Inhibition of ochratoxin a teratogenesis by zearalenone and diethylstilboestrol

Arora, Ram Gopal; Frölén, H.; Fellner-Feldegg, Hugo

doi:10.1016/0278-6915(83)90212-0

Cited by 26 publications

(14 citation statements)

References 5 publications

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“…188 Thus, it appears that the teratogenic effects mediated by OTA are caused by a direct action of the parent compound on the developing fetus. The observations of Arora and coworkers 189 seem to corroborate these observations, as simultaneous administration of diethylstilbestrol and zearalenone, both of which have been shown to reduce transplacental blood flow, resulted in an overall reduction or absence of abnormal fetuses in rats exposed to OTA. In contrast to these reports of teratogenesis in several species, a study carried out by Shreeve and coworkers indicated OTA to have no teratogenic potential in pigs.…”

Section: Ota Causes Specific Developmental Defectssupporting

confidence: 76%

Ochratoxin A: The Continuing Enigma

O'Brien

Dietrich

2005

Critical Reviews in Toxicology

357

212

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The mycotoxin ochratoxin A (OTA) has been linked to the genesis of several disease states in both animals and humans. It has been described as nephrotoxic, carcinogenic, teratogenic, immunotoxic, and hepatotoxic in laboratory and domestic animals, as well as being thought to be the probable causal agent in the development of nephropathies (Balkan Endemic Nephropathy, BEN and Chronic Interstitial Nephropathy, CIN) and urothelial tumors in humans. As a result, several international agencies are currently attempting to define safe legal limits for OTA concentration in foodstuffs (e.g., grain, meat, wine, and coffee), in processed foods, and in animal fodder. In order to achieve this goal, an accurate risk assessment of OTA toxicity including mechanistic and epidemiological studies must be carried out. Ochratoxin has been suggested by various researchers to mediate its toxic effects via induction of apoptosis, disruption of mitochondrial respiration and/or the cytoskeleton, or, indeed, via the generation of DNA adducts. Thus, it is still unclear if the predominant mechanism is of a genotoxic or an epigenetic nature. One aspect that is clear, however, is that the toxicity of OTA is subject to and characterized by large species-and sex-specific differences, as well as an apparently strict structure-activity relationship. These considerations could be crucial in the investigation of OTA-mediated toxicity. Furthermore, the use of appropriate in vivo and in vitro model systems appears to be vital in the generation of relevant experimental data. The intention of this review is to collate and discuss the currently available data on OTA-mediated toxicity with particular focus on their relevance for the in vivo situation, and also to suggest possible future strategies for unlocking the secrets of ochratoxin A.

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Section: Ota Causes Specific Developmental Defectssupporting

confidence: 76%

Ochratoxin A: The Continuing Enigma

O'Brien

Dietrich

2005

Critical Reviews in Toxicology

357

212

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“…Both OTA and citrinin are well-known nephrotoxins. OTA is also carcinogenic to rodents (Creppy et al, 1985) and possesses teratogenic (Arora et al, 1983), immunotoxic (Stormer and Lea, 1995), neurotoxic (Bruinink and Sidler, 1997;Sava et al, 2006), mutagenic (Stetina and Votava, 1986), and genotoxic (Meisner et al, 1983) properties. Compared to OTA, ochratoxin B is rarely found and very less toxic.…”

Section: Importance Of Mycotoxinsmentioning

confidence: 97%

Occurrence, importance and control of mycotoxins: A review

Tola¹,

Kebede

2016

Cogent Food & Agriculture

190

144

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Mycotoxins are poisonous chemical compounds produced by certain fungi. There are five mycotoxins or groups of mycotoxins that occur quite often in food: deoxynivalenol/Nivalenol, zearalenone, ochratoxin, fumonisins and aflatoxins. The fungi that produce mycotoxins in food fall broadly into two groups: those that invade before harvest, commonly called field fungi, and those that occur only after harvest, called storage fungi. There are three types of toxicogenic field fungi: plant pathogens such as Fusarium graminearum (deoxynivalenol, nivalenol); fungi that grow on senescent or stressed plants, such as Fusarium moniliforme (fumonisin) andsometimes Aspergillus flavus (aflatoxin); and fungi that initially colonise the plant before harvest and predispose the commodity to mycotoxin contamination after harvest, such as Penicillium verrucosum (ochratoxin) and Aspergillus flavus (aflatoxin). The favourable conditions for mycotoxins production are instigated with poor hygienic conditions at the time of transportation and storage, high temperature and moisture content and heavy rains. Mycotoxins are distributed in different items such as animal feeds, cereal crops, leguminous plants and animal products.Concentrated animal feed stuffs harbor highest level of mycotoxins. Noug cake and sorghum was warranted as the main source of aflatoxin contaminant among those concentrated animal feeds.Health effects occur in companion animals, livestock, poultry and humans because aflatoxins are potent hepatotoxins, immunosuppressant, and mutagens and carcinogens. Factors that affect mycotoxins production and contamination can be categorized as physical, chemical and biological. Therefore, African countries particularly Ethiopian governmental jurisdictions should implement and regulate level of mycotoxins in animal feed stuffs and human foods.

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“…Although unexpectedly ob served in the rather few reproducing rats and not an objec tive of the experimental design, the apparent lack of re sponse in the pregnant or lactating dam is rather stricking and raises fundamental questions concerning hormonal mediation of P. aurantiogriseum nephrotoxin effects on rat renal proximal tubules. Hormonal modulation of the teratagenicity of ochratoxin A is already strongly implied by the highly significant protection afforded when diethylstilbestrol or the estrogenic mycotoxin zearalenone were admin istered concurrently with ochratoxin A to mice on day 9 of pregnancy [15], 97 …”

Section: Discussionmentioning

confidence: 99%

Renal Histopathological Responses to Nephrotoxic <i>Penicillium aurantiogriseum</i> in the Rat during Pregnancy, Lactation and after Weaning

Mantle

1994

Nephron

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The typical renal histopathological changes in proximal tubules of rats consuming food containing shredded wheat moulded by Penicillium aurantiogriseum did not occur in neonates of rats ingesting the nephrotoxic diet during pregnancy nor in pups fed only by lactation from a treated dam. In contrast, weanlings consuming the moulded diet consistently showed within a few days densely staining mitosis-like structures in the proximal tubules which was the first step leading to development of the prominent tubular cytomegaly and karyomegaly seen when 16 weeks old. Karyomegaly and cytomegaly became evident also when mouldy shredded wheat constituted only 1% of a diet consumed on 45 days during the first 8 weeks after weaning, demonstrating the potency of the active component. Relevance to the putative involvement of nephrotoxic mycotoxins in human renal disease is discussed, as is the apparent absence of a renal histopathological response in adult rats during pregnancy and lactation.

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Inhibition of ochratoxin a teratogenesis by zearalenone and diethylstilboestrol

Cited by 26 publications

References 5 publications

Ochratoxin A: The Continuing Enigma

Ochratoxin A: The Continuing Enigma

Occurrence, importance and control of mycotoxins: A review

Renal Histopathological Responses to Nephrotoxic <i>Penicillium aurantiogriseum</i> in the Rat during Pregnancy, Lactation and after Weaning

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