Citrinin Exposure Induced Testicular Damage and Spermatogenesis Disorder by Triggering Endoplasmic Reticulum Stress

Area of Science:

• Toxicology
• Reproductive Biology
• Molecular Biology

Background:

• Male infertility is often linked to reproductive system damage.
• Citrinin (CTN), a mycotoxin found in food and feed, is known to harm male fertility, but its toxic mechanisms remain unclear.

Purpose of the Study:

• To investigate the toxic mechanisms of Citrinin (CTN) on male mouse reproductive organs.
• To elucidate the role of endoplasmic reticulum stress (ERS) in CTN-induced male reproductive toxicity.

Main Methods:

• Male Kunming mice were administered varying doses of CTN.
• Evaluated sperm quality, testicular histopathology, blood-testis barrier integrity, oxidative stress markers, apoptosis, and ERS-related protein expression.
• Assessed the protective effect of 4-Phenylbutyric Acid (4-PBA), an ERS inhibitor.

Main Results:

• CTN exposure led to androgen disorder, reduced sperm quality, and testicular damage.
• CTN disrupted the blood-testis barrier (BTB) and induced oxidative stress by inhibiting antioxidant enzymes and increasing reactive oxygen species (ROS) and malondialdehyde (MDA).
• CTN induced apoptosis and activated ERS-related proteins; 4-PBA treatment mitigated these adverse effects.

Conclusions:

• CTN exposure causes significant damage to mouse testis tissue.
• Endoplasmic reticulum stress (ERS) is a critical mediator in CTN-induced male reproductive toxicity.
• Targeting ERS may offer a therapeutic strategy against CTN-induced male infertility.