Olusegun L Adebayo, Vivian A Agu, Grace A Idowu, Blessing C Ezejiaku, Adeleke K Atunnise
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引用次数: 0
Abstract
Monosodium glutamate (MSG) is a silent excitotoxin used as a flavour enhancer but exerts serious health hazards to consumers. MSG plays a role in neuronal function as the dominant excitatory neurotransmitter. It is transferred into the blood and ultimately increases brain glutamate levels, causing functional disruptions notably via oxidative stress. The study evaluated the toxic effect of high consumption of MSG and the modulatory role of vitamin C on ATPase activities in the striatum and cerebellum of male Wistar rats for five weeks. Rats were grouped into four (A-D): group A was fed with rat's show only; Group B was fed with diet containing 15% MSG; Group C was treated with vitamin C (200 mg/kg b.wgt orally in 0.9% saline solution) only for 3 weeks; and group D rats were fed with MSG and vitamin C. The findings show that MSG does not affect body and cerebellum weights but increases striatal weight. MSG increases the malondialdehyde (MDA) level and significantly decreases catalase (CAT) and superoxide dismutase (SOD) activities and glutathione (GSH) levels. MSG significantly impaired striatal and cerebellar ATPases activities (Na+/K+-, Ca2+-, Mg2+- and total ATPases). Vitamin C treatment abolishes MSG-induced oxidative stress and improves ATPase activities. The findings show that vitamin C has beneficial effects in improving the functions of membrane-bound ATPases against MSG toxicity in rat's striatum and cerebellum.
谷氨酸一钠(味精)是一种无声的兴奋性毒素,被用作增味剂,但却对消费者的健康造成严重危害。味精作为主要的兴奋性神经递质在神经元功能中发挥作用。味精进入血液后,最终会增加大脑谷氨酸含量,主要通过氧化应激造成功能紊乱。这项研究评估了大量摄入味精的毒性效应以及维生素 C 对雄性 Wistar 大鼠纹状体和小脑中 ATP 酶活性的调节作用。研究将大鼠分为四组(A-D):A 组仅喂食大鼠表演;B 组喂食含 15% 味精的食物;C 组仅口服维生素 C(200 毫克/千克体重,溶于 0.9% 生理盐水中)3 周;D 组大鼠喂食味精和维生素 C。味精会增加丙二醛(MDA)水平,并显著降低过氧化氢酶(CAT)和超氧化物歧化酶(SOD)活性以及谷胱甘肽(GSH)水平。味精会明显损害纹状体和小脑 ATP 酶(Na+/K+-、Ca2+-、Mg2+- 和总 ATP 酶)的活性。维生素 C 可消除味精诱导的氧化应激并改善 ATP 酶的活性。研究结果表明,维生素 C 有助于改善大鼠纹状体和小脑中膜结合 ATP 酶的功能,从而抵御味精的毒性。
期刊介绍:
Neurotoxicity Research is an international, interdisciplinary broad-based journal for reporting both basic and clinical research on classical neurotoxicity effects and mechanisms associated with neurodegeneration, necrosis, neuronal apoptosis, nerve regeneration, neurotrophin mechanisms, and topics related to these themes.
Published papers have focused on:
NEURODEGENERATION and INJURY
Neuropathologies
Neuronal apoptosis
Neuronal necrosis
Neural death processes (anatomical, histochemical, neurochemical)
Neurodegenerative Disorders
Neural Effects of Substances of Abuse
NERVE REGENERATION and RESPONSES TO INJURY
Neural Adaptations
Neurotrophin mechanisms and actions
NEURO(CYTO)TOXICITY PROCESSES and NEUROPROTECTION
Excitatory amino acids
Neurotoxins, endogenous and synthetic
Reactive oxygen (nitrogen) species
Neuroprotection by endogenous and exogenous agents
Papers on related themes are welcome.