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Anti-oxidative hormetic effects of cellular autophagy induced by nutrient deprivation in a molluscan animal model.
Marine Environmental Research ( IF 3.0 ) Pub Date : 2020-02-04 , DOI: 10.1016/j.marenvres.2020.104903 M N Moore 1 , J P Shaw 2 , C Pascoe 2 , A Beesley 2 , A Viarengo 3 , D M Lowe 2
Marine Environmental Research ( IF 3.0 ) Pub Date : 2020-02-04 , DOI: 10.1016/j.marenvres.2020.104903 M N Moore 1 , J P Shaw 2 , C Pascoe 2 , A Beesley 2 , A Viarengo 3 , D M Lowe 2
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This investigation using a molluscan animal model tested the hypothesis that experimentally induced lysosomal autophagy protects against oxidative cell injury. Induction of augmented lysosomal autophagy has previously been implicated in this protective process. Four treatment groups of blue mussels (Mytilus galloprovincialis) were used: Group 1 (fed - control), Group 2 (fasted), Group 3 (copper + fed) and Group 4 (copper + fasted). Groups 2 and 4 were fasted in order to trigger autophagy; and samples of hepatopancreas (liver analogue or digestive gland) from all 4 groups were taken at 3, 6 and 15 days. Treatment with copper provided a positive reference for oxidative stress: Groups 3 and 4 were treated with copper (10 μg Cu2+/animal/day) for three days only. Oxidative damage and cellular injury in hepatopancreatic digestive cells was found to decrease in Group 2 (fasted) compared to Group 1 (fed - control). Group 3 (fed + copper) showed clear evidence of oxidative stress and cell injury, as well as induction of antioxidant activities. Group 4 (copper + fasted) had a reduced uptake of copper and toxicity of copper was also reduced, compared with Group 3. It was concluded that augmented autophagy had a hormetic cytoprotective anti-oxidant effect.
中文翻译：
在软体动物模型中营养剥夺引起的细胞自噬的抗氧化药性作用。
使用软体动物模型进行的这项研究检验了以下假设：实验诱导的溶酶体自噬可防止氧化性细胞损伤。先前已经暗示了溶酶体自噬增强的诱导与该保护过程有关。蓝贻贝（Mytilus galloprovincialis）的四个治疗组被使用：第1组（喂食-对照），第2组（禁食），第3组（铜+喂食）和第4组（铜+禁食）。第2和第4组禁食以触发自噬。在第3、6和15天时从所有4组中采集肝胰腺（肝类似物或消化腺）样品。铜处理为氧化应激提供了积极的参考：第3组和第4组仅用铜（10μgCu2 + /动物/天）处理三天。与第1组（喂食-对照）相比，第2组（禁食）的肝胰腺消化细胞的氧化损伤和细胞损伤减少。第3组（进食+铜）显示出氧化应激和细胞损伤以及抗氧化活性的明显证据。与第3组相比，第4组（铜+空腹）的铜吸收减少，并且铜的毒性也降低了。结论是，增强的自噬具有抑制细胞的抗氧化作用。
更新日期：2020-02-04
中文翻译：
在软体动物模型中营养剥夺引起的细胞自噬的抗氧化药性作用。
使用软体动物模型进行的这项研究检验了以下假设：实验诱导的溶酶体自噬可防止氧化性细胞损伤。先前已经暗示了溶酶体自噬增强的诱导与该保护过程有关。蓝贻贝（Mytilus galloprovincialis）的四个治疗组被使用：第1组（喂食-对照），第2组（禁食），第3组（铜+喂食）和第4组（铜+禁食）。第2和第4组禁食以触发自噬。在第3、6和15天时从所有4组中采集肝胰腺（肝类似物或消化腺）样品。铜处理为氧化应激提供了积极的参考：第3组和第4组仅用铜（10μgCu2 + /动物/天）处理三天。与第1组（喂食-对照）相比，第2组（禁食）的肝胰腺消化细胞的氧化损伤和细胞损伤减少。第3组（进食+铜）显示出氧化应激和细胞损伤以及抗氧化活性的明显证据。与第3组相比，第4组（铜+空腹）的铜吸收减少，并且铜的毒性也降低了。结论是，增强的自噬具有抑制细胞的抗氧化作用。
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