Zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cells

Bai, Jun; Li, Jun; Liu, Ning; Hai, Jian; Si, Xuemeng; Zhou, Yusong; Zhai, Zhian; Yang, Ying; Ren, Fazheng; Wu, Zhenlong

doi:10.1016/j.aninu.2022.08.016

Cited by 5 publications

(4 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hoechst 33258 staining confirmed that ZEA led to apoptosis in sheep follicular granulosa cells. This result is consistent with that of previous studies that showed that ZEA induces apoptosis in chicken granulosa and porcine trophoblast cells [ 17 , 31 ]. There are reports that, in general, pigs and sheep are more susceptible to ZEA infection than poultry [ 20 ].…”

Section: Discussionsupporting

confidence: 94%

“…Accumulation of ZEA in the food chain can be hazardous to human health and may even affect the pathogenesis and prevalence of estrogen-related carcinogenicity [ 28 , 29 ]. Both in vitro and in vivo tests confirmed that ZEA causes reproductive system damage in mice, pigs, cattle, and chickens [ 17 , 30 , 31 , 32 ]; however, few studies have focused on the mechanism underlying the toxicity of ZEA in sheep. In this study, we researched the toxic effects of ZEA on follicular granulosa cells of sheep cultured in vitro and the potential mechanism of action, providing theoretical support for ZEA-mediated reproductive damage.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Heme Oxygenase-1 Regulates Zearalenone-Induced Oxidative Stress and Apoptosis in Sheep Follicular Granulosa Cells

Li,

Gao,

Yao

et al. 2024

IJMS

View full text Add to dashboard Cite

Zearalenone (ZEA) is a common non-steroidal estrogenic mycotoxin found in a range of animal feeds and poses a serious threat to the reproductive health of farm animals and humans. However, the mechanism underlying ZEA-induced reproductive toxicity in sheep remains unknown. Granulosa cells are crucial for egg maturation and the fertility of female sheep. In this study, we aimed to examine the impact of different ZEA concentrations on sheep follicular granulosa cells and to elucidate the potential molecular mechanism underlying ZEA-induced toxicity using transcriptome sequencing and molecular biological approaches. Treating primary sheep follicular granulosa cells with different concentrations of ZEA promoted the overproduction of reactive oxygen species (ROS), increased lipid peroxidation products, led to cellular oxidative stress, decreased antioxidant enzyme activities, and induced cell apoptosis. Using transcriptome approaches, 1395 differentially expressed genes were obtained from sheep follicular granulosa cells cultured in vitro after ZEA treatment. Among them, heme oxygenase-1 (HMOX1) was involved in 11 biological processes. The protein interaction network indicated interactions between HMOX1 and oxidative and apoptotic proteins. In addition, N-acetylcysteine pretreatment effectively reduced the ZEA-induced increase in the expression of HMOX1 and Caspase3 by eliminating ROS. Hence, we suggest that HMOX1 is a key differential gene involved in the regulation of ZEA-induced oxidative stress and apoptosis in follicular granulosa cells. These findings provide novel insights into the prevention and control of mycotoxins in livestock.

show abstract

Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Heme Oxygenase-1 Regulates Zearalenone-Induced Oxidative Stress and Apoptosis in Sheep Follicular Granulosa Cells

Li,

Gao,

Yao

et al. 2024

IJMS

View full text Add to dashboard Cite

show abstract

“…ZEA reduces the protein expression of Nrf2 and HO‐1 to further induce oxidative stress and cause cell apoptosis via the p38, JNK, and ERK MAPK pathways 63 , 64 , 65 . Bai et al found that ZEA can induce apoptosis by modulating EnR stress though the PERK and ATF6 signaling pathways in porcine trophectoderm cells 66 . In addition to the classical signaling pathways, ZEA induces apoptosis through the ERK/p53/Caspase 3 signaling pathway and the Caspase 12 signaling pathway activated by Ca 2+ release from the EnR 67 , 68 .…”

Section: Main Fusarium Mycotoxinsmentioning

confidence: 99%

Fusarium mycotoxins: The major food contaminants

Qu,

Ren,

et al. 2024

mLife

View full text Add to dashboard Cite

Mycotoxins, which are secondary metabolites produced by toxicogenic fungi, are natural food toxins that cause acute and chronic adverse reactions in humans and animals. The genus Fusarium is one of three major genera of mycotoxin‐producing fungi. Trichothecenes, fumonisins, and zearalenone are the major Fusarium mycotoxins that occur worldwide. Fusarium mycotoxins have the potential to infiltrate the human food chain via contamination during crop production and food processing, eventually threatening human health. The occurrence and development of Fusarium mycotoxin contamination will change with climate change, especially with variations in temperature, precipitation, and carbon dioxide concentration. To address these challenges, researchers have built a series of effective models to forecast the occurrence of Fusarium mycotoxins and provide guidance for crop production. Fusarium mycotoxins frequently exist in food products at extremely low levels, thus necessitating the development of highly sensitive and reliable detection techniques. Numerous successful detection methods have been developed to meet the requirements of various situations, and an increasing number of methods are moving toward high‐throughput features. Although Fusarium mycotoxins cannot be completely eliminated, numerous agronomic, chemical, physical, and biological methods can lower Fusarium mycotoxin contamination to safe levels during the preharvest and postharvest stages. These theoretical innovations and technological advances have the potential to facilitate the development of comprehensive strategies for effectively managing Fusarium mycotoxin contamination in the future.

show abstract

“…Similarly, a mixture of deoxynivalenol and zearalenone has synergistic effects on the levels of pro-in ammatory cytokines in piglets[65]. Endoplasmic reticulum stress has also been observed in numerous studies conducted with fumonisins[12, 46,[66][67][68], deoxynivalenol [69-73], and zearalenone[74][75][76][77][78][79]. This mechanism could play a key role in mitochondrial-induced apoptosis when deoxynivalenol and zearalenone were used in combination[80].…”

mentioning

confidence: 99%

Fumonisins alone or mixed with other fusariotoxins increase the C22–24:C16 sphingolipid ratios in chickens and ducks, while deoxynivalenol and zearalenone have no effect

Guerre,

Lassallette,

Beaujardin-Daurian

et al. 2023

Preprint

View full text Add to dashboard Cite

Background The inhibitory effect of fumonisins on ceramide synthases results in several effects on the sphingolipidome, and recent results in chickens suggest that the C22–24:C16 sphingolipid ratios may be complementary biomarkers to Sa:So. Feeding diets containing fumonisins, deoxynivalenol, or zearalenone alone or in combination up to the maximum levels recommended by the European Commission for 35 days in chickens and 12 days in ducks resulted in no effects on performance or toxicity. The aim of this study was to investigate their effects on the liver sphingolipidome. Results Sphingolipids were characterised by UHPLC-MSMS. Numerous significant effects of fusariotoxins on sphingolipids were observed at the class and analyte levels. Fusariotoxins alone decreased sphingolipids in chickens but had weak effects in ducks. Feeding fumonisins in combination with deoxynivalenol and zearalenone increased sphingolipid levels in chickens but not in ducks. These increases were mainly due to an increase in C22–24 sphingolipids, whereas C16 sphingolipids decreased. The Sa:So ratio and the C22–24:C16 ratio for ceramides, sphingomyelins, monohexosylceramides, dihydroceramides, and dihydrosphingomyelins were unaffected in chickens and ducks fed the diets containing deoxynivalenol or zearalenone but increased in animals fed the fumonisin diets. Interestingly, while the effects of feeding fumonisins alone or in combination on the total amount of sphingolipids differed in chickens, the Sa:So and C22-24:C16 ratios were similar. Partial least squares-discriminant analysis of sphingolipids did not allow discrimination of the animals exposed to deoxynivalenol or zearalenone from the unexposed animals. By contrast, good discrimination of the animals fed the diets containing fumonisins was achieved. Sphinganine, d20 sphinganine, a large number of C16 sphingolipids, and dihydrosphingomyelins for which the fatty acid contains more than 18 carbon atoms, were important variables in the models obtained in chickens and ducks. Conclusions The C22–24:C16 ratios of sphingolipids are increased in chickens and ducks by intake of fumonisins but not deoxynivalenol or zearalenone. The increases were similar when fumonisins were fed alone or in combination with deoxynivalenol or zearalenone. The increase in the C22–24:C16 ratio may be an important factor in explaining the interspecies differences in sensitivity to fumonisin toxicity.

show abstract

Zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cells

Cited by 5 publications

References 47 publications

Heme Oxygenase-1 Regulates Zearalenone-Induced Oxidative Stress and Apoptosis in Sheep Follicular Granulosa Cells

Heme Oxygenase-1 Regulates Zearalenone-Induced Oxidative Stress and Apoptosis in Sheep Follicular Granulosa Cells

Fusarium mycotoxins: The major food contaminants

Fumonisins alone or mixed with other fusariotoxins increase the C22–24:C16 sphingolipid ratios in chickens and ducks, while deoxynivalenol and zearalenone have no effect

Contact Info

Product

Resources

About