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Adulthood and driving in the candida telomerase RNP: building new things using reused components.
In this chapter, we first gave a brief introduction to the detriments of cigarette smoking, with an emphasis on its adverse effects on female reproductive health. Then, we outlined recent advances about the impacts of cigarette smoke on preimplantation embryo development. Additionally, toxicities of cadmium and benzo(a)pyrene (BaP) at this specific developmental window were also discussed, to illustrate the potential mechanisms involved in cigarette smoke-associated embryotoxicity. Finally, we provide an overview of the issues to be solved in the future research. Further studies about the molecular mechanism of cigarette smoking-associated female infertility may provide vital insights into developing new interventions for the women smokers and thus improving their reproductive outcomes.Anovulatory disorder comprises around 30% of female infertility. The origin of ovulatory failure is rooted in pituitary FSH secretion. Any factor or process that disrupts the finely tuned interactions of hypothalamo-pituitary-ovarian axis can potentially lead to anovulation. The World Health Organization (WHO) has classified anovulatory disorders into three categories hypothalamic-pituitary failure, hypothalamic-pituitary dysregulation, and ovarian failure. Due to industrial development, environmental pollution, and global warming, the human living environment has undergone tremendous changes. Abivertinib Industrial waste, noise, pesticides, fertilizers, and vehicular emission are visible pollutants responsible for environmental contamination and ill effects on health of all living systems. A considerable body of research suggests that chemical exposures in the environment or workplace may be associated with endocrine disruption of the synthesis, secretion, transport, binding, or elimination of natural hormones. For instance, some advanced biological mechanisms suggest that heavy metals may affect progesterone production, which possibly disturbs endocrine function in pregnant women. On the other hand, our lifestyle factors have also changed accordingly, which greatly influence overall health and well-being, including fertility. Many lifestyle factors such as nutrition, weight, exercise, and psychological stress can have substantial effects on female ovulation.Premature ovarian insufficiency (POI) or primary ovarian failure is defined as a cessation of the menstrual cycle in women younger than 40 years old. It is strictly defined as more than 4 months of oligomenorrhea or amenorrhea in a woman 25 U/L in the menopausal range, detected more than 4 weeks apart. It is estimated that POI was affected 1 and 2% of women. Although 80% of POI cases are of unknown etiology, it is suggested that genetic disorder, autoimmune origin, toxins, and environmental factors, as well as personal lifestyles, may be risk factors of developing POI. In this section, we will discuss the influences of environmental and lifestyle factors on POI. Moreover updated basic research findings regarding how these environmental factors affect female ovarian function via epigenetic regulations will also be discussed.Endocrine-disrupting chemicals (EDCs) exist ubiquitously in the environment. Epidemiological data suggest that the increasing prevalence of infertility may be related to the numerous chemicals. Exposure to EDCs may have significant adverse impacts on the reproductive system including fertility, ovarian reserve, and sex steroid hormone levels. This chapter covers the common exposure ways, the origins of EDCs, and their effects on ovarian function, follicular genesis, and oocyte quality. Furthermore, we will review the origin and the physiology of ovarian development, as well as explore the mechanisms in which EDCs act on the ovary from human and animal data. And then, we will focus on the bisphenol A (BPA), which has been shown to reduce fertility and ovarian reserve, as well as disrupt steroidogenesis in animal and human models. Finally, we will discuss the future direction of prevention and solution methods.The female reproductive process is very complicated, including multiple processes. Each process is different and plays a vital role in reproduction. If some reproductive diseases occur, these processes will be abnormal, causing infertility problem. In this Chapter, we will describe the female reproductive process and their corresponding reproductive diseases.In this Chapter, we systematically and comprehensively described various environmental harmful factors. They were classified into four aspects physical factors, chemical factors, biological factors, and physiological and psychological stress factors. Their classification, modes of presence, toxicity and carcinogenicity, routes of exposure to human and toxic effects on the female reproductive health were introduced. It is expected that the exposure routes could be controlled and eliminated, and the pathogenic mechanism of environmental harmful factors should be investigated and explained to protect female reproductive health.Preeclampsia complicates 5-8% of all pregnancies worldwide, and although its pathophysiology remains obscure, placental oxidative stress and mitochondrial abnormalities are considered to play a key role. Mitochondrial abnormalities in preeclamptic placentae have been described, but the extent to which mitochondrial content and the molecular pathways controlling this (mitochondrial biogenesis and mitophagy) are affected in preeclamptic placentae is unknown. Therefore, in preeclamptic (n = 12) and control (n = 11) placentae, we comprehensively assessed multiple indices of placental antioxidant status, mitochondrial content, mitochondrial biogenesis, mitophagy, and mitochondrial fusion and fission. In addition, we also explored gene expression profiles related to inflammation and apoptosis. Preeclamptic placentae were characterized by higher levels of oxidized glutathione, a higher total antioxidant capacity, and higher mRNA levels of the mitochondrial-located antioxidant enzyme manganese-dependent superoxide dismutase 2 compared to controls. Furthermore, mitochondrial content was significantly lower in preeclamptic placentae, which was accompanied by an increased abundance of key constituents of glycolysis. Moreover, mRNA and protein levels of key molecules involved in the regulation of mitochondrial biogenesis were lower in preeclamptic placentae, while the abundance of constituents of the mitophagy, autophagy, and mitochondrial fission machinery was higher compared to controls. In addition, we found evidence for activation of apoptosis and inflammation in preeclamptic placentae. This study is the first to comprehensively demonstrate abnormalities at the level of the mitochondrion and the molecular pathways controlling mitochondrial content/function in preeclamptic placentae. These aberrations may well contribute to the pathophysiology of preeclampsia by upregulating placental inflammation, oxidative stress, and apoptosis. Graphical Abstract.
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