Yang Jian Ying, Zhang Yong Fa, Li Yuan Xiao, Guan Gui Ping, Kong Xiang Feng, Liang Ai Min, Ma Kai Wang, Da Li Guang, Bai Xue Fei
College of Medical Technology and Engineering, Henan University of Science and Technology, Luoyang, Henan, China Laboratory of Animal Nutrition and Health and Key Laboratory of Subtropical Agro-ecology, Institute of Subtropical Agriculture, The Chinese Academy of Sciences, Changsha, Hunan, China.
Laboratory of Animal Nutrition and Health and Key Laboratory of Subtropical Agro-ecology, Institute of Subtropical Agriculture, The Chinese Academy of Sciences, Changsha, Hunan, China College of Food and Bioengineering, Henan University of Science and Technology, Luoyang, Henan, China
Toxicol Ind Health. 2016 Oct;32(10):1801-7. doi: 10.1177/0748233715590516. Epub 2015 Jun 17.
T-2 toxin is one of the mycotoxins, a group of type A trichothecenes produced by several fungal genera including Fusarium species, which may lead to the decrease of testosterone secretion in primary Leydig cells derived from mouse testis. The previous study demonstrated T-2 toxin decrease the testosterone biosynthesis in the primary Leydig cells derived from the mouse testis directly. In this study, we further examined the direct biological effects of T-2 toxin on the process of steroidogenesis, primarily in Leydig cells of mice. Leydig cells of mature mouse were purified by Percoll gradient centrifugation and the cell purity was determined by 3β-hydroxysteroid dehydrogenase (3β-HSD) staining. To examine the decrease in T-2 toxin-induced testosterone secretion, we measured the transcription level of three key steroidogenic enzymes including 3β-HSD-1, cytochrome P450 side-chain cleavage (P450scc) enzyme, and steroidogenic acute regulatory (StAR) protein in T-2 toxin/human chorionic gonadotropin (hCG) co-treated cells. Our previous study showed that T-2 toxin (10(-7), 10(-8), and 10(-9) M) significantly suppressed hCG (10 ng/ml)-induced testosterone secretion. The studies demonstrated that the suppressive effect is correlated with a decrease in the level of transcription of 3β-HSD-1, P450scc, and StAR (p < 0.05).
T-2毒素是一种霉菌毒素,属于A类单端孢霉烯族毒素,由包括镰刀菌属在内的多个真菌属产生,可能导致源自小鼠睾丸的原代睾丸间质细胞中睾酮分泌减少。先前的研究表明,T-2毒素直接降低了源自小鼠睾丸的原代睾丸间质细胞中的睾酮生物合成。在本研究中,我们进一步研究了T-2毒素对类固醇生成过程的直接生物学效应,主要是在小鼠的睾丸间质细胞中。通过Percoll梯度离心法纯化成熟小鼠的睾丸间质细胞,并通过3β-羟基类固醇脱氢酶(3β-HSD)染色确定细胞纯度。为了检测T-2毒素诱导的睾酮分泌减少情况,我们测量了在T-2毒素/人绒毛膜促性腺激素(hCG)共同处理的细胞中三种关键类固醇生成酶的转录水平,这三种酶包括3β-HSD-1、细胞色素P450侧链裂解酶(P450scc)和类固醇生成急性调节蛋白(StAR)。我们先前的研究表明,T-2毒素(10^(-7)、10^(-8)和10^(-9) M)显著抑制hCG(10 ng/ml)诱导的睾酮分泌。研究表明,这种抑制作用与3β-HSD-1、P450scc和StAR转录水平的降低相关(p < 0.05)。