The purpose of this study was to investigate whether boric acid (BA) can reduce the acute lung injury caused by acrylamide (ACR) in rats. ACR was orally given to produce acute lung damage. Group 1 (saline), Group 2 (ACR, 38.27 mg/kg)), Group 3 (20 mg/kg BA), Group 4 (10 mg/kg BA+ACR), and Group 5 (20 mg/kg BA+ACR) were five equal groups of thirty rats.  Lungs were taken for histological analysis, immunohistochemical staining and biochemical evaluations after the experimental trial. Malondialdehyde (MDA) levels, a marker of lipid peroxidation and oxidative stress, increased after ACR administration. Nevertheless, it caused the reduction of glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) in lungs. The administration of BA efficiently inhibited the activities of CAT, GSH, SOD, and GPx in lung tissue and protected the lipid peroxidation caused by ACR. Moreover, increased expression of Bax, Caspase-3 and reduced Bcl-2 were found in the lung tissue of rats given ACR, which indicated enhanced congestion, inflammation, alveolar damage, and apoptosis. Interestingly, in rats given ACR injections, BA enhanced the expression of indicators of histological damage and lung injury. These results indicate the efficacy of BA treatment in preventing lipid peroxidation caused by ACR and reducing the negative effects on antioxidant capacity.