## 1 Introduction  
Over the past three decades there has been a pronounced increase in the number of births by older women, especially in their late 30s and 40s, in many high-income countries [1; 2; 3]. The mean age of women at birth of their first child has gradually increased from 27.0 in 1987 to 29.3 in 2018 in the European Union [4]. Women are evidently delaying childbearing. However, advanced maternal age can have detrimental effects on fertility and pregnancy outcome. It is well known that the developmental potential of oocytes declines with increasing age, referred to as ovarian aging. This phenomenon is characteristic not only for humans, but for all mammals [5; 6; 7]. Advanced maternal age is associated with a range of adverse pregnancy outcomes, including low birth weight, preterm birth and stillbirth [8; 9; 10; 11]. It has been proposed that during the reproductive lifespan, ovarian follicles and reproductive tissues become exposed to factors that accumulate irreversibly, leading to an age-related decline of fertility [12; 13].  
Accumulation of harmful compounds such as advanced glycation end products (AGEs) is strongly associated with aging [14]. Furthermore, higher AGE levels correlate with aging-related diseases;for example with diabetes, cancer and neurodegenerative diseases [15; 16]. A major precursor of AGEs is the \(\alpha\)-oxoaldehyde methylglyoxal (MG), a dicarbonyl, which is physiologically formed during glycolysis, and to a lesser extent in cellular lipid and amino acid metabolism [17; 18]. Dicarbonyl species are highly reactive, promoting posttranslational modifications of proteins, lipids and nucleic acids [19] and thus interfering with physiological functions of these molecules. MG reacts with arginine residuals to form argpyrimidine [20].  
In physiological systems, defence against dicarbonyl glycation and particularly detoxification of MG mainly occurs via the glyoxalase system [21; 22]. The glyoxalase system limits carbonyl stress toxicity [23]. It consists of two enzymes: the important rate-limiting glyoxalase 1 (GLO1) and glyoxalase 2 (GLO2, also known as hydroxyacyl glutathione hydrolase, HAGH) [24]. GLO1, the main component of the MG elimination system, is significantly decreased and associated with increased MG-AGEs in ovaries from mice with an advanced reproductive age in comparison to their young control group [25]. Moreover, studies have shown that AGEs are closely associated with female infertility and that AGE accumulation promotes ovarian oxidative stress and steroid hormone production, in consequence leading to ovarian dysfunction [26].  
The reproductive dysfunction associated with aging has been so far characterised in terms of reduction of ovarian follicles and oocyte quality, as well as pregnancy complications (reviewed by [PERSON] [27]). While the extent of literature in this area is profound, there is currently limited knowledge on the molecular pathways leading to the impact that advanced maternal age has on the developmental competences of oocytes and embryos. We have recently shown that AGEs are present in ovarian tissues and embryos in rabbits [28]. Furthermore, the GLO1 enzyme is active in rabbit blastocysts as early as during preimplantation. The GLO1 amount decreases under pathophysiological conditions of maternal diabetes mellitus in embryos [29].  
In the current study, we investigated the impact of maternal age on GLO1 expression and localisation in female reproductive organs and embryos at the preimplantation stage. For this purpose, we quantified GLO1 amounts and enzymatic activity of reproductive young (16-20 weeks) and old (over 108 weeks) rabbits in the uterus, oviduct and ovary, as well as in blastocysts on day 6 of pregnancy.