Introduction. The widely used antiarrhythmic amiodarone (AD) has been linked to many health problems, including pulmonary toxicity.
The objective of the study. In the present study we assessed the protective effect of 21-aminosteroid U-74389 G due to its antioxidative and membrane-stabilizing potency on amiodarone-induced pneumotoxicity in rats.
Material and methods. The study was carried out on 72 male Wistar rats, divided into four groups: (1) – control; (2) – treated with AD intratracheally; (3) – treated with AD and U-74389G; (4) – treated with U-74389G alone. AD was instilled twice on days 0 and 2 (6.25 mg/kg with a concentration 3.125 mg/mL). U-74389G was injected intraperitoneally on days 0, 1 and 2 in a dose of 5 mg/kg. The activity of super-oxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GP), malondialdehyde (MDA) content and hydroxyproline content were performed on days 3, 7, 14 and 28 in lung homogenate. Hydroperoxide concentrations were measured in the plasma.
Results. AD administration affected antioxidant defense system in the lungs, promoted lipid peroxidation, and caused pulmonary fibrosis.
Conclusions. The 21-aminosteroid U-74389G significantly inhibited lipid peroxidation and mitigated fibrous changes in rat lungs provoked by AD.
Keywords: amiodarone, U-74389G, antioxidant system, lipid peroxidation.
AD – amiodarone
CAT – catalase
GP – glutathione peroxidase
ROOH – hydroperoxide
LH – lung homogenate
MDA – malondialdehyde
SOD – super-oxide dismutase
Department of Pharmacology and Toxicology, Medical University of Pleven, Bulgaria
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