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首页> 外文期刊>Neuroscience Research: The Official Journal of the Japan Neuroscience Society >Effect of melatonin on PCB (Aroclor 1254) induced neuronal damage and changes in Cu/Zn superoxide dismutase and glutathione peroxidase-4 mRNA expression in cerebral cortex, cerebellum and hippocampus of adult rats.
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Effect of melatonin on PCB (Aroclor 1254) induced neuronal damage and changes in Cu/Zn superoxide dismutase and glutathione peroxidase-4 mRNA expression in cerebral cortex, cerebellum and hippocampus of adult rats.

机译：褪黑素对多氯联苯（Aroclor 1254）诱导的神经元损伤以及成年大鼠大脑皮层，小脑和海马中铜锌超氧化物歧化酶和谷胱甘肽过氧化物酶-4 mRNA表达的影响。

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Polychlorinated biphenyls (PCBs) are one of the environmental toxicants and neurotoxic compounds which induce the production of free radicals leading to oxidative stress. Free radicals represent a class of biologically generated species that pose a potential threat to neuronal survival. Cu/Zn superoxide dismutase (SOD) and glutathione peroxidase-4 (GPx-4) are the key cellular antioxidant enzymes by which neurons and other cells detoxify free radicals and protect themselves from damage. Melatonin, an indoleamine plays an important role in neurodegenerative diseases as an antioxidant and neuroprotector. The aim was to carry out to investigate the effect of melatonin on PCB (Aroclor 1254) induced changes in histomorphology and Cu/Zn SOD, GPx-4 mRNA expression in selected brain regions of adult rats. Group I: rats intraperitoneally (i.p.) administered with corn oil (vehicle) for 30 days. Group II: rats injected (i.p.) with Aroclor 1254 (PCB) at 2mg/kgbw/day for 30 days. Groups III and IV: rats (i.p.) received melatonin (5 or 10mg/kgbw/day) simultaneously with PCB for 30 days. Groups V and VI: rats (i.p.) received melatonin (5 or 10mg/kgbw/day) alone for 30 days. After 30 days, rats were sacrificed and the brain regions were dissected to cerebral cortex, cerebellum and hippocampus. Activities of enzymatic antioxidants such as total SOD, Cu/Zn SOD, Mn SOD, glutathione peroxidase (GPx) were estimated. mRNA expressions of Cu/Zn SOD and GPx-4 were quantified by reverse transcriptase polymerase chain reaction (RT-PCR) method. Histological study was also observed. Specific activities of all antioxidant enzymes and mRNA expression of Cu/Zn SOD and GPx-4 were decreased in brain regions of PCB exposed animals. Neuronal damages were observed in all the brain regions. Exogenous melatonin supplementation retrieved all the parameters. These results suggest that melatonin protects PCB-induced oxidative stress and prevents neuronal damage in brain regions.
机译：多氯联苯（PCBs）是环境毒物和神经毒性化合物之一，会诱导自由基的产生，从而导致氧化应激。自由基代表一类生物产生的物种，对神经元的生存构成潜在威胁。铜/锌超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶4（GPx-4）是关键的细胞抗氧化酶，神经元和其他细胞可通过该酶使自由基解毒并保护自己免受损害。褪黑素（一种吲哚胺）作为抗氧化剂和神经保护剂，在神经退行性疾病中起着重要的作用。目的是研究褪黑激素对PCB（Aroclor 1254）诱导的成年大鼠选定脑区域组织形态学变化以及Cu / Zn SOD，GPx-4 mRNA表达的影响。第一组：给大鼠腹膜内（i.p.）施用玉米油（车辆）30天。第二组：以2mg / kgbw /天向大鼠腹膜内注射Aroclor 1254（PCB）30天。 III和IV组：大鼠（i.p.）接受褪黑激素（5或10mg / kgbw /天），同时接受PCB治疗30天。第五和第六组：大鼠（腹膜内）单独接受褪黑激素（5或10mg / kgbw /天）持续30天。 30天后，处死大鼠，将大脑区域解剖至大脑皮层，小脑和海马。估算了酶促抗氧化剂的活性，例如总SOD，Cu / Zn SOD，Mn SOD，谷胱甘肽过氧化物酶（GPx）。采用逆转录聚合酶链反应（RT-PCR）方法定量检测Cu / Zn SOD和GPx-4的mRNA表达。还观察了组织学研究。在PCB暴露的动物的大脑区域中，所有抗氧化酶的比活性和Cu / Zn SOD和GPx-4的mRNA表达均降低。在所有脑区域均观察到神经元损伤。外源褪黑激素补充可检索所有参数。这些结果表明褪黑素可以保护PCB诱导的氧化应激并防止大脑区域的神经元损伤。

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