首页> 外文期刊>Toxicon: An International Journal Devoted to the Exchange of Knowledge on the Poisons Derived from Animals, Plants and Microorganisms >Basal expression of metallothionein suppresses butenolide-induced oxidative stress in liver homogenates in vitro.
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Basal expression of metallothionein suppresses butenolide-induced oxidative stress in liver homogenates in vitro.

机译:金属硫蛋白的基础表达可在体外抑制肝匀浆中丁烯内酯诱导的氧化应激。

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摘要

Butenolide (4-acetamido-4-hydroxy-2-butenoic acid gamma -lactone) is a Fusarium mycotoxin which is frequently detected in foodstuffs and feedstuffs for human and animal consumption. It can evoke a broad spectrum of toxicities, thus posing a potential health risk to both humans and animals. Previous study showed that this mycotoxin produced a significant oxidative stress, and several antioxidants abated this effect. Metallothionein (MT) has been proposed as a potent antioxidant, therefore, this study attempts to determine whether endogenous expression of MT protects against butenolide-induced hepatic oxidative stress by using an in vitro incubation system of liver homogenates prepared from MT-I/II null (MT-/-) mice, and the corresponding wild type (MT+/+) mice. The results showed that butenolide elicited significant oxidative stress in both MT-/- mice and MT+/+ mice; however, MT-/- mice were more sensitive than MT+/+ mice to butenolide-induced hepatic oxidative stress, as evidenced by more production of thiobarbituric acid reactive substances and nitric oxide, and by more severe reductions of glutathione, superoxide dismutase and glutathione peroxidase in the liver homogenates of MT-/- mice than those of MT+/+ mice. These findings implicated the antioxidant potency of basal expression of MT in suppression of the oxidative stress of butenolide.
机译:丁烯内酯(4-乙酰氨基-4-羟基-2-丁烯酸γ-内酯)是霉菌毒素,经常在人类和动物食用的食品和饲料中被检测到。它会引起广泛的毒性,从而对人类和动物都构成潜在的健康风险。先前的研究表明,这种霉菌毒素会产生明显的氧化应激,并且几种抗氧化剂可以减轻这种影响。金属硫蛋白(MT)已被提议作为有效的抗氧化剂,因此,本研究试图通过使用制备的肝匀浆的体外培养系统来确定MT的内源表达是否能抵抗丁烯内酯诱导的肝氧化应激。来自MT-I / II无效(MT-/-)小鼠和相应的野生型(MT + / +)小鼠。结果表明,丁烯内酯在MT-/-和MT + / +小鼠中均引起明显的氧化应激。但是,MT-/-小鼠比MT + / +小鼠对丁烯内酯诱导的肝氧化应激更敏感,这可以通过硫代巴比妥酸反应性物质和一氧化氮的更多产生以及更严重地降低谷胱甘肽,超氧化物歧化酶和谷胱甘肽过氧化物酶来证明。 MT-/-小鼠的肝匀浆中的平均分子量高于MT + / +小鼠。这些发现暗示MT的基础表达的抗氧化能力在抑制丁烯内酯的氧化应激中。

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