Rachelle Abouchedid, Sarah Hodgson, Anselm Wong, Ingrid Berling, Thomas Sullivan, Joshua Bloom, Gar Chan, Mark Su, Kate Cleary, Natasha Tile, Aisling Kiely, R. Syrjanen, Jennifer Schumann, Shaun Greene, A. Holford, Christopher Martin, Andrew Staib, Keith Harris, K. Isoardi, Benjamin Horan, Benjamin Learmont, Christina Needham, Lucy Shieffelbien, Brian O’Riordan, Jonathan Lee, Joseph Rotella, Rowena Penafiel, Gina Chowdhury, Darren M Roberts, Nazila Jamshidi, Stuart Duffin
{"title":"Proceedings of the Toxicology and Poisons Network Australasia (TAPNA) 2023 Annual Scientific Meeting","authors":"Rachelle Abouchedid, Sarah Hodgson, Anselm Wong, Ingrid Berling, Thomas Sullivan, Joshua Bloom, Gar Chan, Mark Su, Kate Cleary, Natasha Tile, Aisling Kiely, R. Syrjanen, Jennifer Schumann, Shaun Greene, A. Holford, Christopher Martin, Andrew Staib, Keith Harris, K. Isoardi, Benjamin Horan, Benjamin Learmont, Christina Needham, Lucy Shieffelbien, Brian O’Riordan, Jonathan Lee, Joseph Rotella, Rowena Penafiel, Gina Chowdhury, Darren M Roberts, Nazila Jamshidi, Stuart Duffin","doi":"10.1080/24734306.2023.2222509","DOIUrl":null,"url":null,"abstract":"Arsenicals induce their toxic effects by binding to sulfhydryl groups in multiple enzyme systems, inhibiting metabolism and disrupting oxidative phosphorylation generating reactive oxygen species. In animal studies NAC has been shown to decrease arsenic mediated oxidative damage and in in vitro studies NAC was shown to chelate arsenic. The optimal time to commence NAC therapy has not been studied, but animal studies have shown earlier treatment improved survival. Given its favourable safety profile, low cost and the findings from animal studies, NAC should be used as an adjunct to standard chelation therapy in arsenic poisoning. Further investigation is required to establish the optimal duration of treatment and dosing.","PeriodicalId":23139,"journal":{"name":"Toxicology communications","volume":"16 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2023-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology communications","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/24734306.2023.2222509","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Arsenicals induce their toxic effects by binding to sulfhydryl groups in multiple enzyme systems, inhibiting metabolism and disrupting oxidative phosphorylation generating reactive oxygen species. In animal studies NAC has been shown to decrease arsenic mediated oxidative damage and in in vitro studies NAC was shown to chelate arsenic. The optimal time to commence NAC therapy has not been studied, but animal studies have shown earlier treatment improved survival. Given its favourable safety profile, low cost and the findings from animal studies, NAC should be used as an adjunct to standard chelation therapy in arsenic poisoning. Further investigation is required to establish the optimal duration of treatment and dosing.