Effects of T-2 toxin on the regulation of steroidogenesis in mouse Leydig cells

Toxicol Ind Health. 2016 Oct;32(10):1801-7. doi: 10.1177/0748233715590516. Epub 2015 Jun 17.

Abstract

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).

Keywords: 3β-HSD-1; P450scc; StAR; T-2 toxin; mouse Leydig cells.

MeSH terms

  • 17-Hydroxysteroid Dehydrogenases / analysis
  • 17-Hydroxysteroid Dehydrogenases / genetics
  • 17-Hydroxysteroid Dehydrogenases / metabolism*
  • Animals
  • Cells, Cultured
  • Centrifugation
  • Leydig Cells / drug effects*
  • Leydig Cells / enzymology
  • Leydig Cells / metabolism*
  • Male
  • Mice
  • Phosphoproteins / analysis
  • Phosphoproteins / genetics
  • Phosphoproteins / metabolism
  • RNA, Messenger / analysis
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • T-2 Toxin / toxicity*

Substances

  • Phosphoproteins
  • RNA, Messenger
  • steroidogenic acute regulatory protein
  • 17-Hydroxysteroid Dehydrogenases
  • 3 (or 17)-beta-hydroxysteroid dehydrogenase
  • T-2 Toxin