Abstract Title:

Melatonin prevents abnormal mitochondrial dynamics resulting from the neurotoxicity of cadmium by blocking calcium-dependent translocation of Drp1 to the mitochondria.

Abstract Source:

J Pineal Res. 2016 Jan 6. Epub 2016 Jan 6. PMID: 26732476

Abstract Author(s):

Shangcheng Xu, Huifeng Pi, Lei Zhang, Nixian Zhang, YuMing Li, Huiliang Zhang, Ju Tang, Huijuan Li, Min Feng, Pan Guo, Li Tian, Jia Xie, Mindi He, Yonghui Lu, Min Zhong, Yanwen Zhang, Wang Wang, Russel J Reiter, Zhengping Yu, Zhou Zhou

Article Affiliation:

Shangcheng Xu


Cadmium (Cd) is a persistent environmental toxin and occupational pollutant that is considered to be a potential risk factor in the development of neurodegenerative diseases. Abnormal mitochondrial dynamics are increasingly implicated in mitochondrial damage in various neurological pathologies. The aim of the present study was to investigate whether the disturbance of mitochondrial dysnamics contributed to Cd-induced neurotoxicity and whether melatonin has any neuroprotective properties. After cortical neurons were exposed to 10μM cadmium chloride (CdCl2 ) for various periods (0, 3, 6, 12, and 24 hr), the morphology of their mitochondria significantly changed from the normal tubular networks into punctuated structures within 3 hrs. Following this pronounced mitochondrial fragmentation, Cd treatment led to signs of mitochondrial dysfunction, including excess reactive oxygen species (ROS) production, decreased ATP content and mitochondrial membrane potential (△Ψm) loss. However, 1 mM melatonin pretreatment efficiently attenuated the Cd-induced mitochondrial fragmentation, which improved the turnover of mitochondrial function. In the brain tissues of rats that were intraperitoneally given 1 mg/kg CdCl2 for 7 days, melatonin also ameliorated excessive mitochondrial fragmentation and mitochondrial damage in vivo. Melatonin's protective effects were attributed to its roles in preventing cytosolic calcium ([Ca(2+)]i ) overload, which blocked the recruitment of Drp1 from the cytoplasm to the mitochondria. Taken together, our results are the first to demonstrate that abnormal mitochondrial dynamics is involved in cadmium-induced neurotoxicity. Melatonin has significant pharmacological potential in protectingagainst the neurotoxicity of Cd by blocking the disbalance of mitochondrial fusion and fission. This article is protected by copyright. All rights reserved.

Study Type : In Vitro Study

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