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HT-2 toxin impairs porcine oocyte in vitro maturation through disruption of endomembrane system.

Authors :
Li, Jia-Rui
Wu, Si-Le
Hu, Lin-Lin
Liao, Bi-Yun
Sun, Shao-Chen
Source :
Theriogenology. Sep2024, Vol. 226, p286-293. 8p.
Publication Year :
2024

Abstract

HT-2 toxin is a type of mycotoxin which is shown to affect gastric and intestinal lesions, hematopoietic and immunosuppressive effects, anorexia, lethargy, nausea. Recently, emerging evidences indicate that HT-2 also disturbs the reproductive system. In this study, we investigated the impact of HT-2 toxin exposure on the organelles of porcine oocytes. Our results found that the abnormal distribution of endoplasmic reticulum increased after HT-2 treatment, with the perturbation of ribosome protein RPS3 and GRP78 expression; Golgi apparatus showed diffused localization pattern and GM130 localization was also impaired, thereby affecting the Rab10-based vesicular transport; Due to the impairment of ribosomes, ER, and Golgi apparatus, the protein supply to lysosomes was hindered, resulting in lysosomal damage, which further disrupted the LC3-based autophagy. Moreover, the results indicated that the function and distribution of mitochondria were also affected by HT-2 toxin, showing with fragments of mitochondria, decreased TMRE and ATP level. Taken together, our study suggested that HT-2 toxin exposure induces damage to the organelles for endomembrane system, which further inhibited the meiotic maturation of porcine oocytes. • HT-2 caused abnormal distribution of ER and GRP78-based ER stress in oocytes. • HT-2 disrupted GM130-based Golgi apparatus and Rab10-based vesicular transport. • HT-2 induced lysosome damage and disrupted LC3-based autophagy in oocytes. • HT-2 disturbed mitochondria distribution, MMP and ATP production in oocytes. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
0093691X
Volume :
226
Database :
Academic Search Index
Journal :
Theriogenology
Publication Type :
Academic Journal
Accession number :
178535941
Full Text :
https://doi.org/10.1016/j.theriogenology.2024.06.019