2. Academic Validation
  3. Citrinin Exposure Induced Testicular Damage and Spermatogenesis Disorder by Triggering Endoplasmic Reticulum Stress

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

  • Foods. 2023 Apr 11;12(8):1616. doi: 10.3390/foods12081616.
Jing Wu 1 2,  You Wu 1 2,  Hui Fan 1 2,  Chenglin Yang 1 2,  Mengran Yang 1 2,  Xiangyi Kong 1 2,  Can Ning 1 2,  Siqi Wang 1 2,  Wenguang Xiao 1 2,  Naidong Wang 1 3,  Jine Yi 1 2,  Zhihang Yuan 1 2
Affiliations

Affiliations

  • 1 Colleges of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, China.
  • 2 Hunan Engineering Research Center of Livestock and Poultry Health Care, Hunan Agricultural University, Changsha 410128, China.
  • 3 Hunan Provincial Key Laboratory of Protein Engineering in Animal Vaccines, Laboratory of Functional Proteomics, Research Center of Reverse Vaccinology, Changsha 410128, China.
PMID: 37107412 DOI: 10.3390/foods12081616
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.

Keywords

Citrinin; apoptosis; endoplasmic reticulum stress; oxidative stress; reproductive disorders; testicular damage.

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