{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,29]],"date-time":"2026-10-29T03:49:51Z","timestamp":1793245791282,"version":"4.5.0"},"reference-count":89,"publisher":"MDPI AG","issue":"11","license":[{"start":{"date-parts":[[2024,11,7]],"date-time":"2024-11-07T00:00:00Z","timestamp":1730937600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Biomolecules"],"abstract":"<jats:p>Cyanide (CN) is a well-known mitochondrial poison. CN poisoning may result from acute or long-term exposure to a number of CN compounds. Recent insight into the chemical affinities of the CN anion has increased our understanding of its toxicity and the mechanisms of antidotal actions, which, together with information on various exposure sources, are reviewed in the present article. A literature search in Scopus, Embase, Web of Science, PubMed, and Google Scholar for the period 2001\u20132024 revealed that the CN anion after exposure or degradation of CN compounds is distributed to vulnerable copper and iron-containing targets, especially in mitochondria, thus blocking the electron transport chain. Intake of cyanogenic compounds may exert subacute or chronic toxic effects, also because of the interaction with cobalt in vitamin B12. Antidotal agents exert their effects through the affinity of CN for cobalt- or iron-containing compounds. Research on CN interactions with metalloproteins may increase our insight into CN toxicity and efficient antidotal regimens.<\/jats:p>","DOI":"10.3390\/biom14111420","type":"journal-article","created":{"date-parts":[[2024,11,7]],"date-time":"2024-11-07T12:12:13Z","timestamp":1730981533000},"page":"1420","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":72,"title":["Cyanide and Cyanogenic Compounds\u2014Toxicity, Molecular Targets, and Therapeutic Agents"],"prefix":"10.3390","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4644-761X","authenticated-orcid":false,"given":"Joanna Izabela","family":"Lachowicz","sequence":"first","affiliation":[{"name":"Department of Population Health, Division of Environmental Health, Occupational Medicine and Epidemiology, Wroclaw Medical University, Mikulicza-Radeckiego 7, PL 50-368 Wroclaw, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6381-5720","authenticated-orcid":false,"given":"Jan","family":"Alexander","sequence":"additional","affiliation":[{"name":"Norwegian Institute of Public Health (NIPH), N-0213 Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7518-5703","authenticated-orcid":false,"given":"Jan O.","family":"Aaseth","sequence":"additional","affiliation":[{"name":"Department of Research, Innlandet Hospital Trust, N-2381 Brumunddal, Norway"},{"name":"Faculty of Health and Social Sciences, Inland Norway University of Applied Sciences, N-2418 Elverum, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,11,7]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"565","DOI":"10.1016\/j.chembiol.2017.03.013","article-title":"Cisplatin Analogs Confer Protection against Cyanide Poisoning","volume":"24","author":"Nath","year":"2017","journal-title":"Cell Chem. 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