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DS Irvine

The excessive generation of reactive oxygen species (ROS) by abnormal spermatozoa and by contaminating leukocytes has been identified as one of the few defined aetiologies for male infertility. As a consequence, work has begun on evaluating the role of antioxidants in the management of these patients. Glutathione plays a significant role in the antioxidant defences of the spermatogenic epithelium, the epididymis, and perhaps in ejaculated spermatozoa. The use of antioxidants in vitro appears to be of value in preserving fertilizing capacity, although no clinical data are available. Glutathione administered in vivo to patients who may have infertility secondary to excessive oxidative stress appears to act at the epididymis and during spermatogenesis, to improve the function of ejaculated spermatozoa. However, fertility studies have not yet been conducted. Controlled studies of glutathione and other antioxidants in patients with defined ROS pathology are urgently required.

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M Ozawa, M Hirabayashi, and Y Kanai

Mammalian preimplantation embryos are sensitive to maternal and direct heat stress. However, the mechanisms by which heat stress affects early embryonic development in vivo or in vitro are unknown. This study examined whether heat-stress-induced loss of developmental competence in mouse embryos was mediated by physiological changes in the maternal environment or by high temperatures alone. After fertilization, zygotes at the same stage were heat-stressed at 39.5 degrees C for 12 h either maternally (measured by maternal rectal temperature) or directly in culture. Zygotes in each group were cultured at 37.5 degrees C for a further 84 h to assess their developmental ability. Neither type of heat stress affected the first cleavage rate. However, the proportion of embryos that developed to morulae or blastocysts was significantly lower in the maternally heat-stressed group, but not in the directly heat-stressed group. Moreover, maternal heat stress significantly reduced intracellular glutathione concentrations and enhanced hydrogen peroxide concentrations in both zygotes and two-cell embryos that were recovered immediately after heat stress or 12 h later, respectively. In contrast, direct heat stress had little effect on concentrations of glutathione or hydrogen peroxide in cultured early embryos. These results demonstrate that maternal heat stress at the zygote stage reduces the developmental ability of mouse embryos via physiological changes in the maternal environment that lead to an increase in intracellular oxidative stress on the embryo.

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S. Natsuyama, Y. Noda, K. Narimoto, Y. Umaoka, and T. Mori

Summary. The development of mouse pronuclear-stage embryos in media containing various concentrations of thioredoxin was monitored and the influence of antithioredoxin immunoglobulin G (IgG) and heat-treated thioredoxin on the thioredoxin-induced effects was evaluated. A significant increase in the number of four-cell embryos (76·3%) and blastocysts (37·3%) was observed when embryos were cultured in the medium containing 50 μg thioredoxin ml−1 compared with the rates (55·8 and 3·8%, respectively) in the basic medium. The number of blastocysts increased significantly to a maximum of 70·2% at 500 μg ml−1. The biological activity of thioredoxin was evident after dialysis, but was markedly impaired by the addition of anti-thioredoxin IgG to the culture medium. Treatment at 60°C for 5 min did not affect the enzymatic and biological activity of thioredoxin. More severe heat treatment (121°C for 30 min) attenuated the enzymatic activity to 40% of its initial value and reduced the biological activity (number of blastocysts, from 77·8 to 51·6%).

These results indicate that the effect of thioredoxin on the two-cell block is due to the thioredoxin molecule itself, and suggest that disulfide formation within or between proteins resulting from oxidative stress is one of the major causes of the two-cell block.

Keywords: thioredoxin; embryo; mouse

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Morgane Robles, Shavahn Loux, Amanda M de Mestre, and Pascale Chavatte-Palmer

Equine placental development is a long process with unique features. Implantation occurs around 40 days of gestation (dpo) with the presence of a transient invasive placenta from 25–35 to 100–120 dpo. The definitive, non-invasive placenta remains until term (330 days). This definitive placenta is diffuse and epitheliochorial, exchanging nutrients, gas and waste with the endometrium through microvilli, called microcotyledons. These are lined by an external layer of haemotrophic trophoblast. Moreover, histotrophic exchange remains active through the histotrophic trophoblast located along the areolae. Placental development is dependent on the maternal environment that can be affected by several factors (e.g. nutrition, metabolism, age, embryo technologies, pathologies) that may affect fetal development as well as long-term offspring health. The first section of the review focuses on normal placental development as well as definitive placental structure. Differences between the various regions of the placenta are also highlighted. The latter sections provide an overview of the effects of the maternal environment and reproductive pathologies, respectively, on trophoblast/placental gene expression and structure. So far, only pre-implantation and late gestation/term data are available, which demonstrate important placental plasticity in response to environmental variation, with genes involved in oxidative stress and tissue differentiation mostly involved in the pre-implantation period, whereas genes involved in feto-placental growth and nutrient transfers are mostly perturbed at term.

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R John Aitken

suggest that the origin of this age-dependent increase in DNA damage in the germ line is oxidative, reflecting the general relationship between oxidative stress and ageing observed in most biological systems ( Paul et al . 2011 , Smith et al . 2013 a

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D G Valcarce and V Robles

problem for sperm survival and fertility ( Guthrie & Welch 2012 ). In mammals, oxidative stress damage competence of spermatozoa by peroxidation of lipids, induction of oxidative DNA damage and formation of protein adducts are well known ( Aitken et al

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L Vandaele, M Thys, J Bijttebier, A Van Langendonckt, I Donnay, D Maes, E Meyer, and A Van Soom

Introduction In vitro embryo culture conditions never completely mimic the in vivo situation which prevails in the oviduct and uterus, and may represent a source of increased oxidative stress for the in vitro produced embryo ( Nasr-Esfahani et

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R John Aitken, Jock K Findlay, Karla J Hutt, and Jeff B Kerr

variety of environmental factors can conspire to induce a state of oxidative stress in the male germ line. The DNA-damaged spermatozoa then fertilize the egg and the latter rapidly engages in a round of DNA repair. If this DNA repair is incomplete or

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B J Houston, B Nixon, B V King, G N De Iuliis, and R J Aitken

certain exposure conditions. Generation of oxidative stress It has previously been hypothesised that the biological effects of EMR could be attributed solely to heat stress, which is induced at the higher intensities of approximately ≥4 W

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Qingling Yang, Shanjun Dai, Xiaoyan Luo, Jing Zhu, Fangyuan Li, Jinhao Liu, Guidong Yao, and Yingpu Sun

intracellular signals that control postovulatory oocyte aging have not been well defined, previous studies have shown that the postovulatory aging of mammalian oocytes is inherently linked to oxidative stress and that the ROS content increases in a time