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HT-2 toxin affects cell viability of goat spermatogonial stem cells through AMPK-ULK1 autophagy pathways.
- Source :
-
Theriogenology [Theriogenology] 2021 Apr 01; Vol. 164, pp. 22-30. Date of Electronic Publication: 2021 Jan 24. - Publication Year :
- 2021
-
Abstract
- HT-2 toxin is widely found in moldy crops and is the major metabolite of T-2 toxin, which has been shown to exert various toxic effects in farm animals. However, little is known about the effects of HT-2 toxin on male reproduction, particularly spermatogenesis. This study aims to investigate the toxic effects of HT-2 toxin on goat spermatogonial stem cells (SSCs) and related autophagy-regulated mechanisms. Our results showed that HT-2 toxin exposure resulted in decreased cell viability and proliferation, disrupted SSCs self-renewal, and reduced germ cell-related gene expression. HT-2 toxin exposure also induced oxidative stress and cell apoptosis, as shown by ROS accumulation, increased antioxidant enzyme activity levels, decreased the mitochondrial membrane potential, and increased caspase-9 mRNA and Bcl/bax protein levels. Additionally, HT-2 toxin exposure increased the expression of the autophagy-inducing genes Atg5, Atg7 and Beclin1 and the number of autophagosomes, which indicated that HT-2 toxin induced autophagy in the goat SSCs. Moreover, we also examined a possible mechanism by which HT-2 toxin exposure induced higher expression of AMPK, mTOR and ULK at both the mRNA and protein levels. our results indicated that HT-2 toxin caused apoptosis and autophagy by activating AMPK-mTOR-ULK1 pathway, which further affected SSCs viability.<br />Competing Interests: Declaration of competing interest The authors have declared that they have no potential conflicts of interest.<br /> (Copyright © 2021 Elsevier Inc. All rights reserved.)
Details
- Language :
- English
- ISSN :
- 1879-3231
- Volume :
- 164
- Database :
- MEDLINE
- Journal :
- Theriogenology
- Publication Type :
- Academic Journal
- Accession number :
- 33529808
- Full Text :
- https://doi.org/10.1016/j.theriogenology.2021.01.015