1,721,067 research outputs found
Development of female germcells
No full textEichenlaub-Ritter U. Development of female germcells. Gynäkologische Endokrinologie . 2018;16(4):220-229
Environmental Hazard in the Aetiology of Somatic and Germ Cell Aneuploidy
No full textPacchierotti F, Eichenlaub-Ritter U. Environmental Hazard in the Aetiology of Somatic and Germ Cell Aneuploidy. Cytogenetic and Genome Research. 2011;133(2-4):254-268
Nondisjunction, disturbances in spindle structure, and characteristics of chromosome alignment in maturing oocytes of mice heterozygous for Robertsonian translocations
No full textEichenlaub-Ritter U, Winking H. Nondisjunction, disturbances in spindle structure, and characteristics of chromosome alignment in maturing oocytes of mice heterozygous for Robertsonian translocations. Cytogenetic and Genome Research. 1990;54(1-2):47-54
Dicarbonyl stress and glyoxalases in ovarian function
No full textThe ovary is the main regulator of female fertility. Changes in maternal health and physiology can disrupt intraovarian homoeostasis thereby compromising oocyte competence and fertility. Research has only recently devoted attention to the involvement of dicarbonyl stress in ovarian function. On this basis, the present review focuses on clinical and experimental research supporting the role of dicarbonyl overload and AGEs (advanced glycation end-products) as key contributors to perturbations of the ovarian microenvironment leading to lower fertility. Particular emphasis has been given to oocyte susceptibility to methylglyoxal, a powerful glycating agent, whose levels are known to increase during aging and metabolic disorders. According to the literature, the ovary and the oocyte itself can rely on the glyoxalase system to counteract the possible dicarbonyl overload such as that which may occur in reproductive-age women and patients with PCOS (polycystic ovarian syndrome) or diabetes. Overall, although biochemical methods for proper evaluation of dicarbonyl stress in oocytes and the ovarian microenvironment need to be established, AGEs can be proposed as predictive markers and/or therapeutic targets in new strategies for improving reproductive counselling and infertility therapies.The ovary is the main regulator of female fertility. Changes in maternal health and physiology can disrupt intraovarian homoeostasis thereby compromising oocyte competence and fertility. Research has only recently devoted attention to the involvement of dicarbonyl stress in ovarian function. On this basis, the present review focuses on clinical and experimental research supporting the role of dicarbonyl overload and AGEs (advanced glycation end-products) as key contributors to perturbations of the ovarian microenvironment leading to lower fertility. Particular emphasis has been given to oocyte susceptibility to methylglyoxal, a powerful glycating agent, whose levels are known to increase during aging and metabolic disorders. According to the literature, the ovary and the oocyte itself can rely on the glyoxalase system to counteract the possible dicarbonyl overload such as that which may occur in reproductive-age women and patients with PCOS (polycystic ovarian syndrome) or diabetes. Overall, although biochemical methods for proper evaluation of dicarbonyl stress in oocytes and the ovarian microenvironment need to be established, AGEs can be proposed as predictive markers and/or therapeutic targets in new strategies for improving reproductive counselling and infertility therapies. ©The Authors Journal compilation ©2014 Biochemical Society
Reconstitution of gametes for assisted reproduction
No full textEichenlaub-Ritter U. Reconstitution of gametes for assisted reproduction. HUMAN REPRODUCTION. 2003;18(3):473-475.There are basically two major problems in the genesis of 'cloned' gametes in mammals, which have not been addressed in the original debate article. There is no adequate discussion on the mechanisms providing for high fidelity of chromosome segregation in mitosis and meiosis, and for proper imprinting in construction of 'reconstituted gametes'. The original debate article is uncritical with respect to the currently insufficient database and the incomplete documentation of results
Mechanisms underlying age-related defects in the mammalian oocyte: potential deleterious effects of methylglyoxal, a reactive dicarbonyl compound
No full textTatone C., Carbone M., Heizenrieder T., Gualtieri R., Eichenlaub-Ritter U. Mechanisms underlying age-related defects in the mammalian oocyte: potential deleterious effects of methylglyoxal, a reactive dicarbonyl compound University of L’Aquila, Dept of Health Sciences, L’Aquila (Italy) University of Bielefeld, Faculty of Biology, Gene Technolo/Microbiol, Bielefeld (Germany) University of Naples “Federico II”, Dept of Structural and Functional Biology, Naples (Italy) Methylglyoxal (MG) is a reactive dicarbonyl compound physiologically produced by various metabolic pathways. It causes inhibition of proliferation, and mitochondrial respiration,and increases reactive oxygen species, apoptosis and formation of advanced glycation end-products. Recent findings revealed a reduced MG scavenging efficiency in aged mouse ovaries. Therefore, we have investigated potential deleterious effects of MG on female gametes by exposing denuded (DO) and cumulus enclosed (COC) mouse oocytes from adult outbred mice (MF1,CD1) to 50-300M MG during in vitro maturation (IVM) for 16h or 19h. MG negatively affected the rate of polar body formation in both CEO and DO at 16h, with a more pronounced effect in DO. Oocytes with normal metaphase-II spindles decreased from about 73% (control) to 18% after 16h maturation in 75M MG. Moreover, oocytes in ana/telophase-I or with unaligned chromosomes were about three-to four-fold more abundant in the MG-exposed than in the control group. When maturation was prolonged to 19h MG-exposed oocytes exhibited normal appearing spindles and aligned chromosomes and increased PB rate. Time lapse analysis by polarisation microscopy confirmed that MG induced a pronounced meiotic delay. There was no increase in hyperploidy in the MG-exposed oocytes after 19h-IVM, while about 70% of meiosis I arrested oocytes had unaligned chromosomes at 16h-IVM suggesting that young oocytes are capable of dealing with a disturbance by MG by prolonging the spindle assembly checkpoint and progressing to meiosis II only when chromosomes are properly aligned and attached. CEO staining with JC-1 dye showed that MG was capable to induce changes in cytoplasmic localization of high polarized mitochondria. Furthermore, the number of foci of histone gamma H2AX increased in the nuclei of GV-arrested oocytes exposed for 5h to 75M MG, consistent with induction of DNA damage by MG. In accordance, TUNEL assay revealed about 30% apoptosis rate in CEO exposed to 300M MG. In conclusion, the present results indicate that MG may be one of the factors, which act synergistically to cause age-related changes in the ovarian and/or follicle microenvironment resulting in high susceptibility to meiotic errors and reduced developmental potential of aged oocytes
EVIDENCE FOR INTERMEDIATE-LIKE FILAMENTS IN A HETEROTRICHOUS CILIATE
No full textMOHR M, RUTHMANN A, Eichenlaub-Ritter U, KUHN S, TRAUB P. EVIDENCE FOR INTERMEDIATE-LIKE FILAMENTS IN A HETEROTRICHOUS CILIATE. EUROPEAN JOURNAL OF PROTISTOLOGY. 1990;25(3):255-263
Risks of aneuploidy induction from chemical exposure: Twenty years of collaborative research in Europe from basic science to regulatory implications
No full textKirsch-Volders M, Pacchierotti F, Parry EM, Russo A, Eichenlaub-Ritter U, Adler I-D. Risks of aneuploidy induction from chemical exposure: Twenty years of collaborative research in Europe from basic science to regulatory implications. MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH. 2019;779:126-147.Although Theodor Boveri linked abnormal chromosome numbers and disease more than a century ago, an in-depth understanding of the impact of mitotic and meiotic chromosome segregation errors on cell proliferation and diseases is still lacking. This review reflects on the efforts and results of a large European research network that, from the 1980's until 2004, focused on protection against aneuploidy-inducing factors and tackled the following problems: 1) the origin and consequences of chromosome imbalance in somatic and germ cells; 2) aneuploidy as a result of environmental factors; 3) dose-effect relationships; 4) the need for validated assays to identify aneugenic factors and classify them according to their modes of action; 5) the need for reliable, quantitative data suitable for regulating exposure and preventing aneuploidy induction; 6) the need for mechanistic insight into the consequences of aneuploidy for human health. This activity brought together a consortium of experts from basic science and applied genetic toxicology to prepare the basis for defining guidelines and to encourage regulatory activities for the prevention of induced aneuploidy. Major strengths of the EU research programmes on aneuploidy were having a valuable scientific approach based on well-selected compounds and accurate methods that allow the determination of precise dose-effect relationships, reproducibility and inter-laboratory comparisons. The work was conducted by experienced scientists stimulated by a fascination with the complex scientific issues surrounding aneuploidy; a key strength was asking the right questions at the right time. The strength of the data permitted evaluation at the regulatory level. Finally, the entire enterprise benefited from a solid partnership under the lead of an inspired and stimulating coordinator. The research programme elucidated the major modes of action of aneugens, developed scientifically sound assays to assess aneugens in different tissues, and achieved the international validation of relevant assays with the goal of protecting human populations from aneugenic chemicals. The role of aneuploidy in tumorigenesis will require additional research, and the study of effects of exposure to multiple agents should become a priority. It is hoped that these reflections will stimulate the implementation of aneuploidy testing in national and OECD guidelines
Effects of methylglyoxal-induced carbonyl stress on mitochondrial distribution and GSH-dependent redox potential in mouse oocytes
No full textTatone C, Heizenrieder T, Di Emidio G, Treffon P, Seidel T, Eichenlaub-Ritter U. Effects of methylglyoxal-induced carbonyl stress on mitochondrial distribution and GSH-dependent redox potential in mouse oocytes. Human Reproduction. 2011;26(Suppl.):I165
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