Related Experiment Video
Updated: Aug 1, 2025
Transgenic Rodent Assay for Quantifying Male Germ Cell Mutant Frequency
Published on: August 6, 2014
Citrinin Exposure Induced Testicular Damage and Spermatogenesis Disorder by Triggering Endoplasmic Reticulum Stress
Jing Wu1,2, You Wu1,2, Hui Fan1,2
1Colleges of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, China.
Abstract:
Damage to the reproductive system is the key factor leading to male infertility. Citrinin (CTN) is produced by Penicillium and Aspergillus in nature, and is definitely found in food and animal feed. Studies have revealed that CTN can cause damage to male reproductive organs and reduce fertility, but the mechanism of toxicity has not been revealed. In the present study, male Kunming mice were given different doses of CTN (0, 1.25, 5 or 20 mg/kg BW) by intragastric administration. The results demonstrated that CTN exposure caused disorder of androgen, a decline in sperm quality, and histopathological damage of testis. The inhibition of the expression of ZO-1, claudin-1 and occludin suggests that the blood-testis barrier (BTB) was damaged. Simultaneously, CTN inhibited the activity of antioxidant enzymes such as CAT and SOD, and promoted the production of MDA and ROS, resulting in oxidative damage of testis. Additionally, apoptotic cells were detected and the ratio of Bax/Bcl-2 was increased. Not only that, CTN activated the expression of endoplasmic reticulum stress (ERS)-related proteins IRE1, ATF6, CHOP, and GRP78. Interestingly, 4-Phenylbutyric Acid (4-PBA, an ERS inhibitor) treatment blocked the adverse effects of CTN exposure on male reproduction. In short, the findings suggested that CTN exposure can cause damage to mouse testis tissue, in which ERS exhibited an important regulatory role.
Insights
Citrinin (CTN) exposure damages male mouse reproductive health by impairing the blood-testis barrier and causing oxidative stress. Endoplasmic reticulum stress (ERS) plays a key role in CTN-induced male infertility.
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.
Related Concept Videos
01:17Role of ER in the Secretory Pathway
Components of the secretory pathway
About a third of proteins synthesized in the cell are sorted via the secretory route. They shuffle between different compartments in membrane-bound vesicles until they reach their final destination. The main intracellular compartments involved...
01:41Spermatogenesis