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ROS-induced oxidative damage in lymphocytes ex vivo/in vitro from healthy individuals and MGUS patients: protection by myricetin bulk and nanoforms.
Archives of Toxicology ( IF 4.8 ) Pub Date : 2020-02-27 , DOI: 10.1007/s00204-020-02688-4
Shabana Akhtar 1 , Mojgan Najafzadeh 1 , Mohammad Isreb 2 , Lisa Newton 3 , Rajendran C Gopalan 2 , Diana Anderson 1
Affiliation  

We investigated the protective role of myricetin bulk and nanoforms, against reactive oxygen species (ROS)-induced oxidative stress caused by hydrogen peroxide and tertiary-butyl hydro peroxide in lymphocytes in vitro from healthy individuals and those from pre-cancerous patients suffering with monoclonal gammopathy of undetermined significance (MGUS). The change in intracellular reactive oxygen species was measured once cells were treated with myricetin bulk forms and nanoforms with and without either hydrogen peroxide or tertiary-butyl hydro peroxide co-supplementation. The direct and indirect antioxidant activity of myricetin was spectrofluometrically measured using the fluorescent dye 2',7'-dichlorofluorescin diacetate and using the Comet assay, respectively. Hydrogen peroxide (50 µM) and tertiary-butyl hydro peroxide (300 µM) induced a higher level of reactive oxygen species-related DNA damage and strand breaks. Addition of myricetin nanoform (20 µM) and bulk (10 µM) form could, however, significantly prevent hydrogen peroxide- and tertiary-butyl hydro peroxide-induced oxidative imbalances and the nanoform was more effective. Glutathione levels were also quantified using a non-fluorescent dye. Results suggest that myricetin treatment had no significant effect on the cellular antioxidant enzyme, glutathione. The current study also investigates the effect of myricetin on the induction of double-strand breaks by staining the gamma-H2AX foci immunocytochemically. It was observed that myricetin does not induce double-strand breaks at basal levels rather demonstrated a protective effect.

中文翻译:

ROS 诱导的健康个体和 MGUS 患者离体/体外淋巴细胞的氧化损伤:杨梅素本体和纳米形式的保护。

我们研究了杨梅素本体和纳米形式对活性氧 (ROS) 诱导的氧化应激的保护作用,这些氧化应激是由健康个体和患有单克隆丙种球蛋白病的癌前患者的体外淋巴细胞中的过氧化氢和叔丁基过氧化氢引起的意义未定(MGUS)。一旦细胞用杨梅素散装形式和纳米形式处理,有和没有过氧化氢或叔丁基过氧化氢共补充物,测量细胞内活性氧物质的变化。杨梅素的直接和间接抗氧化活性分别使用荧光染料 2',7'-二氯荧光素二乙酸盐和彗星测定法测量。过氧化氢 (50 µM) 和叔丁基过氧化氢 (300 µM) 可诱导更高水平的活性氧相关 DNA 损伤和链断裂。然而,添加杨梅素纳米形式 (20 µM) 和散装 (10 µM) 形式可以显着防止过氧化氢和叔丁基过氧化氢引起的氧化失衡,并且纳米形式更有效。谷胱甘肽水平也使用非荧光染料进行量化。结果表明杨梅素处理对细胞抗氧化酶谷胱甘肽没有显着影响。目前的研究还通过免疫细胞化学染色 gamma-H2AX 病灶来研究杨梅素对诱导双链断裂的影响。据观察,杨梅素不会在基础水平上诱导双链断裂,而是表现出保护作用。
更新日期:2020-02-27
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