Urinary ochratoxin A and ochratoxin alpha in pregnant women

Klapec, Tomislav; Šarkanj, Bojan; Banjari, Ines; Strelec, Ivica

doi:10.1016/j.fct.2012.09.030

Cited by 41 publications

(26 citation statements)

References 34 publications

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“…Samples from Bangladesh showed significantly higher mean concentrations than samples from Germany and Haiti. The data of the present study resemble ranges of OTA concentrations reported for urine samples from Germany, Italy, and Croatia (Gerding et al 2014;Solfrizzo et al 2014;Klapec et al 2012). From a mean urinary concentration of 0.144 ng/mL in Italian urines, Solfrizzo et al (2014) calculated a PDI of 0.139 μg/kg b.w., i.e., a significant exceedance of the established TDI of 0.017 μg/kg b.w.…”

Section: Discussionmentioning

confidence: 89%

A comparative study of the human urinary mycotoxin excretion patterns in Bangladesh, Germany, and Haiti using a rapid and sensitive LC-MS/MS approach

et al. 2015

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An improved "dilute and shoot" LC-MS/MS multibiomarker approach was used to monitor urinary excretion of 23 mycotoxins and their metabolites in human populations from Asia (Bangladesh), Europe (Germany), and the Caribbean region (Haiti). Deoxynivalenol (DON), deoxynivalenol-3-glucuronide (DON-3-GlcA), T-2-toxin (T-2), HT-2-toxin (HT-2), HT-2-toxin-4-glucuronide (HT-2-4-GlcA), fumonisin B1 (FB1), aflatoxins (AFB1, AFB2, AFG1, AFG2, AFM1), zearalenone (ZEA), zearalanone (ZAN), their urinary metabolites α-zearalanol (α-ZEL) and β-zearalanol (β-ZEL), and corresponding 14-O-glucuronic acid conjugates (ZEA-14-GlcA, ZAN-14-GlcA, β-ZEL, α/β-ZEL-14-GlcA), ochratoxin A (OTA), and ochratoxin alpha (OTα) as well as enniatin B (EnB) and dihydrocitrinone (DH-CIT) were among these compounds. Eight urinary mycotoxin biomarkers were detected (AFM1, DH-CIT, DON, DON-GLcA, EnB, FB1, OTA, and α-ZEL). DON and DON-GlcA were exclusively detected in urines from Germany and Haiti whereas urinary OTA and DH-CIT concentrations were significantly higher in Bangladeshi samples. AFM1 was present in samples from Bangladesh and Haiti only. Exposure was estimated by the calculation of probable daily intakes (PDI), and estimates suggested occasional instances of toxin intakes that exceed established tolerable daily intakes (TDI). The detection of individual mycotoxin exposure by biomarker-based approaches is a meaningful addition to the classical monitoring of the mycotoxin content of the food supply.

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Section: Discussionmentioning

confidence: 89%

A comparative study of the human urinary mycotoxin excretion patterns in Bangladesh, Germany, and Haiti using a rapid and sensitive LC-MS/MS approach

et al. 2015

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“…The fetal and neonatal exposure to OTA is likely determined by the analysis of cord blood samples from pregnant women, human blood, colostrum, milk, and urine (Micco et al, 1991;Kovacs et al, 1995;Miraglia et al, 1998;Skaug et al, 1998;Muñoz et al, 2010;Klapec et al, 2012). The fetal and neonatal exposure to OTA is likely determined by the analysis of cord blood samples from pregnant women, human blood, colostrum, milk, and urine (Micco et al, 1991;Kovacs et al, 1995;Miraglia et al, 1998;Skaug et al, 1998;Muñoz et al, 2010;Klapec et al, 2012).…”

Section: Ota Biomonitoringmentioning

confidence: 99%

“…Despite these difficulties, OTA in urine is thought by some authors to be a better indicator of exposure to OTA than OTA in plasma (Gilbert et al, 2001;Castegnaro et al, 2006;Pfohl-Leszkowicz et al, 2006). The first study to determine the exposure of pregnant women to OTA was realized through examination of OTA and ochratoxin alpha in the urine of pregnant women (Klapec et al, 2012). The first study to determine the exposure of pregnant women to OTA was realized through examination of OTA and ochratoxin alpha in the urine of pregnant women (Klapec et al, 2012).…”

Section: Ota Biomonitoringmentioning

confidence: 99%

“…No data on teratogenic dose and teratogenic OTA effects in humans are available. The fetal and neonatal exposure to OTA is likely determined by the analysis of cord blood samples from pregnant women, human blood, colostrum, milk, and urine (Micco et al, 1991;Kovacs et al, 1995;Miraglia et al, 1998;Skaug et al, 1998;Muñoz et al, 2010;Klapec et al, 2012). It is clear that OTA fetal exposure might pose a potential risk in prenatal and postnatal life for the human infants (Micco et al, 1991;Jonsyn et al, 1995;Kovacs et al, 1995;Skaug et al, 1998).…”

Section: Ota Biomonitoringmentioning

confidence: 99%

“…Moreover, analysis of OTA metabolites in urine will give additional information concerning toxicokinetic and genetic susceptibility (Pfohl-Leszkowicz, 2009). The first study to determine the exposure of pregnant women to OTA was realized through examination of OTA and ochratoxin alpha in the urine of pregnant women (Klapec et al, 2012).…”

Section: Ota Biomonitoringmentioning

confidence: 99%

See 2 more Smart Citations

Ochratoxin A: Developmental and Reproductive Toxicity—An Overview

Malíř

Ostrý

Pfohl‐Leszkowicz

et al. 2013

Birth Defects Research Pt B

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Ochratoxin A (OTA) is nephrotoxic, hepatotoxic, reprotoxic, embryotoxic, teratogenic, neurotoxic, immunotoxic, and carcinogenic for laboratory and farm animals. Male and female reproductive health has deteriorated in many countries during the last few decades. A number of toxins in environment are suspected to affect reproductive system in male and female. OTA is one of them. OTA has been found to be teratogenic in several animal models including rat, mouse, hamster, quail, and chick, with reduced birth weight and craniofacial abnormalities being the most common signs. The presence of OTA also results in congenital defects in the fetus. Neither the potential of OTA to cause malformations in human nor its teratogenic mode of action is known. Exposure to OTA leads to increased embryo lethality manifested as resorptions or dead fetuses. The mechanism of OTA transfer across human placenta (e.g., which transporters are involved in the transfer mechanism) is not fully understood. Some of the toxic effects of OTA are potentiated by other mycotoxins or other contaminants. Therefore, OTA exposure of pregnant women should be minimized. OTA has been shown to be an endocrine disruptor and a reproductive toxicant, with abilities of altering sperm quality. Other studies have shown that OTA is a testicular toxin in animals. Thus, OTA is a biologically plausible cause of testicular cancer in man.

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