title: Pregnancy and amyloidogenesis: I. Offspring of amyloidotic mice are not predisposed to develop amyloidosis.
abstract: Amyloid enhancing factor (AEF) is a substance formed during amyloidogenesis that accelerates amyloid deposition in tissues. The administration of AEF followed by AgNO3 (inflammatory stimulus) to mice results in amyloidosis within 6 days. The purpose of the study was to determine whether the offspring of amyloidotic mice are exposed to maternal AEF during pregnancy and therefore become predisposed to the development of amyloidosis on inflammatory stimulus. To that end female mice were made amyloidotic by the administration of AEF and AgNO3, made pre-amyloidotic (a condition associated with self-generation of AEF) with a short course of casein, or treated with exogenous AEF without AgNO3; then mating and conception took place. The possible priming of offspring with maternal AEF was studied by the administration of AgNO3 alone (without AEF) to the offspring and the determination of the presence of amyloid deposits in their spleens. Despite the long-term effect of AEF and its high activity, amyloidosis did not develop in any of the studied offspring, implying that the newborn mice were not primed by maternal AEF. These findings suggest that amyloidotic mothers do not predispose their offspring to the risk of developing amyloidosis, probably because maternal AEF does not cross the placenta.
authors.affiliation: Heller Institute of Medical Research, Department of Obstetrics and Gynecology, Sheba Medical Center Tel-Hashomer, Israel.
authors.forename: S
authors.initials: S
authors.lastname: Shtrasburg
authors.forename: M
authors.initials: M
authors.lastname: Pras
authors.forename: N
authors.initials: N
authors.lastname: Brezniak
authors.forename: M
authors.initials: M
authors.lastname: Dolitzki
authors.forename: A
authors.initials: A
authors.lastname: Livneh
mesh_terms: D000686:Amyloidosis / Q000139:chemically induced / Q000453:epidemiology / Q000378:metabolism*; D000818:Animals; D002364:Caseins / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D005260:Female; D005333:Fetus / Q000378:metabolism; D006023:Glycoproteins / Q000096:biosynthesis / Q000493:pharmacokinetics*; D008297:Male; D008431:Maternal-Fetal Exchange; D051379:Mice; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D011297:Prenatal Exposure Delayed Effects; D012307:Risk Factors; D000685:Serum Amyloid A Protein / Q000378:metabolism*; D012835:Silver Nitrate; D013154:Spleen / Q000378:metabolism
chemical_list: D002364:Caseins; D002614:Chelating Agents; D006023:Glycoproteins; D000685:Serum Amyloid A Protein; C046748:amyloid enhancing factor; D012835:Silver Nitrate