Activation of aryl hydrocarbon receptor reduces carbendazim-induced cell death

Wei, Kuo‐Liang; Chen, Fei-Yun; Lin, Chih-Yi; Gao, Guanlun; Kao, Wen-Ya; Yeh, Chi-Hui; Chen, Chang-Rong; Huang, Hsiao‐Ping; Tsai, Wei-Ren; Jong, Koa-Jen; Li, Wan-Jung; Su, Jyan-Gwo J.

doi:10.1016/j.taap.2016.06.004

Cited by 18 publications

(13 citation statements)

References 30 publications

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“…Benzo(a)pyrene (B[a]P), the major carcinogenic PAH, is listed as a group I human carcinogen by the International Agency for Research on Cancer (IARC; IARC, 2012; Vázquez‐Gómez, Rocha‐Zavaleta, Rodríguez‐Sosa, & Petrosyan, 2018). Although B[a]P shows no genotoxicity, it can be metabolized by xenobiotic‐metabolizing cytochrome P450 (CYP450) to the final metabolite, benzo[a]pyrene‐ trans ‐7,8‐dihydrodiol‐9,10‐epoxide (B[a]PDE), which covalently binds to macromolecules and forms mutagenic DNA adducts, then inhibits DNA synthesis, inducing cell cycle arrest (Shiizaki, Kawanishi, & Yagi, 2013; Wei et al, 2016). The AhR endogenous agonist 6‐formylindolo[3, 2‐b]carbazole (FICZ), as one of the metabolites of the essential amino acids tryptophan, binds to AhR with a higher affinity than any other compounds even the extremely efficient ligand tetrachlorodibenzo‐p‐dioxin (TCDD; Rannug et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

6‐Formylindolo[3,2‐b]carbazole reduces apoptosis induced by benzo[a]pyrene in a mitochondrial‐dependent manner

Gan

Ding

Chen

2020

Cell Biology International

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Benzo[a]pyrene (B[a]P), a potent carcinogen, has been proved that it can induce apoptosis via activation of the aryl hydrocarbon receptor (AhR) pathway. The metabolite of tryptophan 6‐formylindolo[3,2‐b]carbazole (FICZ), an endogenous activator of AhR, plays bifunctional roles in cell growth and apoptosis. However, whether and how FICZ can reduce the toxicity of B[a]P and the mechanism underlying this remain unclear. In this study, FICZ interfered with the toxicity of B[a]P in mouse hepatocarcinoma cell line Hepa1‐6. The results of the MTT assay indicated that FICZ and B[a]P made opposite effects on cell proliferation. The scratch‐wound healing assay showed that B[a]P (1 µM for 24 hr) exposure triggered cell migration and that was inhibited by FICZ (10 nM). In addition, FICZ ameliorated B[a]P‐induced apoptosis by inhibiting reactive oxygen species generation and caspase‐3 activation, as well as increasing reduced glutathione level in mitochondria. Furthermore, gene expression analyses indicated that FICZ competed with B[a]P, which reduced the transcriptional activation of the cyp1a1 and cyp1b1 genes, as well as Bcl2 and P53. Accordingly, the interaction between FICZ and B[a]P in the AhR pathway inhibited apoptosis in a mitochondrial‐dependent manner, suggesting that endogenous compound may reduce the toxicity of exogenous pollutant in vivo and providing an available way to improve health condition related to the hepatic metabolic disorder.

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Section: Introductionmentioning

confidence: 99%

6‐Formylindolo[3,2‐b]carbazole reduces apoptosis induced by benzo[a]pyrene in a mitochondrial‐dependent manner

Gan

Ding

Chen

2020

Cell Biology International

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“…Cell vitality is evaluated by the changes in the intracellular levels of reduced thiols, as described previously 41 . Cells were stained with solution 5, including the fluorescence dyes of VitaBright-48, acridine orange, and propidium iodide (PI) (ChemoMetec A/S, Denmark), and analyzed using the fluorescence to determine various cell populations: the PI-negative cells (the healthy and unhealthy cells), and the PI-positive cells (the necrotic cells).…”

Section: Vitality Assay (Analysis Of the Level Of Cellular Thiols)mentioning

confidence: 99%

“…The complementary (c)DNA was reverse-transcribed from RNA using Magic RT cDNA synthesis kit (Bio-Genesis Technologies Inc., Taiwan) with oligo-dT (18) and random hexamer. The cDNA was amplified in the quantitative PCR with specific oligonucleotide primers for human CYP1A1 (GenBank: NM_000499), human GAPDH (GenBank: NM002046.5), mouse Cyp1a1 (GenBank: NM_009992), and mouse β-actin (GenBank: NM_007393), as described previously 41 . GAPDH and β-actin mRNA was also analyzed to normalize differences in sample uptake.…”

Section: Reverse-transcription Polymerase Chain Reaction (Rt-pcr) Andmentioning

confidence: 99%

“…Afterwards, the luciferase reporter plasmid and RSV-lacZ plasmids were transfected into cells using the liposome for 6 h, followed by treatment with the test compounds as described previously 34 . Cell lysates were harvested at the appropriate time points after treatment with test compounds and were respectively assayed for both luciferase and β-galactosidase activities using Britelite (PerkinElmer) and the Galacto-Star System (Tropix, Bedford, MA) as described previously 34,41 . Transcription activity of the promoter was indicated by luciferase activity, and β-galactosidase activity of RSV-lacZ was used to normalize the luciferase activity.…”

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confidence: 99%

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Cyproterone acetate acts as a disruptor of the aryl hydrocarbon receptor

Cheng

Gao

et al. 2021

Sci Rep

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Prostate cancer is a major cause of death in males. Cyproterone acetate (CPA), the steroidal anti-androgen for part of androgen deprivation therapy, may block the androgen-receptor interaction and then reduce serum testosterone through its weak anti-gonadotropic action. In addition to CPA inducing hepatitis, CPA is known to cause liver tumors in rats also. Aryl hydrocarbon receptor (AhR) is a cytoplasmic receptor and regulates multiple physiological functions. CYP1A1 is an AhR-targeted gene. We found that CPA induced CYP1A1 expression, transcriptional activity of the aryl hydrocarbon response element (AHRE), and the nuclear localization of AhR in mouse Hepa-1c1c7 cells. However, CPA suppressed CYP1A1 mRNA expression and the transcriptional activity of AHRE in human HepG2 and MCF7 cells, and also decreased AhR ligand-induced CYP1A1 protein expression and transcriptional activity of AHRE in HepG2 cells. In summary, CPA is an AhR agonist in mouse cells, but an AhR antagonist in human cells. Accordingly, CPA potentially plays a role as an endocrine disruptor of the AhR. This study helps us to understand why CPA induces acute hepatitis, gene mutation, and many other side effects. In addition, it may trigger further studies investigating the relationships between CPA, glucocorticoid receptor and castration-resistant prostate cancer in the future.

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“…When benomyl interacts with water, it is broken down rapidly into carbendazim, which belongs to the benzimidazole family, and into n‐butyl isocyanate (BIC). The reported mode of action for carbendazim is the inhibition of microtubule formation, which blocks mitosis and inhibits cell proliferation (Schmidt, Busch, Altenburger, & Kuster, ; Wei et al, ). Model organism research has showed that rats exposed to carbendazim exhibit cytoplasmic destruction and edema in thyroid, parathyroid, pituitary and adrenal medulla glands, which are in part derived from the NC (Table , Barlas, Selmanoglu, Kockaya, & Songur, ).…”

Section: Chemical Agentsmentioning

confidence: 99%

The role of teratogens in neural crest development

Cerrizuela

Vega-Lopez

Aybar

2020

Birth Defects Research

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The neural crest (NC), discovered by Wilhelm His 150 years ago, gives rise to a multipotent migratory embryonic cell population that generates a remarkably diverse and important array of cell types during the development of the vertebrate embryo. These cells originate in the neural plate border (NPB), which is the ectoderm between the neural plate and the epidermis. They give rise to the neurons and glia of the peripheral nervous system, melanocytes, chondrocytes, smooth muscle cells, odontoblasts and neuroendocrine cells, among others. Neurocristopathies are a class of congenital diseases resulting from the abnormal induction, specification, migration, differentiation or death of NC cells (NCCs) during embryonic development and have an important medical and societal impact. In general, congenital defects affect an appreciable percentage of newborns worldwide. Some of these defects are caused by teratogens, which are agents that negatively impact the formation of tissues and organs during development. In this review, we will discuss the teratogens linked to the development of many birth defects, with a strong focus on those that specifically affect the development of the NC, thereby producing neurocristopathies.Although increasing attention is being paid to the effect of teratogens on embryonic development in general, there is a strong need to critically evaluate the specific role of these agents in NC development. Therefore, increased understanding of the role of these factors in NC development will contribute to the planning of strategies aimed at the prevention and treatment of human neurocristopathies, whose etiology was previously not considered.

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Activation of aryl hydrocarbon receptor reduces carbendazim-induced cell death

Cited by 18 publications

References 30 publications

6‐Formylindolo[3,2‐b]carbazole reduces apoptosis induced by benzo[a]pyrene in a mitochondrial‐dependent manner

6‐Formylindolo[3,2‐b]carbazole reduces apoptosis induced by benzo[a]pyrene in a mitochondrial‐dependent manner

Cyproterone acetate acts as a disruptor of the aryl hydrocarbon receptor

The role of teratogens in neural crest development

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