Amiodarone is an orally active antiarrhythmic drug generally used throughout the world, causing pulmonary toxicity as one of its most harmful side effects. The efficacy of two phenolic acids; ferulic acid FA or gallic acid GA or their combination on the lung injury in amiodarone-induced lung toxicity were clarified. Fifty albino rats were divided into five groups as follows; G1: Healthy control kept without treatment, G2: Amiodarone group, rats were administered by Amiodarone AD in a daily oral dose (30 mg/kg bw)by gastric gavage for 6 weeks to induce pulmonary toxicity.G3: AD+FA, after induction of pulmonary toxicity, rats received an oral daily dose of FA (100 mg/kg bw) for 6 consecutive weeks. G4: AD + GA, after induction of pulmonary toxicity, rats received an oral daily dose of GA (200 mg/kg.bw) for 6 consecutive weeks. G5: AD + FA+GA, rats have received Amiodarone and a mixture of GA (200 mg/kg bw) and FA (100 mg/kg.bw) for 6 consecutive weeks. Lung samples were assayed for oxidative stress and inflammatory biomarkers along with lung histology and DNA comet assay. The study found that AD causes pulmonary toxicity manifested by a significant alteration in serum level of Lung Na+-K+ adenosine triphosphatase, lung tissue content of antioxidant enzymes, and inflammatory biomarkers. Also, lung DNA damage was indicated as a significant change in comet assay parameters, in addition to histological alterations. Results showed that oral administration of FA, GA, or a combination of them reversed these biochemical indices, such as histopathological alterations and DNA damage induced by AD. These findings designated that FA and GA have defensive effects against AD-induced pulmonary toxicity due to its anti-inflammatory and antioxidant properties. GA or a combination of both FA and GA has the most potent effect on inflammatory biomarkersand oxidative stress.Therefore, supplementingGA and FA combination as an adjuvant remedypossibly be a promising compound in lowering AD side effects.