Bleomycin, a widely used antineoplastic agent, has been associated with severe pulmonary toxicity, primarily fibrosis. Previous work has shown a reduction in bleomycin-induced lung pathology by long-chain omega-3 fatty acids. Treatment by short-chain omega-3 fatty acids, α-linolenic acid, found in dietary flaxseed oil may also reduce lung fibrosis, as previously evidenced in the kidney. To test this hypothesis, 72 rats were divided between diets receiving either 15% (w/w) flaxseed oil or 15% (w/w) corn oil (control). These groups were further divided to receive either bleomycin or vehicle (saline) via an oropharyngeal delivery, rather than the traditional intratracheal instillation. Lungs were harvested at 2, 7, and 21 days after bleomycin or saline treatment. Animals receiving flaxseed oil showed a delay in edema formation ( ) and a decrease in inflammatory cell infiltrate and vasculitis ( and 0.007, resp.). At days 7 and 21, bleomycin produced a reduction in pulmonary arterial lumen patency ( ), but not in rats that were treated with flaxseed oil. Bleomycin-treated rats receiving flaxseed oil had reduced pulmonary septal thickness ( ), signifying decreased fibrosis. Dietary flaxseed oil may prove beneficial against the side effects of this highly effective chemotherapeutic agent and its known toxic effects on the lung. 1. Introduction Bleomycin is a group of glycopeptides that binds iron and oxygen in vivo to produce an active drug, effective in cancer treatment. In the last few decades, many Americans were diagnosed with Hodgkin’s lymphoma and testicular cancer, and a majority received bleomycin as part of their chemotherapeutic regimen. A large study from 1986 to 2003 found that out of 141 Hodgkin’s lymphoma patients treated with bleomycin, 18% developed pulmonary toxicity, and of those patients 24% died [1]. Currently, no known treatments exist to prevent pulmonary toxicity in these patients. In short, bleomycin’s fibrotic side effects are so common that it is widely used to create animal models of pulmonary fibrosis. Bleomycin’s active intermediate is believed to induce both single-and double-strand DNA cleavage in neoplastic cells [2]. The chemotherapeutic mechanism results from the chelation of iron ions with oxygen, which leads to production of DNA-cleaving superoxide, and also hydroxide free radicals [3–5]. It is the increased production of reactive oxygen species (ROS) that may be critical in producing proinflammatory eicosanoids that lead to bleomycin’s pulmonary toxicity, and may eventually lead to lung fibrosis [6–9]. In recent literature,
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