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Oxidative damage repair by glutamine in fish enterocytes

机译:谷氨酰胺对鱼肠细胞的氧化损伤修复

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Fish intestine is very sensitive to oxidative damage. Repair of damaged enterocytes may be involved to restore normal function of fish intestine. However, studies of fish enterocyte repair are scarce. The present study aimed to investigate the potential repair role of glutamine after a H2O2 challenge. In this study, fish enterocytes were post-treated with graded levels of glutamine (0, 4, 8, 12 and 20 mM of glutamine) after expose to 100 mu M H2O2. The basal control cells were kept in the glutamine-free minimum essential medium only. Results showed that the H2O2-induced decreases in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide optical density, alkaline phosphatase and Na+, K+-ATPase activities were completely restored by subsequent glutamine treatments. In addition, cellular injury (lactate dehydrogenase), lipid peroxidation (malondialdehyde) and protein oxidation (protein carbonyls) caused by H2O2 were reversed by subsequent glutamine treatments. Furthermore, the H2O2-induced decreases in glutathione contents, glutathione reductase, superoxide dismutase and glutathione peroxidase activities were completely restored by subsequent glutamine treatments. In summary, the present study indicated that glutamine improved the repair activity in fish enterocytes after challenge with H2O2.
机译:鱼肠对氧化损伤非常敏感。受损肠细胞的修复可能涉及恢复鱼肠的正常功能。但是,关于鱼肠细胞修复的研究很少。本研究旨在调查过氧化氢攻击后谷氨酰胺的潜在修复作用。在这项研究中,鱼肠细胞在暴露于100μM H2O2之后,用分级水平的谷氨酰胺(0、4、8、12和20 mM谷氨酰胺)进行后处理。基础对照细胞仅保存在无谷氨酰胺的基本必需培养基中。结果表明,H2O2诱导的3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化铵的光密度,碱性磷酸酶和Na +,K + -ATPase活性通过随后的谷氨酰胺处理得以完全恢复。此外,H2O2引起的细胞损伤(乳酸脱氢酶),脂质过氧化(丙二醛)和蛋白质氧化(蛋白质羰基)可通过随后的谷氨酰胺处理来逆转。此外,H2O2诱导的谷胱甘肽含量,谷胱甘肽还原酶,超氧化物歧化酶和谷胱甘肽过氧化物酶活性的降低通过随后的谷氨酰胺处理得以完全恢复。总而言之,本研究表明,谷氨酰胺提高了H2O2攻击后鱼肠细胞的修复活性。

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