The low doses effect of experimental zearalenone (ZEN) intoxication on the presence of Ca2+ in selected ovarian cells from pre-pubertal bitches

Gajęcka, Magdalena; Przybylska‐Gornowicz, Barbara

doi:10.2478/v10181-012-0108-1

Cited by 18 publications

(17 citation statements)

References 21 publications

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“…The effect of endogenous hormones and xenoestrogens on ion channels is an example of such activity. In general, EDs including environmental mycotoxins, such as ZEN and its metabolites, disrupt the activity of Ca 2+ channels and/or Ca 2+ signaling in certain types of cells [9]. These findings indicate that endogenous hormones and EDs exhibit hormonal activity by binding to nuclear hormone receptors.…”

Section: Introductionmentioning

confidence: 96%

The Effect of Different Doses of Zearalenone in Feed on the Bioavailability of Zearalenone and Alpha-Zearalenol, and the Concentrations of Estradiol and Testosterone in the Peripheral Blood of Pre-Pubertal Gilts

Zielonka

Gajęcka

Lisieska-Żołnierczyk³

et al. 2020

Toxins

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The objective of this study was to determine the effect of long-term (48 days), per os administration of specific zearalenone (ZEN) doses (20 and 40 μg ZEN/kg BW in experimental groups EI and EII, which were equivalent to 200% and 400% of the upper range limit of the no-observed-adverse-effect-level (NOAEL), respectively) on the bioavailability of ZEN and the rate of changes in estradiol and testosterone concentrations in the peripheral blood of pre-pubertal gilts. ZEN and α-ZEL levels were similar until day 28. After day 28, α-ZEL concentrations increased significantly in group EI, whereas a significant rise in ZEN levels was noted in group EII. The presence of estradiol in peripheral blood plasma was not observed until day 20 of the experiment. Spontaneous secretion of estradiol was minimal, and it was determined at very low levels of up to 10 pg/mL in EI and EII groups. Testosterone concentrations ranged from 4 to 9 ng/mL in all groups. A decrease in the concentrations of both analyzed hormones was reported in the last stage of the experiment. The results of the experiment indicate that: (i) The bioavailability of ZEN in peripheral blood has low diagnostic value, (ii) exposure to low doses of ZEN induces minor changes in the concentrations of the analyzed hormones, which could lead to situational supraphysiological hormone levels and changes in endogenous hormonal balance.

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Section: Introductionmentioning

confidence: 96%

The Effect of Different Doses of Zearalenone in Feed on the Bioavailability of Zearalenone and Alpha-Zearalenol, and the Concentrations of Estradiol and Testosterone in the Peripheral Blood of Pre-Pubertal Gilts

Zielonka

Gajęcka

Lisieska-Żołnierczyk³

et al. 2020

Toxins

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“…In farming, determination of the ideal conditions for in vitro and in vivo development of preantral follicles will enable breeders to optimize the reproductive performance of females (Brasil et al 2010). Our published results (Gajęcka and Przybylska-Gornowicz 2012) suggest that zearalenone-induced apoptosis of ovarian cells in pre-pubertal bitches is an internal process that begin in the mitochondria. The presence of ZEN and its metabolite, α-zearalenol, leads to hyperestrogenism and increased cellular Ca 2+ levels in mitochondria.…”

Section: Introductionmentioning

confidence: 99%

The effect of experimental low zearalenone intoxication on ovarian follicles in pre-pubertal bitches

Gajęcka¹

2013

Polish Journal of Veterinary Sciences

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Companion animals, including bitches, may be exposed to zearalenone (ZEN) toxins that are often present in feed, and ZEN intoxication may lead to ovarian dysfunction. This study involved evaluation of the degree of ZEN-induced hypo stimulation of ovary by determination of proliferative and apoptotic indices and description of the ultra-structural organization of ovarian follicles in pre-pubertal bitches subjected to experimental, long-term exposure to low-dose ZEN mycotoxicosis. The experiment involved 30 clinically healthy, immature Beagle bitches aged approximately 70 days with initial average body weight of 8 kg, randomly divided into three groups of 10 animals each: two experimental groups (EI and EII) and a control group (C). Over a period of 42 days, ZEN was administered per os to EI animals at a dose of 50 μg/kg BW, and to EII bitches at a dose of 75 μg/kg BW. Control group animals were fed placebo containing no ZEN for 42 days. Analytical samples of the mycotoxin were administered daily in gelatin capsules before morning feeding. All the bitches were subjected to ovario-hysterectomy at the end of the experiment. Proliferation index (PCNA method) and apoptotic index (TUNEL test) values were determined by immune-histological analyses. The median for apoptotic index was determined at 13.45 for group EI, 17.84 for group EII, and 8.59 for group C. The median for proliferation index was determined at 35.25 for group EII, 42.44 for group EI, and 70.60 for group C. The results of ultra-structural examinations of the ovaries revealed that experimental, ZEN-induced hyperestrogenism enhanced apoptosis and lowered the proliferative ability of follicular cells what contributed to organelle destruction in pre-pubertal bitches. The changes observed were particularly advanced in EII animals, which were administered a higher dose of ZEN.

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“…In a similar fashion, zearalenone caused oxidative phosphorylation and mitochondrial dysfunction which led to endocrine dysfunction in H295R . A 42 days of intoxication with zearalenone induced apoptosis‐ like changes, possibly via Ca 2+ accumulation in the mitochondria, followed by cell dysfunction and a decrease in the mitochondrial metabolic activity in oocytes, follicle and interstitial cells of ovarian cells from beagle bitches .…”

Section: Resultsmentioning

confidence: 86%

Mycotoxin‐assisted mitochondrial dysfunction and cytotoxicity: Unexploited tools against proliferative disorders

et al. 2018

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Mitochondria are the powerhouse of cells, which upon dysfunctions may lead to several diseases. Mycotoxins are the toxic secondary metabolites from fungi which are capable of causing diseases and death in humans and animals. They have a versatile mechanism of action in biological systems and can be used as lead compounds to treat some diseases including cancer. The present work encompasses analysis on the effects of mycotoxins on mitochondrial dysfunction. Electronic databases such as PubMed, ScienceDirect, Scopus, Web of Science, and Google Scholar were thoroughly searched for up-to-date published information associated with those mycotoxins and their effect on mitochondrial dysfunction. Findings suggest that mycotoxins such as citrinin, aflatoxin, and T-2 toxin exert multi-edged sword-like effects in test systems causing mitochondrial dysfunction. Mycotoxins can induce oxidative stress even at low concentration/dose that may be one of the major causes of mitochondrial dysfunction. On the other hand, activation of apoptotic caspases and other proteins by mycotoxins may lead to apoptotic cell death. Thus, mycotoxins-mediated mitochondrial dysfunction may be related to several chronic diseases which also makes these mycotoxins considerable as lead compounds for inducing toxic effects in cells. Their cytotoxic effects on cancer cells suggest their possible application as chemotherapeutic tools. © 2018 IUBMB Life, 70(11):1084-1092, 2018.

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The low doses effect of experimental zearalenone (ZEN) intoxication on the presence of Ca2+ in selected ovarian cells from pre-pubertal bitches

Cited by 18 publications

References 21 publications

The Effect of Different Doses of Zearalenone in Feed on the Bioavailability of Zearalenone and Alpha-Zearalenol, and the Concentrations of Estradiol and Testosterone in the Peripheral Blood of Pre-Pubertal Gilts

The Effect of Different Doses of Zearalenone in Feed on the Bioavailability of Zearalenone and Alpha-Zearalenol, and the Concentrations of Estradiol and Testosterone in the Peripheral Blood of Pre-Pubertal Gilts

The effect of experimental low zearalenone intoxication on ovarian follicles in pre-pubertal bitches

Mycotoxin‐assisted mitochondrial dysfunction and cytotoxicity: Unexploited tools against proliferative disorders

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