Inhibin B Response to Testicular Toxicants Hexachlorophene, Ethane Dimethane Sulfonate, Di-(n-butyl)-phthalate, Nitrofurazone, DL-Ethionine, 17-alpha Ethinylestradiol, 2,5-Hexanedione, or Carbendazim Following Short-Term Dosing in Male Rats
Version of Record online: 24 JAN 2013
© 2013 Wiley Periodicals, Inc.
Birth Defects Research Part B: Developmental and Reproductive Toxicology
Special Issue: Part B: Developmental and Reproductive Toxicology
Volume 98, Issue 1, pages 41–53, February 2013
How to Cite
Erdos, Z., Pearson, K., Goedken, M., Menzel, K., Sistare, F. D., Glaab, W. E. and Saldutti, L. P. (2013), Inhibin B Response to Testicular Toxicants Hexachlorophene, Ethane Dimethane Sulfonate, Di-(n-butyl)-phthalate, Nitrofurazone, DL-Ethionine, 17-alpha Ethinylestradiol, 2,5-Hexanedione, or Carbendazim Following Short-Term Dosing in Male Rats. Birth Defects Research Part B: Developmental and Reproductive Toxicology, 98: 41–53. doi: 10.1002/bdrb.21035
- Issue online: 5 FEB 2013
- Version of Record online: 24 JAN 2013
- Manuscript Received: 26 NOV 2012
- Manuscript Accepted: 26 NOV 2012
- Inhibin B;
- testicular toxicity;
- seminiferous tubule toxicity
Inhibin B is a heterodimer glycoprotein that downregulates follicle-stimulating hormone and is produced predominantly by Sertoli cells. The potential correlation between changes in plasma Inhibin B and Sertoli cell toxicity was evaluated in male rats administered testicular toxicants in eight studies. Inhibin B fluctuations over 24 hr were also measured.
Adult rats were administered one of eight testicular toxicants for 1 to 29 days. The toxicants were DL-ethionine, dibutyl phthalate, nitrofurazone, 2,5-hexanedione, 17-alpha ethinylestradiol, ethane dimethane sulfonate, hexachlorophene, and carbendazim. In a separate study plasma was collected throughout a 24-hr period via an automatic blood sampler.
Histomorphologic testicular findings included seminiferous tubule degeneration, round and elongate spermatid degeneration/necrosis, seminiferous tubule vacuolation, aspermatogenesis, and interstitial cell degeneration. There was a varying response of plasma Inhibin B levels to seminiferous tubule toxicity, with three studies showing high correlation, three studies with a response only at a certain time or dose, and two studies with no Inhibin B changes. In a receiver operating characteristics exclusion model analysis, where treated samples without histopathology were excluded, Inhibin B showed a sensitivity of 70% at 90% specificity in studies targeting seminiferous tubule toxicity.
Decreases in Inhibin B correlated with Sertoli cell toxicity in the majority of studies evaluated, demonstrating the value of Inhibin B as a potential biomarker of testicular toxicity. There was no correlation between decreases in Inhibin B and interstitial cell degeneration. In addition, a pattern of Inhibin B secretion could not be identified over 24 hr.