Deoxynivalenol as potential modulator of human steroidogenesis

Urbanek, Kinga Anna; Habrowska-Górczyńska, Dominika Ewa; Kowalska, Karolina; Stańczyk, Anna; Domińska, Kamila; Piastowska-Ciesielska, Agnieszka Wanda

doi:10.1002/jat.3623

Cited by 29 publications

(24 citation statements)

References 83 publications

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“…DON is discussed as one of the potential disruptors of the male reproductive system. It is postulated that the steroidogenesis-dysregulating effect of DON is associated with the modulation of steroidogenic enzymes [4] as well as germ cell degeneration, sperm retention, and abnormal morphology in male mice [24]. DON is also reported to have a toxic effect in the mice Leydig cell line MA-10 [33], affecting steroidogenesis and inducing oxidative stress [34].…”

Section: Discussionmentioning

confidence: 99%

“…DON is only partially destroyed in food processing during the high temperature stage, and is thus present in processed cereals [3]. After consumption, DON is quickly metabolized and is no longer present in the serum after 24 h due to its quick absorption in the gastrointestinal tract and excretion in the urine, mainly in glucuronidated forms [4]. The temporary tolerable daily intake of DON established by the World Health Organization (WHO) is 1 µg kg −1 body weight.…”

Section: Introductionmentioning

confidence: 99%

“…Although a considerable body of animal studies has shown that DON is genotoxic, impairs the immune response, and exhibits both developmental and reproductive toxicity through the reduction of fertility, embryotoxicity, and postnatal mortality [4], accordingly to the newest report of the International Agency for Research on Cancer (IARC) DON is classified as not classifiable as to its carcinogenicity to humans (Group 3). This group of agents include both non-cancerogenic agents with documented toxicity as well as agents with no sufficient evidence to be determined as toxic, which trigger a different animal and human effect or indicating gaps in research studies [7].…”

Section: Introductionmentioning

confidence: 99%

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Deoxynivalenol Modulates the Viability, ROS Production and Apoptosis in Prostate Cancer Cells

Habrowska-Górczyńska

Kowalska

Urbanek

et al. 2019

Toxins

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Deoxynivalenol (DON), known as vomitoxin, a type B trichothecene, is produced by Fusarium. DON frequently contaminates cereal grains such as wheat, maize, oats, barley, rye, and rice. At the molecular level, it induces ribosomal stress, inflammation and apoptosis in eukaryotic cells. Our findings indicate that DON modulates the viability of prostate cancer (PCa) cells and that the response to a single high dose of DON is dependent on the androgen-sensitivity of cells. DON appears to increase reactive oxygen species (ROS) production in cells, induces DNA damage, and triggers apoptosis. The effects of DON application in PCa cells are influenced by the mitogen-activated protein kinase (MAPK) and NFΚB- HIF-1α signaling pathways. Our results indicate that p53 is a crucial factor in DON-associated apoptosis in PCa cells. Taken together, our findings show that a single exposure to high concentrations of DON (2–5 µM) modulates the progression of PCa.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Deoxynivalenol Modulates the Viability, ROS Production and Apoptosis in Prostate Cancer Cells

Habrowska-Górczyńska

Kowalska

Urbanek

et al. 2019

Toxins

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“…Immunosuppressive/immunostimulatory a 0.06 Wu et al (2017) Nevertheless, all studies confirmed that the Nrf2 pathways is attributed to cellular oxidative stress caused by T-2. Deoxynivalenol (vomitoxin; DON) belongs to type B of the trichothecenes family of mycotoxin produced mainly by Fusarium species (Urbanek et al 2018) and is considered one of the best known mycotoxins. It is detected in 90% of tested samples (Sobrova et al 2010).…”

Section: Trichothecenesmentioning

confidence: 99%

“…Deoxynivalenol (vomitoxin; DON) belongs to type B of the trichothecenes family of mycotoxin produced mainly by Fusarium species (Urbanek et al 2018 ) and is considered one of the best known mycotoxins. It is detected in 90% of tested samples (Sobrova et al 2010 ).…”

Section: Mycotoxinsmentioning

confidence: 99%

Nrf2: a main responsive element in cells to mycotoxin-induced toxicity

Kozieł

Kowalska

Piastowska-Ciesielska

2021

Arch Toxicol

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Nuclear factor erythroid 2-like 2 (Nrf2) is a transcription factor participating in response to cellular oxidative stress to maintain the redox balance. Generation of reactive oxygen species (ROS) and, in consequence, oxidative stress, are physiological as well as pathological processes which take place in almost all types of cells. Nrf2, in response to oxidative stress, activates expression and production of antioxidant enzymes to remove free radicals. However, the role of Nrf2 seems to be more sophisticated and its increased expression observed in cancer cells allows to draw a conclusion that its role is tissue—and condition—dependent. Interestingly, Nrf2 might also play a crucial role in response to environmental factors like mycotoxins. Thus, the aim of the study is to review the role of Nrf2 in cells exposed to most common mycotoxins to check if the Nrf2 signaling pathway serves as the main response element to mycotoxin-induced oxidative stress in human and animal cells and if it can be a target of detoxifying agents.

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Mechanisms underlying protective effects of vitamin E against mycotoxin deoxynivalenol‐induced oxidative stress and its related cytotoxicity in primary human brain endothelial cells

Shieh

Hsu

Liang

2021

Environmental Toxicology

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Fusarium mycotoxins are one of the largest families of mycotoxins. Among these mycotoxins, deoxynivalenol is the most widespread pollutant of grains. However, the mechanism underlying the effect of deoxynivalenol on cytotoxicity in human brain endothelial cells was still unclear. This study examined whether deoxynivalenol induced oxidative stress‐associated cytotoxicity in primary human brain endothelial cells (HBEC‐5i), and explored whether Vitamin E (VE), a selective antioxidant, had protective effects on deoxynivalenol‐treated cells. Deoxynivalenol (10‐50 μM) concentration‐dependently induced cytotoxicity in HBEC‐5i cells. Deoxynivalenol (IC50 = 20 μM) activated mitochondrial apoptotic pathway by modulating antioxidant protein expressions (Nrf2, HO‐1 and NQO1). More significantly, pre‐treatment with VE (20 μM) attenuated the deoxynivalenol‐induced cytotoxicity in this cell model. Together, VE significantly alleviated the apoptotic effects of deoxynivalenol in HBEC‐5i cells suggesting that it protected the cells against deoxynivalenol‐induced oxidative damage. Our findings provided new insight that VE had the potential to ameliorate neurotoxicity of deoxynivalenol.

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Deoxynivalenol as potential modulator of human steroidogenesis

Cited by 29 publications

References 83 publications

Deoxynivalenol Modulates the Viability, ROS Production and Apoptosis in Prostate Cancer Cells

Deoxynivalenol Modulates the Viability, ROS Production and Apoptosis in Prostate Cancer Cells

Nrf2: a main responsive element in cells to mycotoxin-induced toxicity

Mechanisms underlying protective effects of vitamin E against mycotoxin deoxynivalenol‐induced oxidative stress and its related cytotoxicity in primary human brain endothelial cells

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