BACKGROUND DNA damage is a hazard that affects all cells of the body. DNA-damage repair (DDR) mechanisms are in place to repair damage and restore cellular function, as are other damage-induced processes such as apoptosis, autophagy and senescence. The resilience of germ cells and embryos in response to DNA damage is less well studied compared with other cell types. Given that recent studies have described links between embryonic handling techniques and an increased likelihood of disease in post-natal life, an update is needed to summarize the sources of DNA damage in embryos and their capacity to repair it. In addition, numerous recent publications have detailed novel techniques for detecting and repairing DNA damage in embryos. This information is of interest to medical or scientific personnel who wish to obtain undamaged embryos for use in offspring generation by ART. OBJECTIVE AND RATIONALE This review aims to thoroughly discuss sources of DNA damage in male and female gametes and preimplantation embryos. Special consideration is given to current knowledge and limits in DNA damage detection and screening strategies. Finally, obstacles and future perspectives in clinical diagnosis and treatment (repair) of DNA damaged embryos are discussed. SEARCH METHODS Using PubMed and Google Scholar until May 2021, a comprehensive search for peer-reviewed original English-language articles was carried out using keywords relevant to the topic with no limits placed on time. Keywords included ‘DNA damage repair’, ‘gametes’, ‘sperm’, ‘oocyte’, ‘zygote’, ‘blastocyst’ and ‘embryo’. References from retrieved articles were also used to obtain additional articles. Literature on the sources and consequences of DNA damage on germ cells and embryos was also searched. Additional papers cited by primary references were included. Results from our own studies were included where relevant. OUTCOMES DNA damage in gametes and embryos can differ greatly based on the source and severity. This damage affects the development of the embryo and can lead to long-term health effects on offspring. DDR mechanisms can repair damage to a certain extent, but the factors that play a role in this process are numerous and altogether not well characterized. In this review, we describe the multifactorial origin of DNA damage in male and female gametes and in the embryo, and suggest screening strategies for the selection of healthy gametes and embryos. Furthermore, possible therapeutic solutions to decrease the frequency of DNA damaged gametes and embryos and eventually to repair DNA and increase mitochondrial quality in embryos before their implantation is discussed. WIDER IMPLICATIONS Understanding DNA damage in gametes and embryos is essential for the improvement of techniques that could enhance embryo implantation and pregnancy success. While our knowledge about DNA damage factors and regulatory mechanisms in cells has advanced greatly, the number of feasible practical techniques to avoid or repair damaged embryos remains scarce. Our intention is therefore to focus on strategies to obtain embryos with as little DNA damage as possible, which will impact reproductive biology research with particular significance for reproductive clinicians and embryologists.

Inflammation is an organism’s physiological response to harmful septic and aseptic stimuli. This process begins locally through the influx of immune system cells to the damaged tissue and the subsequent activation and secretion of inflammatory mediators to restore homeostasis in the organism. Inflammation is regulated at many levels, and one of these levels is post-transcriptional regulation, which controls the half-life of transcripts that encode inflammatory mediators. One of the proteins responsible for controlling the amount of mRNA in a cell is the RNase monocyte chemoattractant protein-induced protein 1 (MCPIP1). The studies conducted so far have shown that MCPIP1 is involved not only in the regulation of inflammation but also in many other physiological and pathological processes. This paper provides a summary of the information on the role of MCPIP1 in adipogenesis, angiogenesis, cell differentiation, cancer, and skin inflammation obtained to date.

Poczęcie dziecka w zaawansowanym wieku rozrodczym (>35 lat) w ostatnich dekadach stale wzrasta, szczególnie w krajach rozwiniętych. Bezpośredni wpływ na odsuwanie decyzji o urodzeniu dziecka mają czynniki społeczno-ekonomiczne, skuteczne środki antykoncepcyjne, oraz dostępność technologii wspomaganego rozrodu (ang. Assisted Reproduction Technologies, ART). Rozród wspomagany umożliwia sukces rozrodczy osobom diagnozowanym jako niepłodne lub o obniżonych możliwościach naturalnego zajścia w ciążę z uwagi na współistniejące patologie lub styl życia. Badania epidemiologiczne wskazują, że zarówno zaawansowany wiek rodzicielski jak i ART są związane z patologiami ciąży, życia okołoporodowego i poporodowego, takimi jak cukrzyca ciążowa, ryzyko stanu przedrzucawkowego, poronienia, oderwanie łożyska, poród przedwczesny, urodzenie martwego dziecka, zaburzenia neurorozwojowe i pogorszone wskaźniki ogólnego stanu zdrowia potomstwa [1–4]. W naszej pracy skupimy się na dostępnych informacjach dotyczących zmian metabolicznych zwiększających ryzyko rozwoju chorób sercowo-naczyniowych u potomstwa rodziców w zaawansowanym wieku oraz urodzonego przy pomocy ART. Na koniec odniesiemy się do źródeł powstawania obserwowanych zaburzeń na poziomie gamety i zarodka, dotyczących stresu tlenowego, modyfikacji epigenetycznych oraz uszkodzeń DNA, rozpatrując możliwe działania naprawcze.