Ghosh Buddhadeb, Sharma Ravi Kant, Yadav Suman
Department of Anatomy, Government Medical College, Amritsar, Punjab, India.
Department of Anatomy, Dr Rajendra Prasad Government Medical College, Kangra, Himachal Pradesh, India.
J Pharm Bioallied Sci. 2021 Nov;13(Suppl 2):S1228-S1233. doi: 10.4103/jpbs.jpbs_377_21. Epub 2021 Nov 10.
Both aluminium and ethanol are pro-oxidants and neurotoxic. Moderately intake of alcohol may favor the body in coronary heart disease and diabetes mellitus etc. Being cheaper aluminium and increasing consumption of alcohol in India mixed with each other and may induce neurotoxicity. The present study was planned to identify the level of aluminium induced neurodegeneration in presence of ethanol coexposure in the cerebellum.
An experimental study was carried out at Dr. RP Government Medical College, Kangra, and Government Medical College, Amritsar, India after due approval from the Institute Animal Ethics Committee. Thirty-two Wistar rats were divided into one vehicle control and three experimental groups. Group I received the normal saline water as the vehicle control group. Group II received aluminium chloride 4.2 mg/kg body weight as the experimental group. Group III received ethanol 1 g/kg body weight as the experimental group. Group IV received both aluminium chloride 4.2 mg/kg body weight and ethanol 1 g/kg body weight as the experimental group. After 3 months of treatment, cerebellum was processed for histopathological observation under the microscope.
Experimental group treated with aluminium and ethanol separately showed reduction in the number of Purkinje cells, without a prominent nucleolus and well-defined nuclear membrane. Eosinophilic swelling adjacent to Purkinje cell bodies observed. The effects of combined administration of aluminium ethanol treated groups showed with acute neurodegeneration of Purkinje cell layer and granular layer. Pyknosis and neurofibrillary tangle seen in Purkinje cells.
It has been suggested that the ethanol-induced the effects of aluminium on the cerebellum and plays a significant role in neurotoxicity.
铝和乙醇都是促氧化剂且具有神经毒性。适度饮酒可能对身体在冠心病和糖尿病等方面有益。在印度,价格低廉的铝与酒精消费量的增加相互交织,可能会诱发神经毒性。本研究旨在确定在乙醇共同暴露的情况下,铝在小脑诱发的神经退行性变的程度。
在获得印度坎格拉的RP政府医学院和阿姆利则政府医学院的动物伦理委员会正式批准后,开展了一项实验研究。32只Wistar大鼠被分为一个溶剂对照组和三个实验组。第一组接受生理盐水作为溶剂对照组。第二组接受4.2毫克/千克体重的氯化铝作为实验组。第三组接受1克/千克体重的乙醇作为实验组。第四组接受4.2毫克/千克体重的氯化铝和1克/千克体重的乙醇作为实验组。治疗3个月后,对小脑进行处理,以便在显微镜下进行组织病理学观察。
单独用铝和乙醇处理的实验组显示浦肯野细胞数量减少,核仁不明显且核膜清晰。在浦肯野细胞体附近观察到嗜酸性肿胀。铝乙醇联合给药处理组的效果显示浦肯野细胞层和颗粒层出现急性神经退行性变。在浦肯野细胞中可见核固缩和神经原纤维缠结。
有人提出,乙醇会增强铝对小脑的影响,并在神经毒性中起重要作用。