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首页> 外文期刊>International journal of developmental neuroscience: the official journal of the International Society for Developmental Neuroscience >The neuroprotective role of melatonin in a gestational hypermethioninemia model
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The neuroprotective role of melatonin in a gestational hypermethioninemia model

机译：褪黑素在妊娠高血症血症模型中的神经保护作用

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Elevated levels of methionine in blood characterize the hypermethioninemia, which may have genetic or non-genetic origin, as for example from high protein diet. Born rats from hypermethioninemic mothers presented cerebral oxidative stress, inhibition of Na (+),K+ -ATPase, memory deficit and ultrastructure cerebral changes. Melatonin is a hormone involved in circadian rhythm and has antioxidant effects. The aim of this study was to verify the possible neuroprotective effects of melatonin administration in hypermethioninemic pregnant rats on damage to biomolecules (Na+, K+-ATPase, sulfhydryl content and DNA damage index) and behavior (open field, novel object recognition and water maze tasks), as well as its effect on cells morphology by electron microscopy in offspring. Wistar female rats received methionine (2.68 mu mol/g body weight) and/or melatonin (10 mg/kg body weight) by subcutaneous injections during entire pregnancy. Control rats received saline. Biochemical analyzes were performed at 21 and 30 days of life of offspring and behavioral analyzes were performed only at 30 days of age in male pups. Results showed that gestational hypermethioninemia diminished Na+, K+-tATPase activity and sulfhydryl content and increased DNA damage at 21 and 30 days of life. Melatonin was able to totally prevent Na+, K+-ATPase activity alteration at 21 days and partially prevent its alteration at 30 days of rats life. Melatonin was unable in to prevent sulfhydryl and DNA damage at two ages. It also improved DNA damage, but not at level of saline animals (controls). Regarding to behavioral tests, data showed that pups exposed to gestational hypermethioninemia decreased reference memory in water maze, spent more time to the center of the open field and did not differentiate the objects in the recognition test. Melatonin was able to prevent the deficit in novel object recognition task. Electron microscopy revealed ultrastructure alterations in neurons of hypermethioninemic at both ages of offspring, whose were prevented by melatonin. These findings suggest that melatonin may be a good neuroprotective to minimize the harmful effects of gestational hypermethioninemia on offspring.
机译：血液中甲硫氨酸水平升高，表征了高血硫血症，其可具有遗传或非遗传来源，例如高蛋白质饮食。来自高血管素患者的出生的大鼠呈现脑氧化应激，抑制Na（+），K + -ATP酶，记忆缺损和超微结构脑变化。褪黑激素是涉及昼夜节律的激素，具有抗氧化作用。本研究的目的是验证褪黑素给药在高精度血症孕妇对生物分子（Na +，K + -AtPase，巯基含量和DNA损伤指数）和行为（开放场，新的对象识别和水迷宫任务的损伤中的可能神经保护作用），以及其在后代电子显微镜通过电子显微镜对细胞形态的影响。 Wistar雌性大鼠通过皮下注射在整个妊娠期间接受甲硫氨酸（2.68μmmol/ g体重）和/或褪黑激素（10mg / kg体重）。对照大鼠接受盐水。生物化学分析在后代的21和30天的后代寿命中进行，行为分析仅在雄性幼崽30天时进行。结果表明，妊娠期高甲型肝癌血症降低Na +，K + -Tatpase活性和巯基含量，并在生命的21和30天内增加DNA损伤。褪黑素能够在21天内完全防止Na +，K + -AtPase活性改变，并部分防止其在大鼠寿命的30天内改变。褪黑激素无法防止巯基和DNA损伤两年龄段。它还改善了DNA损伤，但不是盐水动物（对照）的水平。关于行为测试，数据显示暴露于妊娠期高血症患者的幼崽在水迷宫中降低了参考记忆，花费更多时间到开放场的中心，并且没有区分识别测试中的物体。褪黑激素能够防止新的对象识别任务中的缺陷。电子显微镜揭示了在后代两年龄段的高精度血症神经元的超微结构改变，褪黑素预防其。这些发现表明褪黑激素可能是一种良好的神经保护，以最大限度地减少妊娠期高血症患者对后代的有害影响。

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