Copper overload induces lifespan shortening through activating mitochondrial respiration in Caenorhabditis elegans.

Jia Zhang, Chang Liu, Yuxin Liao, Wanqiao He, Yantao Zheng, Hao Shi, Qiong Liu, Jiajie Lin, Chong Gao, Xuanbin Wang, Lei Gao

School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China.School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China. · pubmed

Paper

Abstract

Despite being a common environmental heavy metal, copper is an essential trace element for organisms, playing a vital role in the assembly and function of the mitochondrial respiratory chain. However, excessive copper exposure induces significant biological toxicity. Copper overload can lead to mitochondrial dysfunction, growth inhibition, and cytotoxicity, but its impact on lifespan and the underlying mechanism remains largely unexplored. Caenorhabditis elegans, characterized by a short life cycle, transparency, and high genetic homology (60-80 %) with humans, serves as an ideal model for researching the homeostasis and toxicity of metal ions. In this study, we utilized CuCl

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Research summary

Copper overload shortens lifespan in Caenorhabditis elegans by activating mitochondrial respiration. The study investigates the effects of copper toxicity on lifespan, which is directly related to aging mechanisms and could provide insights into the biological processes that influence longevity.

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