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RAD51 m6A and PARylation modification orchestrate benzene-induced haematological toxicity.

Lin Chen1, Fengzhen Cui1, Han Li1

  • 1School of Public Health, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, Guangdong 523808, China.

Journal of Hazardous Materials
|December 31, 2025
PubMed
Summary

RAD51, a DNA repair protein, is upregulated by benzene metabolite hydroquinone, suppressing DNA damage. This suggests RAD51 could be a biomarker for benzene-induced blood toxicity in exposed individuals.

Keywords:
BenzeneHematotoxicityM6APARylationRAD51

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Area of Science:

  • Environmental Health
  • Molecular Biology
  • Toxicology

Background:

  • Occupational benzene exposure is a known cause of leukemia.
  • The role of RAD51 in DNA damage repair concerning benzene toxicity is not well understood.

Purpose of the Study:

  • To investigate the role of RAD51 in benzene-induced hematotoxicity.
  • To identify potential biomarkers for monitoring benzene exposure health risks.

Main Methods:

  • Exposure of human lymphoblast cells (TK6) to hydroquinone (HQ), a benzene metabolite.
  • Analysis of RAD51 expression and its regulation by METTL3 and YTHDC1.
  • Investigation of PARP1-mediated PARylation on RAD51.
  • Examination of protein expression in lymphocytes from occupationally benzene-exposed workers.

Main Results:

  • Hydroquinone exposure upregulates RAD51 expression in TK6 cells, suppressing DNA damage.
  • METTL3-mediated m6A modification and YTHDC1 binding enhance RAD51 expression.
  • PARP1-mediated PARylation further reduces HQ-induced DNA damage.
  • RAD51, PARP1, YTHDC1, and METTL3 were upregulated in benzene-exposed workers' lymphocytes.

Conclusions:

  • RAD51 plays a protective role against hydroquinone-induced DNA damage.
  • The METTL3-YTHDC1 pathway regulates RAD51 expression in response to benzene metabolite exposure.
  • RAD51 shows potential as a biomarker for assessing benzene-induced hematological toxicity in exposed populations.