Microcystin-LR induces autophagy and apoptosis in rat Sertoli cells in vitro

Yu Chen1, Yuan Zhou, Xueting Wang

  • 1Immunology and Reproduction Biology Laboratory, Medical School, Nanjing University, Nanjing, Jiangsu 210093, China; Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing, Jiangsu 210093, China; State Key Laboratory of Analytical Chemistry for Life Science, Nanjing University, Nanjing, Jiangsu 210093, China.

Insights

Microcystin-LR (MC-LR) from cyanobacteria harms reproductive cells. This study shows MC-LR induces autophagy and apoptosis in Sertoli cells, linking these processes to its toxicity.

Area of Science:

  • Environmental Toxicology
  • Cell Biology
  • Reproductive Toxicology

Background:

  • Cyanobacteria produce microcystin-LR (MC-LR), a toxin with known reproductive toxicity.
  • The precise mechanisms underlying MC-LR's toxicity, particularly in Sertoli cells, remain incompletely understood.

Purpose of the Study:

  • To investigate the impact of MC-LR on autophagy induction in Sertoli cells.
  • To elucidate the relationship between MC-LR-induced autophagy and apoptosis in these cells.

Main Methods:

  • Sertoli cells were exposed to varying concentrations of MC-LR (0.5-500 nM) for 24 or 48 hours.
  • Cell viability, membrane integrity, and the autophagosome marker LC3 were assessed.
  • The role of autophagy in MC-LR toxicity was examined using an autophagy inhibitor (3-MA).

Main Results:

  • MC-LR exposure at high concentrations (50-500 nM) reduced Sertoli cell viability and membrane integrity.
  • Mild MC-LR concentrations (0.5-5 nM) increased the autophagosome marker LC3.
  • High MC-LR concentrations led to significant autophagosome accumulation and increased apoptosis, which was mitigated by 3-MA.

Conclusions:

  • MC-LR exerts toxic effects on Sertoli cells through the induction of both autophagy and apoptosis.
  • Autophagosome accumulation appears to be a key factor in the apoptosis pathway triggered by MC-LR exposure.

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