镉对大鼠海马抗氧化系统及神经元死亡的影响

IF 1.6 4区 医学 Q4 NEUROSCIENCES Synapse Pub Date : 2022-06-16 DOI:10.1002/syn.22242
S. Treviño, Guadalupe Pulido, Estefania Fuentes, Anabella Handal-Silva, A. Moreno-Rodríguez, Berenice Venegas, Gonzalo Flores, J. Guevara, Alfonso Díaz
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引用次数: 4

摘要

镉(Cd)是一种重金属,被列为致癌物,其暴露可能影响中枢神经系统的功能。研究表明,镉改变了海马体的神经元形态,并影响了认知任务。氧化应激途径被认为是一种毒性机制。然而,这种机制还不精确。本研究旨在评估镉对雄性大鼠海马氧化应激标志物的影响。雄性Wistar大鼠被分为(1)对照(饮用水)和(2)用Cd(水中32.5ppm的氯化镉(CdCl2))处理。Cd给药时间分别为2、3和4个月。结果表明,口服CdCl2会增加血浆和海马中Cd的浓度,这种反应与给药时间有关。同样,它导致脂质过氧化和亚硝化应激标志物的增加。
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Effect of cadmium administration on the antioxidant system and neuronal death in the hippocampus of rats
Cadmium (Cd) is a heavy metal classified as a carcinogen whose exposure could affect the function of the central nervous system. Studies suggest that Cd modifies neuronal morphology in the hippocampus and affects cognitive tasks. The oxidative stress pathway is proposed as a mechanism of toxicity. However, this mechanism is not precise yet. This study aimed to evaluate the effect of Cd administration on oxidative stress markers in the male rat's hippocampus. Male Wistar rats were divided into (1) control (drinking water) and (2) treatment with Cd (32.5 ppm of cadmium chloride (CdCl2) in water). The Cd was administered for 2, 3, and 4 months. The results show that the oral administration of CdCl2 increased the concentration of Cd in plasma and hippocampus, and this response is time‐dependent on its administration. Likewise, it caused an increase in lipid peroxidation and nitrosative stress markers.
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来源期刊
Synapse
Synapse 医学-神经科学
CiteScore
3.80
自引率
0.00%
发文量
38
审稿时长
4-8 weeks
期刊介绍: SYNAPSE publishes articles concerned with all aspects of synaptic structure and function. This includes neurotransmitters, neuropeptides, neuromodulators, receptors, gap junctions, metabolism, plasticity, circuitry, mathematical modeling, ion channels, patch recording, single unit recording, development, behavior, pathology, toxicology, etc.
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