title: Disposition of inorganic mercury in pregnant rats and their offspring.
abstract: Environmental toxicants such as methylmercury have been shown to negatively impact fetal health. Despite the prevalence of inorganic mercury (Hg(2+)) in the environment and the ability of methylmercury to biotransform into Hg(2+), little is known about the ability of Hg(2+) to cross the placenta into fetal tissues. Therefore, it is important to understand the handing and disposition of Hg(2+) in the reproductive system. The purpose of the current study was to assess the disposition and transport of Hg(2+) in placental and fetal tissues, and to test the hypothesis that acute renal injury in dams can alter the accumulation of Hg(2+) in fetal tissues. Pregnant Wistar rats were injected intravenously with 0.5 or 2.5 μmol kg(-1) HgCl2 for 6 or 48 h and the disposition of Hg(2+) was measured. Accumulation of Hg(2+) in the placenta was rapid and dose-dependent. Very little Hg(2+) was eliminated during the initial 48 h after exposure. When dams were exposed to the low dose of HgCl2, fetal accumulation of Hg(2+) increased between 6h and 48 h, while at the higher dose, accumulation was similar at each time point. Within fetal organs, the greatest concentration of Hg(2+) (nmol/g) was localized in the kidneys, followed by the liver and brain. A dose-dependent increase in the accumulation of Hg(2+) in fetal organs was observed, suggesting that continued maternal exposure may lead to increased fetal exposure. Taken together, these data indicate that Hg(2+) is capable of crossing the placenta and gaining access to fetal organs in a dose-dependent manner.
authors.affiliation: Mercer University School of Medicine, Division of Basic Medical Sciences, Macon, GA, USA.
authors.forename: Cláudia S
authors.initials: CS
authors.lastname: Oliveira
authors.affiliation: Mercer University School of Medicine, Division of Basic Medical Sciences, Macon, GA, USA.
authors.forename: Lucy
authors.initials: L
authors.lastname: Joshee
authors.affiliation: Mercer University School of Medicine, Division of Basic Medical Sciences, Macon, GA, USA.
authors.forename: Rudolfs K
authors.initials: RK
authors.lastname: Zalups
authors.affiliation: Mercer University School of Medicine, Division of Basic Medical Sciences, Macon, GA, USA.
authors.forename: Maria E
authors.initials: ME
authors.lastname: Pereira
authors.affiliation: Mercer University School of Medicine, Division of Basic Medical Sciences, Macon, GA, USA. Electronic address: bridges_cc@mercer.edu.
authors.forename: Christy C
authors.initials: CC
authors.lastname: Bridges
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004785:Environmental Pollutants / Q000008:administration & dosage / Q000097:blood / Q000493:pharmacokinetics* / Q000633:toxicity; D005243:Feces / Q000737:chemistry; D005260:Female; D005333:Fetus / Q000378:metabolism*; D007275:Injections, Intravenous; D007668:Kidney / Q000378:metabolism; D007674:Kidney Diseases / Q000139:chemically induced; D008099:Liver / Q000378:metabolism; D018811:Maternal Exposure; D008431:Maternal-Fetal Exchange; D008627:Mercuric Chloride / Q000008:administration & dosage / Q000097:blood / Q000493:pharmacokinetics* / Q000633:toxicity; D010539:Permeability; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D017208:Rats, Wistar; D018570:Risk Assessment; D014018:Tissue Distribution
chemical_list: D004785:Environmental Pollutants; D008627:Mercuric Chloride
keywords: Mercury; Nephrotoxicity; Placenta; Transport