Therapeutic Chemistry Department, National Research Center, Al Bouhooth Street, Dokki, Giza, Egypt.
Biol Trace Elem Res. 2021 Jan;199(1):227-236. doi: 10.1007/s12011-020-02132-9. Epub 2020 Apr 11.
Aluminum chloride (AlCl) is commonly used in daily life; meanwhile, it is the potential etiology of various neurodegenerative as well as hepatorenal diseases. Therefore, the present study was carried out to investigate the correlation between AlCl-induced biochemical alterations and the toxicity induced in various organs such as the brain, liver, and kidney. Male mice received AlCl in an oral dose of 50 mg kg in addition to (50 mg) in drinking water for 2 weeks. Two weeks post-AlCl intoxication, the brain, liver, and kidney biochemical indices were assessed via molecular and western blot analysis. The results are as follows: AlCl intoxication induced a significant elevation in serum malondialdehyde in addition to a significant reduction in serum glutathione (GSH) and superoxide dismutase (SOD) levels. Brain β-secretase (tubulin-binding protein) and tau proteins which are responsible for the synthesis of β-amyloid protein that may interfere with neuronal communication in Alzheimer's disease (AD) were also upregulated; regarding hepatic function, AlCl elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities. Moreover, it upregulated hepatic mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK) protein expressions as well as renal kidney-inducible molecule-1 (KIM-1) which indicated the deleterious effect of AlCl on these organs. These results were confirmed by histopathological investigations. So, we hypothesize that acute AlCl administration is responsible for oxidative cell damage that interferes with brain function inducing β-amyloid accumulation, Alzheimer's disease, and neurodegenerative damage as well as hepatorenal injuries.
氯化铝（AlCl）在日常生活中被广泛应用；同时，它也是多种神经退行性疾病和肝肾功能疾病的潜在病因。因此，本研究旨在探究 AlCl 引起的生化改变与脑、肝、肾等器官毒性之间的相关性。雄性小鼠接受 50mg/kg 的 AlCl 灌胃剂量，同时给予 50mg 的 AlCl 于饮用水中，连续 2 周。AlCl 染毒 2 周后，通过分子和 Western blot 分析评估脑、肝、肾的生化指标。结果如下：AlCl 染毒可显著升高血清丙二醛（MDA），同时显著降低血清谷胱甘肽（GSH）和超氧化物歧化酶（SOD）水平。大脑中的β-分泌酶（微管结合蛋白）和 tau 蛋白也被上调，它们负责合成β-淀粉样蛋白，可能会干扰阿尔茨海默病（AD）中的神经元通讯；关于肝功能，AlCl 可升高血清丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）活性。此外，它还上调了肝丝裂原活化蛋白激酶（MAPK）和 c-Jun N-末端激酶（JNK）蛋白的表达，以及肾诱导的分子-1（KIM-1），这表明 AlCl 对这些器官有有害影响。这些结果通过组织病理学研究得到了证实。因此，我们假设急性 AlCl 给药会导致细胞氧化损伤，从而干扰大脑功能，导致β-淀粉样蛋白积累、阿尔茨海默病和神经退行性损伤以及肝肾功能损伤。
