Evaluation of reactive oxygen species involvement in amiodarone pulmonary toxicity in vivo and in vitro

Leeder, Randall G.; Rafeiro, Elizabeth; Brien, James F.; Mandin, Colin C.; Massey, Thomas E.

doi:10.1002/(sici)1522-7146(1996)11:3<147::aid-jbt7>3.0.co;2-k

Cited by 20 publications

(5 citation statements)

References 33 publications

(49 reference statements)

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“…BCNU , a glutathione reductase inhib itor preventin g reduction of GSSG to GSH , has been shown to inhibit pulm onary glutathione reductase activity and to magnify toxicity of oxygen and [ 13,24] . I n the current study, H 2 O 2 BCNU and cotreatment resulted in a decrease in SP -A and -B mR NA s H 2 O 2 and an increase in the GSSG/GSH ratio.…”

Section: Discussionmentioning

confidence: 99%

ANTAGONISTIC EFFECTS OF PYRROLIDINE DITHIOCARBAMATE AND N-ACETYL-L-CYSTEINE ON SURFACTANT PROTEIN A AND B mRNAs

Khalak

Huyck²,

Pryhuber³

1999

Experimental Lung Research

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Pulmonary surfactant, a mixture of phospholipids and specific associated proteins, reduces surface tension at the air-liquid interface of the lung and protects the large epithelial surface of the lung from infectious organisms. Surfactant proteins, SP-A and SP-B, are required for normal surfactant function. In the current work, increased levels of oxidized glutathione (GSSG) are demonstrated at doses of pyrrolidine dithiocarbamate (PDTC) which decrease SP-A and SP-B mRNAs, suggesting that cellular oxidation reduces surfactant protein expression. Similarly, reduction of SP-A and SP-B mRNA levels following accumulation of GSSG induced by glutathione reductase inhibitor 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU), supports the hypothesis that surfactant protein synthesis is reduced in response to oxidation of pulmonary epithelial glutathione. Concurrent induction of apolipoprotein J (apoJ) mRNA by PDTC demonstrates the selectivity of pulmonary gene regulation by the dithiocarbamate. In contrast, the glutathione precursor N-acetyl-l-cysteine (NAC) prevented PDTC-dependent increase in GSSG/GSH ratio, inhibition of SP-A and -B mRNAs, and induction of apoJ. Insufficiency of SP-A and -B, which occurs in inflammatory lung diseases, may result from the exposure of the pulmonary epithelium to oxidant stress and may be reversed by the antioxidant NAC.

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Section: Discussionmentioning

confidence: 99%

ANTAGONISTIC EFFECTS OF PYRROLIDINE DITHIOCARBAMATE AND N-ACETYL-L-CYSTEINE ON SURFACTANT PROTEIN A AND B mRNAs

Khalak

Huyck²,

Pryhuber³

1999

Experimental Lung Research

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“…Acute renal toxicity was also observed for amiodarone in rats after intraperitoneal injection . Another extremely common side effect of amiodarone therapy is pulmonary toxicity, for which evidence of involvement of reactive oxygen species was provided by Leeder et al . Other reported causes behind the toxicity of amiodarone are oxidative stress, lipid peroxidation, phospholipidosis, free radical generation, formation of N ‐desethyl and N ‐didesethyl metabolites, reductive deiodination, etc .…”

mentioning

confidence: 91%

Metabolite identification studies on amiodarone in in vitro (rat liver microsomes, rat and human liver S9 fractions) and in vivo (rat feces, urine, plasma) matrices by using liquid chromatography with high‐resolution mass spectrometry and multiple‐stage mass spectrometry: Characterization of the diquinone metabolite supposedly responsible for the drug's hepatotoxicity

Varkhede

Jhajra

Ahire

et al. 2013

Rapid Comm Mass Spectrometry

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“…7,8 Amiodarone pulmonary toxicity is a common and serious side effect of amiodarone, but the exact mechanism for this toxicity is unclear. 9 Some authors have postulated that direct cytotoxic lung injury or an indirect hypersensitivity reaction are the main mechanisms. 10 The risk for amiodarone pulmonary toxicity is associated with a high cumulative dose of amiodarone rather than plasma concentration or daily dose.…”

Section: Discussionmentioning

confidence: 99%

Amiodarone pulmonary toxicity: a report on two cases

Zedan

Mukarram

Burns³

et al. 2015

SW Resp Crit Care Chron

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Amiodarone is an iodine-containing antiarrhythmic drug commonly used for the treatment of ventricular and supraventricular arrhythmias. Amiodarone toxicity has several clinical presentations and affects multiple organs. One well-known serious side effect of amiodarone is pulmonary toxicity which can be acute, sub-acute, or chronic. Amiodarone pulmonary toxicity may present a diagnostic dilemma, particularly when clinical suspicion of pulmonary infection is high. Here we report two cases of amiodarone lung toxicity that were diagnosed in an early stage and improved after the discontinuation of amiodarone.

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Evaluation of reactive oxygen species involvement in amiodarone pulmonary toxicity in vivo and in vitro

Cited by 20 publications

References 33 publications

ANTAGONISTIC EFFECTS OF PYRROLIDINE DITHIOCARBAMATE AND N-ACETYL-L-CYSTEINE ON SURFACTANT PROTEIN A AND B mRNAs

ANTAGONISTIC EFFECTS OF PYRROLIDINE DITHIOCARBAMATE AND N-ACETYL-L-CYSTEINE ON SURFACTANT PROTEIN A AND B mRNAs

Amiodarone pulmonary toxicity: a report on two cases

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