Cigarette smoke condensate induces aryl hydrocarbon receptor-dependent changes in gene expression in spermatocytes

Prabagaran Esakky, Deborah A. Hansen, Andrea M. Drury, Kelle H. Moley

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

Cigarette smoke contains numerous compounds that cause oxidative stress and alter gene expression in many tissues, and cigarette smoking is correlated with male infertility. To identify mechanisms by which this occurs, we evaluated expression of antioxidant genes in mouse spermatocytes in response to cigarette smoke condensate (CSC). CSC exposure led to oxidative stress and dose-dependent up-regulation of Hsp90aa1, Ahr, Arnt, Sod1, Sod2, and Cyp1a1 expression in a mouse spermatocyte cell line. An antagonist of the aryl hydrocarbon receptor (AHR) abrogated several CSC-mediated changes in mRNA and protein levels. Consistent with these results, spermatocytes isolated by laser-capture microdissection from CSC-treated mice showed increased expression of several antioxidant genes. In vivo exposure to CSC was genotoxic to spermatocytes, resulting in apoptosis and disruptions to the seminiferous tubules. Our in vivo and in vitro data indicate that CSC-mediated damage to murine spermatocytes is AHR-dependent and is mediated by oxidative stress.

Original languageEnglish
Pages (from-to)665-676
Number of pages12
JournalReproductive Toxicology
Volume34
Issue number4
DOIs
StatePublished - Dec 2012

Keywords

  • AHR
  • Apoptosis
  • CSC
  • Cyp1a1
  • Oxidative stress
  • Spermatocytes

Fingerprint

Dive into the research topics of 'Cigarette smoke condensate induces aryl hydrocarbon receptor-dependent changes in gene expression in spermatocytes'. Together they form a unique fingerprint.

Cite this