Acrolein exerts a genotoxic effect in the Leydig cells by stimulating DNA damage-induced apoptosis

Yildizbayrak N., Orta-Yilmaz B. , Aydın Y. , Erkan M.

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH, 2020 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume:
  • Publication Date: 2020
  • Doi Number: 10.1007/s11356-020-08124-5
  • Journal Indexes: Science Citation Index Expanded, Scopus, IBZ Online, ABI/INFORM, Aerospace Database, Agricultural & Environmental Science Database, Aqualine, Aquatic Science & Fisheries Abstracts (ASFA), BIOSIS, CAB Abstracts, EMBASE, Environment Index, Geobase, MEDLINE, Pollution Abstracts, Veterinary Science Database, Civil Engineering Abstracts
  • Keywords: Acrolein, Leydig cell, Steroidogenesis, Apoptosis, DNA damage, Testosterone, EXPRESSION


Acrolein is a highly reactive unsaturated organic molecule and has harmful effects on human health. Acrolein is generally formed in heat-treated foods above 150 degrees C, as well as in the combustion of gasoline, wood industry, plastic waste, and tobacco smoke. In this study, the effects of acrolein on genotoxicity in Leydig cells and the underlying mechanisms are aimed to be clarified. In addition, the toxicogenomic profile of acrolein was studied in terms of both apoptosis and steroidogenesis. Real-time PCR and ELISA tests were used to analyses of steroidogenic endpoints. Apoptosis was evaluated with double fluorescence staining and gene expression analyses of related genes. Comet assay was used to determine the genotoxicity. The results showed that acrolein caused concentration-dependent inhibition on cell viability at 8 mu M and above concentrations, decreased testosterone production at 13.6 and 19.7 mu M concentrations, and suppressed expression levels of genes that play an important role in steroidogenic pathway. Furthermore, acrolein downregulated expression of anti-apoptotic Bcl2 gene and upregulated expression of pro-apoptotic Bax, Casp3, and Trp53 gene after 24-h treatment in 7.4, 13.6, and 19.7 mu M acrolein-exposed Leydig cells. The results of comet assay showed that acrolein significantly induced tail length, tail % DNA, and Olive tail moment. Overall, it was concluded that acrolein-induced cell damage in Leydig cells may be due to formation of genetic damage in steroidogenesis and apoptosis.