Mazzocco John C, Jagadapillai Rekha, Gozal Evelyne, Kong Maiying, Xu Qian, Barnes Gregory N, Freedman Jonathan H
Department of Pediatrics, University of Louisville School of Medicine, USA.
Department of Pharmacology and Toxicology, University of Louisville School of Medicine, USA.
Toxicol Rep. 2020 Aug 23;7:1164-1169. doi: 10.1016/j.toxrep.2020.08.005. eCollection 2020.
Analyses of human cohort data support the roles of cadmium and obesity in the development of several neurocognitive disorders. To explore the effects of cadmium exposure in the brain, mice were subjected to whole life oral cadmium exposure. There were significant increases in cadmium levels with female animals accumulating more metal than males (p < 0.001). Both genders fed a high fat diet showed significant increases in cadmium levels compared to low fat diet fed mice (p < 0.001). Cadmium and high fat diet significantly affected the levels of several essential metals, including magnesium, potassium, chromium, iron, cobalt, copper, zinc and selenium. Additionally, these treatments resulted in increased superoxide levels within the cortex, amygdala and hippocampus. These findings support a model where cadmium and high fat diet affect the levels of redox-active, essential metal homeostasis. This phenomenon may contribute to the underlying mechanism(s) responsible for the development of neurocognitive disorders.
对人类队列数据的分析支持镉和肥胖在几种神经认知障碍发展中的作用。为了探究镉暴露对大脑的影响,对小鼠进行了终生口服镉暴露实验。镉水平显著升高,雌性动物比雄性积累更多的金属(p < 0.001)。与喂食低脂饮食的小鼠相比,两种性别喂食高脂饮食的小鼠镉水平均显著升高(p < 0.001)。镉和高脂饮食显著影响了几种必需金属的水平,包括镁、钾、铬、铁、钴、铜、锌和硒。此外,这些处理导致皮质、杏仁核和海马体内超氧化物水平升高。这些发现支持了一个模型,即镉和高脂饮食会影响氧化还原活性必需金属稳态的水平。这种现象可能有助于解释神经认知障碍发展的潜在机制。