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低分子量壳聚糖(∼20 kDa)通过恢复多巴胺和 KIF5B 水平来保护秀丽隐杆线虫免受丙烯酰胺诱导的氧化应激。

Low Molecular Weight Chitosan (∼20 kDa) protects acrylamide induced oxidative stress in D. melanogaster by restoring dopamine and KIF5B levels.

机构信息

Functional Biopolymer Lab, Department of Biochemistry, CSIR-Central Food Technological Research Institute, Mysuru, 570020, Karnataka State, India.

Functional Biopolymer Lab, Department of Biochemistry, CSIR-Central Food Technological Research Institute, Mysuru, 570020, Karnataka State, India.

出版信息

Carbohydr Polym. 2019 Oct 15;222:115005. doi: 10.1016/j.carbpol.2019.115005. Epub 2019 Jun 18.

Abstract

Acrylamide (AA) presence and formation are predominant in fried, baked and heat-processed foods. Using Drosophila model, we have investigated the dietary AA-arbitrate oxidative stress induced neurotoxicity and the effect of soluble Low Molecular Weight Chitosan (LMWC) supplementation. We assessed the neurodegenerative and behavioural effect of AA (0-10 mM) exposure in Drosophila (adult males). As a result, the exposed flies showed distinctive locomotor impairments and incident of mortality [51% in 5 mM AA (sub-toxic level) for 7 days] and higher mortality with increased concentration of acrylamide. Further, exposure of AA toxicity was also correlated with changing levels of oxidative markers, ETC complexes and cholinergic function of flies. Decreased dopamine (25 μg/mg) and kinesin motor protein levels were confirmed by HPLC and Immunoblotting studies, respectively. Interestingly, the co-exposure of LMWC alongside AA ameliorates respective biochemical changes with restoring dopamine (30 μg/mg, control groups 32 μg/mg) and kinesin motor protein (KIF5B) levels. These results indicated that supplementation of biocompatible LMWC may be promising candidate for complete protection against AA induced oxidative stress.

摘要

丙烯酰胺(AA)存在于油炸、烘焙和热加工食品中,且是主要形成物。我们使用果蝇模型,研究了饮食中 AA 引起的氧化应激诱导的神经毒性,以及可溶性低分子量壳聚糖(LMWC)补充的影响。我们评估了 AA(0-10mM)暴露在果蝇(成年雄性)中的神经退行性和行为效应。结果表明,暴露的果蝇表现出明显的运动障碍和死亡率(5mM AA 暴露 7 天的死亡率为 51%),并且随着丙烯酰胺浓度的增加死亡率更高。此外,AA 毒性的暴露也与果蝇的氧化标记物、ETC 复合物和胆碱能功能的变化水平相关。通过 HPLC 和免疫印迹研究分别证实了多巴胺(25μg/mg)和驱动蛋白运动蛋白水平的降低。有趣的是,LMWC 与 AA 共同暴露可改善相应的生化变化,恢复多巴胺(30μg/mg,对照组 32μg/mg)和驱动蛋白运动蛋白(KIF5B)水平。这些结果表明,生物相容性 LMWC 的补充可能是对抗 AA 诱导的氧化应激的有前途的候选物。

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