2013
DOI: 10.3109/15376516.2013.812170
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In vitrostudy on the pulmonary cytotoxicity of amiodarone

Abstract: Uncoupling oxidative phosphorylation was demonstrated in untreated mouse lung tissues. Amiodarone lowered cellular ATP. Further studies are needed to explore the susceptibility of the lung to these deleterious insults and their relevance to human diseases.

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Cited by 2 publications
(1 citation statement)
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“…Several mechanisms that may work in conjunction with each other and may involve the accumulation of iodine-rich amiodarone into pneumocytes have been suggested for amiodarone-induced pulmonary toxicity [3] [33] [34]. The first potential mechanism involves a direct toxic effect that disrupts cellular membranes through the activation of protein kinase C, release of toxic reactive oxygen species, decreases in glutathione, mitochondrial dysfunction, necrosis, and apoptosis.…”
Section: Lung Massesmentioning
confidence: 99%
“…Several mechanisms that may work in conjunction with each other and may involve the accumulation of iodine-rich amiodarone into pneumocytes have been suggested for amiodarone-induced pulmonary toxicity [3] [33] [34]. The first potential mechanism involves a direct toxic effect that disrupts cellular membranes through the activation of protein kinase C, release of toxic reactive oxygen species, decreases in glutathione, mitochondrial dysfunction, necrosis, and apoptosis.…”
Section: Lung Massesmentioning
confidence: 99%