State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing 210093, People's Republic of China.
Environ Toxicol. 2011 Jun;26(3):217-23. doi: 10.1002/tox.20546.
The aim of this article is to elucidate the mechanism by which eicosapentaenoic acid (EPA) acts against cyclophosphamide (CP)-induced effects. The prevalence of micronuclei, the extent of lipid peroxidation, and the status of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) in both liver and serum of mice were used as intermediate biomarkers of chemoprotection. Lipid peroxidation and associated compromised antioxidant defenses (CAT and GPX) in CP treated mice were observed in the liver, serum, and were accompanied by increased prevalence of micronuclei in bone marrow. The number of MN was significantly different (p < 0.01) between the groups treated with CP (group III, IV, V, VI) and the solvent control (group II) (3.2 ± 0.7‰). There was a dose-dependent reduction in formation CP induced micronuclei by treatment with 100, 200, or 300 mg EPA/kg BW mice. Activities of SOD, CAT, and extent of lipid peroxidation were statistically different in liver cells of mice exposed to EPA only with CP compared with the CP group (group III). The present findings imply that EPA may be a potential antigenotoxic, antioxidant and chemopreventive agent and could be used as an adjuvant in chemotherapeutic applications.
本文旨在阐明二十碳五烯酸（EPA）对抗环磷酰胺（CP）诱导作用的机制。微核的发生率、脂质过氧化的程度以及抗氧化酶超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPX）在小鼠肝脏和血清中的状态，被用作化学保护的中间生物标志物。在 CP 处理的小鼠肝脏、血清中观察到脂质过氧化和相关的抗氧化防御受损（CAT 和 GPX），并伴有骨髓中微核发生率增加。用 CP（第 III、IV、V、VI 组）和溶剂对照（第 II 组）处理的小鼠的 MN 数有显著差异（p < 0.01）（3.2 ± 0.7‰）。用 100、200 或 300mg EPA/kg BW 处理的小鼠可使 CP 诱导的微核形成呈剂量依赖性减少。与 CP 组（第 III 组）相比，仅用 CP 暴露的小鼠肝细胞中的 SOD、CAT 活性和脂质过氧化程度有统计学差异。本研究结果表明，EPA 可能是一种潜在的抗诱变、抗氧化和化学预防剂，并可作为化疗应用中的辅助剂。
