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首页> 外文期刊>Journal of Cellular Physiology >Contribution of increased glutathione content to mechanisms of oxidative stress resistance in hydrogen peroxide resistant hamster fibroblasts.
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Contribution of increased glutathione content to mechanisms of oxidative stress resistance in hydrogen peroxide resistant hamster fibroblasts.

机译：谷胱甘肽含量增加的贡献抗氧化应激机制过氧化氢抗仓鼠成纤维细胞。

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摘要

An H2O2-resistant variant (OC14) of the HA1 Chinese hamster fibroblast cell line, which demonstrates cross resistance to 95% O2 and a 2-fold increase in total glutathione content, was utilized to investigate mechanisms responsible for cellular resistance to H2O2- and O2-toxicity. OC14 and HA1 cells were pretreated with buthionine sulfoximine (BSO) to deplete total cellular glutathione. Following BSO pretreatment, cells were either placed in 250 microM BSO to maintain the glutathione depleted condition and challenged with 95% O2, or challenged with hydrogen peroxide in the absence of BSO. Total glutathione and the activities of CuZn superoxide dismutase, Mn superoxide dismutase, catalase, glutathione peroxidase, and glutathione transferase were evaluated immediately following the BSO pretreatment as well as following 39 to 42 hr of exposure to 250 microM BSO. BSO treatment did not cause significant decreases in any cellular antioxidant tested, except total glutathione. Glutathione depletion resulted in significant (P < 0.05) sensitization to O2-toxicity and H2O2-toxicity in both cell lines at every time point tested. However, glutathione depletion did not completely abolish the resistance to either O2- or H2O2-toxicity demonstrated by OC14 cells, relative to HA1 cells. Also, glutathione depletion did not effect the ability of OC14 cells to metabolize extracellular H2O2. These data indicate that glutathione dependent processes significantly contribute to cellular resistance to acute H2O2- and O2-toxicity, but are not the only determinants of resistance in cell lines. The contribution of aldehydes formed by lipid peroxidation in mechanisms involved with the sensitization to O2-toxicity in glutathione depleted cells was tested by measuring the lipid peroxidation byproduct, 4-hydroxy-2-nonenal (4HNE), bound in Schiff-base linkages or in its free form in cell homogenates at 49 hr of 95% O2-exposure. No significant increase in 4HNE was detected in glutathione depleted cells relative to glutathione competent cells, indicating that glutathione depletion does not sensitize these cells to O2-toxicity by altering the intracellular accumulation of free or Schiff-base bound 4HNE.
机译：一个(OC14) HA1 H2O2-resistant变体中国仓鼠纤维母细胞细胞系展示了交叉95% O2和阻力总谷胱甘肽含量增加2倍,利用调查的责任机制细胞抗过氧化氢和O2-toxicity。OC14 HA1细胞被使用buthionine sulfoximine (BSO)耗尽细胞谷胱甘肽。细胞被放置在250 microM BSO维持谷胱甘肽耗竭条件和挑战有95% O2或挑战过氧化氢在缺乏BSO。谷胱甘肽和CuZn超氧化物的活动岐化酶、锰超氧化物歧化酶、过氧化氢酶谷胱甘肽过氧化物酶,谷胱甘肽转移酶进行评估之后BSO预处理以及后39250 microM BSO 42小时的接触。治疗没有造成显著的减少任何细胞抗氧化测试,除了总谷胱甘肽。显著(P < 0.05)敏化O2-toxicity和H2O2-toxicity细胞系在每一个时间点测试。消耗不完全废除O2 -或H2O2-toxicity阻力证明了OC14细胞,相对于HA1上细胞。OC14细胞代谢的能力细胞外过氧化氢。谷胱甘肽显著相关的流程导致细胞抗急性过氧化氢-和O2-toxicity,但并不是唯一的决定因素的抵抗细胞系。醛脂质形成的贡献过氧化反应的机制敏化O2-toxicity谷胱甘肽耗尽电池测试通过测量脂质过氧化反应副产品,4-hydroxy-2-nonenal在席夫碱(4 hne),联系或在它49岁自由形式在细胞匀浆95%的人力资源O2-exposure。在谷胱甘肽耗竭发现细胞相对谷胱甘肽有能力的细胞,这表明谷胱甘肽耗竭不进行宣传通过改变细胞O2-toxicity细胞内积累的免费或席夫碱绑定4 hne。

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