Nadia Pérez-Fuentes, Rebeca Alvariño*, Amparo Alfonso*, Jesús González-Jartín, Mercedes R. Vieytes and Luis M. Botana,
{"title":"Enniatins A1 and B1 Modulate Calcium Flux through Alternative Pathways beyond Mitochondria","authors":"Nadia Pérez-Fuentes, Rebeca Alvariño*, Amparo Alfonso*, Jesús González-Jartín, Mercedes R. Vieytes and Luis M. Botana, ","doi":"10.1021/acs.jafc.4c04242","DOIUrl":null,"url":null,"abstract":"<p >Enniatins (ENNs) A1 and B1, previously considered ionophores, are emerging mycotoxins with effects on Ca<sup>2+</sup> homeostasis. However, their exact mechanism of action remains unclear. This study investigated how these toxins affect Ca<sup>2+</sup> flux in SH-SY5Y cells. ENN A1 induced Ca<sup>2+</sup> influx through store-operated channels (SOC). The mitochondrial uncoupler FCCP reduced this influx, suggesting that the mitochondrial status influences the toxin effect. Conversely, ENN B1 did not affect SOC but acted on another Ca<sup>2+</sup> channel, as shown when nickel, which directly blocks the Ca<sup>2+</sup> channel pore, is added. Mitochondrial function also influenced the effects of ENN B1, as treatment with FCCP reduced toxin-induced Ca<sup>2+</sup> depletion and uptake. In addition, both ENNs altered mitochondrial function by producing the opening of the mitochondrial permeability transition pore. This study describes for the first time that ENN A1 and B1 are not Ca<sup>2+</sup> ionophores and suggests a different mechanism of action for each toxin.</p>","PeriodicalId":41,"journal":{"name":"Journal of Agricultural and Food Chemistry","volume":null,"pages":null},"PeriodicalIF":5.7000,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/acs.jafc.4c04242","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Agricultural and Food Chemistry","FirstCategoryId":"97","ListUrlMain":"https://pubs.acs.org/doi/10.1021/acs.jafc.4c04242","RegionNum":1,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"AGRICULTURE, MULTIDISCIPLINARY","Score":null,"Total":0}
引用次数: 0
Abstract
Enniatins (ENNs) A1 and B1, previously considered ionophores, are emerging mycotoxins with effects on Ca2+ homeostasis. However, their exact mechanism of action remains unclear. This study investigated how these toxins affect Ca2+ flux in SH-SY5Y cells. ENN A1 induced Ca2+ influx through store-operated channels (SOC). The mitochondrial uncoupler FCCP reduced this influx, suggesting that the mitochondrial status influences the toxin effect. Conversely, ENN B1 did not affect SOC but acted on another Ca2+ channel, as shown when nickel, which directly blocks the Ca2+ channel pore, is added. Mitochondrial function also influenced the effects of ENN B1, as treatment with FCCP reduced toxin-induced Ca2+ depletion and uptake. In addition, both ENNs altered mitochondrial function by producing the opening of the mitochondrial permeability transition pore. This study describes for the first time that ENN A1 and B1 are not Ca2+ ionophores and suggests a different mechanism of action for each toxin.
期刊介绍:
The Journal of Agricultural and Food Chemistry publishes high-quality, cutting edge original research representing complete studies and research advances dealing with the chemistry and biochemistry of agriculture and food. The Journal also encourages papers with chemistry and/or biochemistry as a major component combined with biological/sensory/nutritional/toxicological evaluation related to agriculture and/or food.