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PHTHALATE ESTER-INDUCED GUBERNACULAR LESIONS ARE ASSOCIATED WITH REDUCED INSL-3 GENE EXPRESSION IN THE FETAL RAT TESTIS
Citation:
Wilson, V S., C R. Lambright, J. R. Furr, J S. Ostby, C R. Wood, G A. Held, AND L E. Gray Jr. PHTHALATE ESTER-INDUCED GUBERNACULAR LESIONS ARE ASSOCIATED WITH REDUCED INSL-3 GENE EXPRESSION IN THE FETAL RAT TESTIS. TOXICOLOGY LETTERS 146(3):207-215, (2004).
Description:
Phthalate ester-induced gubernacular ligament lesions are associated with reduced Insl3 gene expression in the fetal rat testis during sexual differentiation.
VS Wilson, C Lambright, J Furr, J Ostby, C Wood, G Held, LE Gray Jr.
U.S. EPA, ORD, NHEERL, Reproductive Toxicology Division, RTP, NC
Abstract
Recently, concern has arisen over the apparent increase in male reproductive health problems and the potential role of endocrine disrupting chemicals (EDCs) in the etiology of these conditions (1). Declining sperm counts, altered sex ratios, and increased incidences of hypospadias, cryptorchidism and testis cancer all have been reported. Of these, the world-wide doubling in the rate of testicular cancer over the last 40 years is one of the more robust of these pathologies (2). Since only a small percentage of these lesions can be linked directly to know genetic defects, developmental exposure to man-made chemicals has been implicated in the increases in these reproductive malformations. The phthalate ester, di-n-ethylhexyl phthalate (DEHP), is a high production volume, ubiquitous environmental chemical that induces male rat reproductive tract malformations when administered during sexual differentiation. In the current study, we report that DEHP-induced lesions of the gubernacular ligaments, which are critical for testis descent, likely result from an inhibition of insulin-like hormone 3 (insl3) gene expression, a recently discovered peptide hormone synthesized by fetal Leydig cells.