Effect of adenosine triphosphate on amiodarone-induced oxidative and inflammatory lung injury in rats

Aim: To investigate the biochemical and histopathological effects of adenosine triphosphate (ATP) on amiodarone-induced oxidative and inflammatory lung damage in rats. Materials and Methods: Experimental animals were divided into four groups: healthy (HG), amiodarone alone (AMD), amiodarone + 2 mg/kg ATP (AATP-2), and amiodarone + 4 mg/kg ATP (AATP-4). Amiodarone was administered orally at a dose of 50 mg/kg, and ATP was administered intraperitoneally at doses of 2 and 4 mg/kg for 14 days. At the end of the experiment, all animals were sacrificed, and lung tissues were collected for biochemical and histopathological examination. Results: Biochemical findings showed that amiodarone increased the levels of oxidative parameters such as malondialdehyde (MDA; p<0.001) and interleukin-6 (IL-6; p<0.001), while reducing antioxidant levels, including total glutathione (tGSH; p<0.001), superoxide dismutase (SOD; p<0.001), and catalase (CAT; p<0.001). ATP administration at 2 mg/kg resulted in less pronounced changes in these parameters, and ATP at 4 mg/kg restored these values to levels similar to the healthy group. Histopathological examination of lung tissues revealed peribronchial dense lymphocyte infiltration, increased connective tissue in the interalveolar septa, and vascular congestion in the AMD group. These findings were mitigated by ATP administration. In the AATP-2 group, lymphocyte infiltration in the peribronchial area, connective tissue density in the interalveolar septa, and vascular congestion were reduced. The histological appearance of lung tissues in the AATP-4 group was similar to that of the healthy group. Conclusion: Biochemical and histopathological data demonstrated that amiodarone disrupts the oxidant/antioxidant balance in lung tissue, shifting it toward oxidants and causing damage. These results suggest that ATP may be beneficial in preventing amiodarone-induced oxidative and inflammatory lung damage.