Weitberg A B
Division of Hematology/Oncology, Roger Williams Cancer Center, Providence, Rhode Island.
Clin Genet. 1988 Nov;34(5):288-92. doi: 10.1111/j.1399-0004.1988.tb02880.x.
Stimulated human phagocytes produce toxic oxygen radicals which induce sister chromatid exchanges in cultured mammalian cells. Oxidative damage to membranes initiates lipid peroxidation chain reactions and stimulation of the arachidonic acid cascade. The products of these reactions may mediate the genetic toxicity of oxygen radicals. Arachidonic acid significantly augmented the number of sister chromatid exchanges in target cells exposed to stimulated phagocytes. This genetic damage was abrogated in radical-treated cells preincubated with inhibitors of the cyclooxygenase (indomethacin), lipoxygenase (nordihydroguaiaretic acid) or both (piroxicam) pathways.
受刺激的人类吞噬细胞会产生有毒的氧自由基，这些自由基会在培养的哺乳动物细胞中诱导姐妹染色单体交换。对细胞膜的氧化损伤引发脂质过氧化链式反应，并刺激花生四烯酸级联反应。这些反应的产物可能介导氧自由基的遗传毒性。花生四烯酸显著增加了暴露于受刺激吞噬细胞的靶细胞中姐妹染色单体交换的数量。在用环氧合酶（吲哚美辛）、脂氧合酶（去甲二氢愈创木酸）或两者（吡罗昔康）途径的抑制剂预孵育的经自由基处理的细胞中，这种遗传损伤被消除。
