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

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

Molecular Mechanisms of Action of Selected Substances Involved in the Reduction of Benzo[a]pyrene-Induced Oxidative Stress

Exposure to Benzo(a)pyrene Enhances Acetaminophen-Induced Liver Injury in Mice at Non-Hepatotoxic Doses

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