Fusarium
Dongyou Liu in Laboratory Models for Foodborne Infections, 2017
It is assumed that ZEA has a role in sexual reproduction of the producing fungi [17], and it also affects the growth, development, and photosynthetic apparatus of the contaminated plant [18]. The nonsteroidal, estrogen-like structure also allows the toxin and its metabolites (α-zearalenol and β-zearalenol) to compete with mammalian endogenous estrogens for specific binding sites on their receptors. This estrogenic activity of ZEA causes hyperestrogenism and fertility disorders in farm animals after consumption of a high dose of affected crops (e.g., >0.25 mg/kg ZEA in maize) [14,19]. Pigs—particularly the prepubertal females—are the most sensitive to the higher concentrations of ZEA, whereas ruminants and poultry are reported as less sensitive [14]. Piglets can be affected as well, as ZEA can be excreted into sows’ milk [19]. ZEA also represents a potential risk to human health. It is assumed that ZEA exposure is associated with precocious pubertal development in girls [15,20], and it was also mentioned as a possible causative agent of cervical cancer [21]. Besides its endocrine-disrupting effects on animals and humans, ZEA has been reported to be hepatotoxic, hematotoxic, immunotoxic, and genotoxic [12].
Zearalenone: Insights into New Mechanisms in Human Health
Dongyou Liu in Handbook of Foodborne Diseases, 2018
Once ingested, ZEA is metabolized in the liver and in the small intestine through redox reactions to α- and β-zearalenol (α- and ß-ZOL) [11]. The second biotransformation is through conjugation with the glucuronic or sulfonic acids, resulting in zearalenone-glucuronide or zearalenone-sulfate. The metabolites are excreted mainly in the bile and finally in the urine [12,13]. It seems that the human placenta cells also have the ability to metabolize ZEA, mainly in α-zearalenol. The enzyme CYP19A1 is involved in this conversion [14].
Toxic and irritant effects induced by zearalenone: prevention by taurine
Published in Toxin Reviews, 2021
Zearalenone (ZEN) is a non-steroidal estrogenic mycotoxin produced by the Fusarium species (Bertero et al. 2018). ZEN is a significant contaminant of many agricultural products thus is a major economic and health problem (Kuiper-Goodman et al. 1987, Zinedine et al. 2007). Several systematic review and meta-analytic approaches reported that 32% of mixed cereal products in Europe were contaminated by ZEN and these products were cornflakes (55%), bread (41%), breakfast cereals (37%), biscuit (22%), pasta (17%), respectively (Mousavi Khaneghah et al. 2018, Al-Jaal et al. 2019). Previous studies declared that the concentration of ZEN in human food could be found at a high level, up to 289 μg/g (Yuwai et al. 1994, Ghedira-Chekir et al. 1999). Therefore, ZEN and its metabolites (α-zearalenol and β-zearalenol) is a potential danger to human and animal health.
Estrogenic activity of zearalenone, α-zearalenol and β-zearalenol assessed using the E-screen assay in MCF-7 cells
Published in Toxicology Mechanisms and Methods, 2018
Elena Tatay, Silvia Espín, Antonio-Juan García-Fernández, María-José Ruiz
Mycotoxins are biologically active metabolites produced by fungal species that are toxic to humans and other animals. They represent a serious problem since mycotoxin contamination of agricultural products can occur worldwide and cause several health disorders. Zearalenone (ZEA) is a resorcylic acid lactone derivate produced by Fusarium fungi. ZEA and its derivatives (α-zearalenol [α-ZOL]; β-zearalenol [β-ZOL]) have structural analogy to estrogen, and their structures are flexible enough to bind to mammalian ERs (Parveen et al. 2009). Thus, they are able to mimic the activity of naturally occurring estrogens (Gajecka 2012). The estrogenic activity of ZEA and its metabolites has been determined both in vivo and in vitro (Le Guevel and Pakdel 2001; Minervini et al. 2005; Caloni et al. 2009; Parveen et al. 2009; Frizzell et al. 2011; Busk et al. 2012; Prouillac et al. 2012; Cortinovis et al. 2013). It is known that these mycotoxins, also called mycoestrogens, induce their toxicity by competitive binding to the ER and modifying steroid metabolism and producing morphological and functional changes in the reproductive system (Salem et al. 2017). It has been shown that ZEA decreases fertility due to reproductive tract disorders and abnormal fetal development, reduces the size and weight of the adrenal and pituitary glands in animals, and alters the ovulation cycle (Parveen et al. 2009; Cortinovis et al. 2013; EFSA Panel on Contaminants in the Food Chain (CONTAM) 2016). Due to the anabolic activity of ZEA, it is used as a hormonal growth-promoter in food animals in the United States and Canada, whereas any use of ZEA as a growth promoter is forbidden in the EU (Le Guevel and Pakdel 2001).
Biomonitoring of mycotoxin exposure using urinary biomarker approaches: a review
Published in Toxin Reviews, 2021
Larissa Tuanny Franco, Amin Mousavi Khaneghah, Sarah Hwa In Lee, Carlos Augusto Fernandes Oliveira
After oral intake of contaminated foods, ZEN is rapidly absorbed and then metabolized in the intestines or liver. There, the toxin undergoes hydroxylation with the production of several metabolites that are usually conjugated with glucuronic acid, thus facilitating their excretion in urine (Borchers et al.2010). In pigs, the calculated plasma half-life was 87 h after the intravenous or oral routes (Riley and Voss 2011). However, there is very little information on the absorption rate and metabolic fate/bioavailability (European Food Safety Authority 2016). ZEN is primarily degraded in the liver after considerable enterohepatic recirculation into α-zearalenol (α-ZEL) and β-zearalenol (β-ZEL), which undergo additional reduction into α-zearalanol (α-ZAL) and β-zearalanol (β-ZAL) (Kiessling and Pettersson 1978; Olsen et al.1981). The α-ZAL is metabolized into its isomer β-ZAL and, to a lesser extent, into zearalenone (ZAN). These compounds are, then, partially conjugated with sulfonic or glucuronic acid and excreted in the urine (Kuiper-Goodman et al.1987; Bernhoft et al.2001; Zinedine et al.2007). The intestinal mucosa is also active in reducing ZEA to α-ZEL as well as conjugating with glucuronic acid (Biehl et al.1993). In humans, urinary excretion of ZEN is approximately 10% of the administered dose, with ZEN glucuronides and α-ZEL as the main metabolites, along with minor amounts of β-ZEL (Fleck et al.2016). Urinary biomarkers in piglets show excretion 36.8% of dietary ZEN in 24 h (Gambacorta et al.2013). Half-life is approximately 3 days after ZEN administration (Ueno et al.1977; Olsen et al.1985; Bernhoft et al.2001).
Related Knowledge Centers
- Epimer
- Estrogen
- Fusarium
- Gastrointestinal Tract
- Metabolite
- Zearalenone
- Liver
- NONsteroidal
- Resorcylic Acid Lactone
- Α-Zearalenol