Spermidine/spermine N1-acetyltransferase1mediates zearalenone-induced toxicity in bovine Leydig cells.

INTRODUCTION

Zearalenone (Zea), a widespread mycotoxin, can impair male reproductive function, but its effects on bovine Leydig cells and the underlying mechanisms remain insufficiently understood.

METHODS

Primary bovine Leydig cells were isolated and identified. The effects of Zea on cell viability, testosterone production, steroidogenic gene expression, oxidative stress, apoptosis, and cell cycle progression were examined. Transcriptomic analysis was performed to identify genes associated with Zea-induced cellular injury, and the role of spermidine/spermine N1-acetyltransferase1 (SAT1) was investigated using siRNA-mediated knockdown.

RESULTS

Zea exposure decreased cell viability in a concentration-dependent manner, with an approximate half-maximal inhibitory concentration of 75 μM, and reduced testosterone production and steroidogenic gene expression. Zea markedly increased intracellular reactive oxygen species levels and lipid peroxidation while suppressing antioxidant enzyme activities. It also promoted apoptosis and induced G2/M phase arrest. SAT1 was identified as one of the most upregulated genes following Zea exposure. SAT1 knockdown attenuated oxidative stress and apoptosis, restored antioxidant capacity, and improved cell proliferation under Zea exposure.

DISCUSSION: These findings demonstrate that SAT1 is involved in Zea-induced oxidative stress and cellular injury in bovine Leydig cells and provide new insight into the molecular basis of mycotoxin-induced reproductive toxicity.