ArticleToxicology research2021
Non-embryotoxic dosage of alternariol aggravates ochratoxin A-triggered deleterious effects on embryonic development through ROS-dependent apoptotic processes.
Article in Toxicology research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Antibacterial insights into alternariol and its derivative alternariol monomethyl ether produced by a marine fungus.Applied and environmental microbiology · 2024Article
- Prevention of methylmercury-triggered ROS-mediated impairment of embryo development by co-culture with adult adipose-derived mesenchymal stem cells.Toxicology research · 2024Article
- Role of caspase-3-cleaved/activated PAK2 in brusatol-triggered apoptosis of human lung cancer A549 cells.Toxicology research · 2022Article
- N-Acetylcysteine, an ROS Inhibitor, Alleviates the Pathophysiology of Hyperthyroidism-Induced Cardiomyopathy via the ROS/CaBiomolecules · 2022Article
- Molecular mechanisms underlying the renal protective effects of coenzyme Q10 in acute kidney injury.Cellular & molecular biology letters · 2022Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
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Abstract
Alternariol (AOH) and ochratoxin A (OTA), two mycotoxins found in many foods worldwide, exhibit cytotoxicity and embryotoxicity, triggering apoptosis and cell cycle arrest in several mammalian cells and mouse embryos. The absorption rate of AOH from dietary foodstuff is low, meaning that the amount of AOH obtained from the diet rarely approaches the cytotoxic threshold. Thus, the potential harm of dietary consumption of AOH is generally neglected. However, previous findings from our group and others led us to question whether a low dosage of AOH could aggravate the cytotoxicity of other mycotoxins. In the present study, we examined how low dosages of AOH affected OTA-triggered apoptosis and embryotoxicity and investigated the underlying regulatory mechanism in mouse blastocysts. Our results revealed that non-cytotoxic concentrations of AOH (1 and 2 μM) could enhance OTA (8 μM)-triggered apoptotic processes and embryotoxicity in mouse blastocysts. We also found that AOH can enhance OTA-evoked intracellular reactive oxygen species (ROS) generation and that this could be prevented by pretreatment with the potent ROS scavenger,
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