Fifty-hertz magnetic fields induce DNA damage through activating mPTP associated mitochondrial permeability transition in senescent human fetal lung fibroblasts

Abstract

Overview

With the rapid development and use of electromagnetic technology, artificial electromagnetic fields (EMFs) have emerged as significant environmental factors in daily life. Among these, extremely-low-frequency (ELF) magnetic fields (MFs)—commonly generated by power lines and electric equipment—are widespread and implicated in potential health risks. The International Agency for Research on Cancer (IARC) has classified ELF-MFs as possible human carcinogens based on limited evidence, but the biological mechanisms underlying these effects remain unclear.

Findings

• Senescent cells, characterized by cell cycle arrest, senescence-associated secretory phenotype (SASP), macromolecular damage accumulation, and metabolic disturbance, play essential roles in fetal development, tissue aging, and carcinogenesis.
• This study demonstrates that exposure to 50 Hz magnetic fields at 1.0 mT for 24 hours induces significant DNA damage in senescent—but not non-senescent—human fetal lung fibroblasts, suggesting increased sensitivity of senescent cells to magnetic field-induced genotoxicity.
• Further investigations reveal that reactive oxygen species (ROS) generation, mediated through mitochondrial permeability transition pore (mPTP) activation, is a critical factor in this DNA damage process.

Conclusion

The results indicate that cellular senescence increases sensitivity to DNA damage caused by 50 Hz magnetic fields, potentially implicating senescent cells in the carcinogenic effects of EMFs. Further research is needed to clarify whether this mechanism significantly contributes to EMF-mediated carcinogenesis.