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Exposure to China dust exacerbates testicular toxicity induced by cyclophosphamide in mice

  • Woong-Il, Kim (College of Veterinary Medicine, Chonnam National University) ;
  • Je-Oh, Lim (College of Veterinary Medicine, Chonnam National University) ;
  • So-Won, Pak (College of Veterinary Medicine, Chonnam National University) ;
  • Se-Jin, Lee (College of Veterinary Medicine, Chonnam National University) ;
  • In-Sik, Shin (College of Veterinary Medicine, Chonnam National University) ;
  • Changjong, Moon (College of Veterinary Medicine, Chonnam National University) ;
  • Jeong-Doo, Heo (Bioenvironmental Science & Technology Division, Korea Institute of Toxicology) ;
  • Jong-Choon, Kim (College of Veterinary Medicine, Chonnam National University)
  • Received : 2022.04.14
  • Accepted : 2022.08.03
  • Published : 2023.01.15

Abstract

This study investigated the potential effects of China dust (CD) exposure on cyclophosphamide (CP)-induced testicular toxicity in mice, focusing on spermatogenesis and oxidative damage. CP treatment reduced testicular and epididymal weight and sperm motility and enhanced sperm abnormality. Histopathological examination presented various morphological alterations in the testis, including increased exfoliation of spermatogenic cells, degeneration of early spermatogenic cells, vacuolation of Sertoli cells, a decreased number of spermatogonia/spermatocytes/spermatids, along with a high number of apoptotic cells. In addition, the testis exhibited reduced glutathione (GSH) levels and glutathione reductase (GR) activity and enhanced malondialdehyde (MDA) concentration. Meanwhile, CD exposure exacerbated testicular histopathological alterations induced by CP. CD exposure also aggravated oxidative damage by increasing the lipid peroxidative product MDA and decreasing GSH levels and antioxidant enzyme activities in the testis. These results suggest that CD exposure exacerbates CP-induced testicular toxicity in mice, which might be attributed to the induction of lipid peroxidation and reduced antioxidant activity.

Keywords

Acknowledgement

The authors would like to thank the researchers at Korea Institute of Toxicology for their technical support.

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