title: Neonatal lead exposure changes quality of sperm and number of macrophages in testes of BALB/c mice.
abstract: BALB/c mice were exposed to 0.1 ppm lead acetate in the drinking water from postnatal day (PND) 1 for 6 weeks. Until PND21, lead exposure was from mother's milk; thereafter, it was directly from the drinking water. The blood lead levels were the highest in pups before weaning (59.5+/-0.9 microg/dL) and significantly lower between PND21 and PND42 (20.3+/-4.7 microg/dL). At PND42, lead-exposed male mice were tested for fertility, sperm DNA, and macrophage number. Mating of lead-treated males with non-treated females confirmed the reduction of fertility in the exposed males. Flow cytometric studies of testicular preparations indicated that the sperm count was not different between lead-exposed and control males; however, the lead-treated mice had a significant increase in the number of testicular cells having a < 1n amount of DNA, which coincided with a decrease in the number of testicular cells with a 2n and 4n amount of DNA. The number of testicular macrophages also was decreased in lead-exposed males, which could reflect altered levels of CSF-1 or response to CSF-1, as previously reported [Kowolenko, M., Tracy, L., Lawrence, D.A., 1989. Lead-induced alterations of in vitro bone marrow cell responses to colony stimulating factor-1. J. Leukoc. Biol. 45, 198-206]. Our study showed that exposure to 0.1 ppm of lead during the neonatal and adolescent period is sufficient to reduce fertility in adult male mice; however, it did not affect sperm count on PND42. The presence of an increased number of apoptotic (< 1n amount of DNA) testicular cells may be diagnostic of defective sperm function. Thus, an administered dose of 0.1 ppm via drinking water ingestion by neonatal male BALB/c mice sufficient to produce PbB of 20-60 mg/dL compromised reproductive function in these mice as adults.
authors.affiliation: Wadsworth Center, NYS Department of Health, Empire State Plaza, P.O. Box 509, Room C505, Albany, NY 12201-0509, USA. pace@wadsworth.org
authors.forename: Beata M
authors.initials: BM
authors.lastname: Pace
authors.forename: David A
authors.initials: DA
authors.lastname: Lawrence
authors.forename: Melissa J
authors.initials: MJ
authors.lastname: Behr
authors.forename: Patrick J
authors.initials: PJ
authors.lastname: Parsons
authors.forename: James A
authors.initials: JA
authors.lastname: Dias
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000831:Animals, Newborn; D000833:Animals, Suckling; D002452:Cell Count; D005260:Female; D007248:Infertility, Male / Q000139:chemically induced*; D007774:Lactation; D007854:Lead / Q000633:toxicity*; D008264:Macrophages / Q000166:cytology / Q000187:drug effects*; D008297:Male; D018811:Maternal Exposure / Q000009:adverse effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D009942:Organometallic Compounds / Q000633:toxicity; D013094:Spermatozoa / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D013737:Testis / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism
chemical_list: D009942:Organometallic Compounds; D007854:Lead; C008261:lead acetate