Editor's Choice for March 2020

The March 2020 Editor’s Choice article is “Effects of micronucleus frequencies and mitochondrial DNA copy numbers among benzene-exposed workers in China” (https://onlinelibrary.wiley.com/doi/pdf/10.1002/em.22354) by Anqi Li, Yuan Sun, Tongshuai Wang, Kan Wang, Tuanwei Wang, Wuzhong Liu, Keyong Li, William W. Au, Zubing Wang, and Zhao-lin Xia.

 

Also known as the “powerhouse” of the cell, mitochondria carry their own genetic information (mitochondrial DNA, MtDNA) that encode for key polypeptides required for the generation of ATP via oxidative phosphorylation. Each cell can contain up to several hundred mitochondria and each mitochondrion has anywhere from 2 – 10 mtDNA molecules. Over the years, MtDNA copy number (MtDNAcn) has gradually become an indication for mitochondrial dysfunction and serves as a potential biomarker for various diseases.  

In this article, Dr. Xia and coworkers have analyzed peripheral blood samples from 174 benzene-exposed and 58 non-exposed workers in China in order to provide a better understanding of how benzene toxicity impacts mitochondrial function and formation of micronuclei (MN). Benzene, a hematotoxicant and a known carcinogen, produces genotoxic damage via the generation of reactive oxygen species resulting in changes to MtDNAcn. As displayed by the authors, MtDNAcn increased and then decreased in response to increasing benzene exposure. A plausible explanation for this unique observation is that higher doses of benzene can result in mitochondrial catastrophe triggering apoptosis and cellular senescence, while at lower doses, cells are able to cope with the damage from an increase in MtDNAcn. On the other hand, appearance of micronuclei displayed a consistent dose-dependent increase in the exposure group and over the control samples.  

Overall, this work presented by Dr. Xia’s team adds to the growing body of evidence that MtDNAcn may be used as a biomarker to signal health hazards from exposure to toxicants such as benzene. In addition, induction of genotoxicities may follow very different dose-dependent responses which are dependent upon the different mechanisms of induction.

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