AI Article Synopsis
- T-2 toxin, produced by Fusarium and found in various foods, causes harm to animals, including reproductive and testicular damage.
- Previous studies showed T-2 toxin triggers apoptosis in Leydig cells through specific cellular pathways, but the role of autophagy in this process was not well understood.
- This study found that T-2 toxin increases autophagy markers, and that manipulating autophagy levels can either enhance or reduce apoptosis in Leydig cells, suggesting autophagy helps protect cells from T-2 toxin toxicity.
Article Abstract
T-2 toxin is a type-A trichothecene produced by Fusarium found in several food commodities worldwide. T-2 toxin causes reproductive disorders, genotoxicity, and testicular toxicity in animals. Our previous research has reported that T-2 toxin can induce apoptosis via the Bax-dependent caspase-3 activation in mouse primary Leydig cells. However, little is known about the functions of autophagy and the cross talk between autophagy and apoptosis after exposure to T-2 toxin in Leydig cells. This study investigated these problems in mouse primary Leydig cells. Results showed that T-2 toxin treatment upregulated LC3-II and Beclin-1 expression, suggesting that T-2 toxin induced a high level of autophagy. Pretreatment with chloroquine (an autophagy inhibitor) and rapamycin (an autophagy inducer) increased and decreased the rate of apoptosis, respectively, in contrast to T-2 toxin-treated group. Autophagy delayed apoptosis in the T-2 toxin-treated Leydig cells. Therefore, autophagy may prevent cells from undergoing apoptosis by reducing T-2 toxin-induced cytotoxicity.
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| http://dx.doi.org/10.1177/0748233719831122 | DOI Listing |
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