title: Relation between serum xenobiotic-induced receptor activities and sperm DNA damage and sperm apoptotic markers in European and Inuit populations.
abstract: Persistent organic pollutants (POPs) can interfere with hormone activities and are suspected as endocrine disrupters involved in disorders, e.g. reproductive disorders. We investigated the possible relation between the actual integrated serum xenoestrogenic, xenoandrogenic and aryl hydrocarbon receptor (AhR) activities, and the sperm DNA damage and sperm apoptotic markers of 262 adult males (54 Inuits from Greenland, 69 from Warsaw (Poland), 81 from Sweden, and 58 from Kharkiv (Ukraine)) exposed to different levels of POPs. Xenobiotic-induced receptor activities were determined by receptor-mediated luciferase reporter gene expression. Sperm DNA damage was measured using terminal deoxynucleotidyl transferase-driven dUTP nick labeling assay (TUNEL) and pro- (Fas) and anti-apoptotic (Bcl-xL) markers were determined by immune methods. Different features of xenobiotic-induced receptor activity in serum and sperm DNA fragmentation and apoptotic markers existed between the Inuits and the European Caucasians. Negative correlations between xenobiotic-induced receptor activities and DNA damage were found for Inuits having relatively lower xenoestrogenic, lower dioxin-like activity, and lower sperm DNA damage, but higher xenoandrogenic activity. In contrast, in the European groups, xenobiotic-induced receptor activities were found to be positively correlated with the DNA damage. Further research must elucidate whether altered receptor activities in concerted action with genetic and/or nutrient factors may have protecting effect on sperm DNA damage of the Inuit population.
authors.affiliation: Unit of Cellular and Molecular Toxicology (CMT), Department of Environmental and Occupational Medicine, Institute of Public Health, University of Aarhus, Vennelyst Boulevard 6, Build 1260, DK-8000 Aarhus C, Denmark.
authors.forename: Manhai
authors.initials: M
authors.lastname: Long
authors.forename: Alessandra
authors.initials: A
authors.lastname: Stronati
authors.forename: Davide
authors.initials: D
authors.lastname: Bizzaro
authors.forename: Tanja
authors.initials: T
authors.lastname: Krüger
authors.forename: Gian-Carlo
authors.initials: GC
authors.lastname: Manicardi
authors.forename: Philip S
authors.initials: PS
authors.lastname: Hjelmborg
authors.forename: Marcello
authors.initials: M
authors.lastname: Spanò
authors.forename: Alexander
authors.initials: A
authors.lastname: Giwercman
authors.forename: Gunnar
authors.initials: G
authors.lastname: Toft
authors.forename: Jens Peter
authors.initials: JP
authors.lastname: Bonde
authors.forename: Eva C
authors.initials: EC
authors.lastname: Bonefeld-Jorgensen
mesh_terms: D000328:Adult; D017209:Apoptosis; D002478:Cells, Cultured; D020552:Comet Assay; D004249:DNA Damage; D004147:Dioxins / Q000633:toxicity; D004305:Dose-Response Relationship, Drug; D052244:Endocrine Disruptors / Q000633:toxicity*; D004781:Environmental Exposure; D004785:Environmental Pollutants / Q000633:toxicity*; D015870:Gene Expression; D006116:Greenland; D006801:Humans; D020287:In Situ Nick-End Labeling; D004930:Inuit; D008156:Luciferases / Q000235:genetics; D008297:Male; D011044:Poland; D011944:Receptors, Androgen / Q000097:blood; D018336:Receptors, Aryl Hydrocarbon / Q000097:blood; D011960:Receptors, Estrogen / Q000097:blood; D013094:Spermatozoa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D013548:Sweden; D014455:Ukraine; D044465:White People; D015262:Xenobiotics
chemical_list: D004147:Dioxins; D052244:Endocrine Disruptors; D004785:Environmental Pollutants; D011944:Receptors, Androgen; D018336:Receptors, Aryl Hydrocarbon; D011960:Receptors, Estrogen; D015262:Xenobiotics; D008156:Luciferases