Reproductive Toxicology 20 (2005) 531–537 Lectin reactivity of expanded mouse blastocysts after exposure to sera from women with unexplained recurrent spontaneous abortion Tahereh Talaei-Khozani a,∗ , Najmeh Aminizadeh a , Elham Aliabadi a , S Fakhroddin Mesbah A a , Jaleh Zolghadr b a Anatomy Department, Medical School, Shiraz University of Medical Sciences, Zand street, Shiraz 71344, Iran b Gynecology Department, Shiraz University of Medical Sciences, Shiraz, Iran Received 1 August 2004; received in revised form 26 March 2005; accepted 23 April 2005 Available online 20 June 2005 Abstract Embryotoxic factors existing in maternal sera may influence their effects via specific binding to, or alteration of cell surface molecules in the conceptus. This study was undertaken to determine the effects of sera from women with unexplained recurrent spontaneous abortion (URSA) on cell surface glycoconjugates of the early conceptus. Four cell stage embryos were cultured in medium supplemented with sera from women with URSA, from normal women, or in medium without serum. Developmental competence was assessed as the stage distribution of embryos advancing to during 96 h in culture. Hatched (expanded) blastocysts were stained with wheat germ agglutinin (WGA), peanut agglutinin (PNA) and dolichos biflorus agglutinin (DBA) to detect surface glucoconjugates. We observed that patient sera could be divided into high- and low-risk groups on the basis of the ability to decrease the number of four-cell embryos reaching the expanded blastocyst stage. Furthermore, the intensity of reactivity to PNA changed after exposure to high-risk sera. Morula formation was reduced and blastocyst formation was delayed. Although the sera from women with URSA had embryotoxic effects, no influence on the glycoconjugate patterns were evident in hatched blastocysts, aside from PNA reactivivity. We suggest altered developmental display of PNA-reactive proteins was a biomarker for poor developmental quality due to emrbyotoxic factors in serum from URSA patients. © 2005 Elsevier Inc. All rights reserved. Keywords: Spontaneous abortion; Glycoconjugates; Lectin; Blastocyst 1. Introduction Recurrent spontaneous abortion (RSA) is commonly defined as three or more consecutive losses of a pregnancy that has lasted less than 20 weeks [1]. One third of the biochemically detected pregnancies failed to survive to deliv- ery. About two thirds of these losses occurred before the pregnancy had been clinically recognized [2]. RSA affects almost 1% of couples [3,4]. The etiologies of RSA are as fol- lows: chromosomal (6%), anatomical (1%), hormonal (5%), immunological (65%) and unexplained (23%) [5]. Abnormal maternal immune reactions have been pro- posed to play a role in RSA [6–11]. In normal condition, ∗ Corresponding author. Tel.: +98 0711 2304372; fax: +98 0711 2304372. E-mail address: talaeit@sums.ac.ir (T. Talaei-Khozani). embryonic cells may be protected by surface expression of carbohydrates that suppress immune effector cell action [12,13]. Endogenous lectins and carbohydrates participate in the innate immune defense by acting as an opsonin and binding to carbohydrate structure and by activating com- plement, inducing cell adhesion, migration and apoptosis [14–16]. Impairment of protein glycosylation can influence cell cycle progression and susceptibility to apoptotic stimuli during embryonic development [17]. Induction of apoptosis and cell cycle impairment in trophoblast cells, or lack of apop- tosis in maternal T-cells, may lead to conceptal resorptions or miscarriage. Studies have shown that specific changes in the expression of plasma membrane glycoproteins take place during apoptosis [18]. Our hypothesis is that changes in the maternal serum com- position may lead to some cases of unexplained recurrent 0890-6238/$ – see front matter © 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.reprotox.2005.04.015