Transcriptomic and proteomic features of a mouse model of sperm DNA damage induced by benzo(a)pyrene

Chenming Zhang1, Yunfeng Ma2, Wenbang Liu2

  • 1Henan University of Chinese Medicine, Zhengzhou, Henan 450046, China; The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, Henan 450003, China.

Insights

Benzo(a)pyrene (BaP) exposure significantly increases sperm DNA damage in mice. This damage impacts key cellular pathways, including those involved in cancer and metabolism.

Area of Science:

  • Reproductive toxicology
  • Environmental health
  • Molecular biology

Background:

  • Benzo(a)pyrene (BaP) is a known environmental toxicant.
  • Sperm DNA damage is a critical factor affecting male fertility and offspring health.
  • Understanding the molecular mechanisms of BaP-induced sperm DNA damage is crucial.

Purpose of the Study:

  • To replicate a mouse model of BaP-induced sperm DNA damage.
  • To investigate the transcriptomic and proteomic alterations in the testis following BaP exposure.
  • To identify molecular pathways affected by BaP-induced sperm DNA damage.

Main Methods:

  • Male mice were exposed to Benzo(a)pyrene (BaP) at 100 mg/kg/d for 60 days.
  • Sperm DNA fragmentation index (DFI) was assessed using sperm chromatin structure assay (SCSA).
  • RNA-sequencing (RNA-seq) and data-independent acquisition (DIA) mass spectrometry were employed for transcriptomic and proteomic analyses.

Main Results:

  • BaP exposure significantly increased the sperm DNA fragmentation index (DFI).
  • Differential expression of 240 genes (DEGs) and 616 proteins (DEPs) was observed in the BaP-exposed group compared to controls.
  • Enriched pathways included those related to cancer, PI3K-Akt signaling, metabolism, and MAPK signaling.

Conclusions:

  • Benzo(a)pyrene (BaP) demonstrably damages sperm DNA in a mouse model.
  • BaP exposure induces significant transcriptomic and proteomic changes in the testis.
  • Affected molecular pathways include cancer signaling, PI3K-Akt, metabolism, and MAPK signaling, highlighting potential mechanisms of toxicity.

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