%0 Journal Article
%T Delayed effects of autophagy on T
%A Jian Ying Yang
%A Xiang Feng Kong
%A Xiang Ping Meng
%A Yong Fa Zhang
%J Toxicology and Industrial Health
%@ 1477-0393
%D 2019
%R 10.1177/0748233719831122
%X 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
%K T-2 toxin
%K autophagy
%K apoptosis
%K cross talk
%K Leydig cells
%U https://journals.sagepub.com/doi/full/10.1177/0748233719831122