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Published in Asim Kurjak, Ultrasound and Infertility, 2020
Joseph G. Schenker, Aby Lewin, Menashe Ben-David
Hyperprolactinemia may result in a decrease of gonadotropin secretion and/or an inhibition of synthesis of adequate amounts of estradiol most needed within the follicular microenvironment for normal folliculogenesis and ovulation.
The role of non-ionizing electromagnetic radiation on female fertility: A review
Published in International Journal of Environmental Health Research, 2023
Pooja Jangid, Umesh Rai, Radhey Shyam Sharma, Rajeev Singh
According to the findings of this review, it can be concluded that non-ionizing EMRs radiated from cell phones, laptops, bluetooth devices, microwave ovens, or wireless networks might have detrimental effects on female fertility. Non-ionizing radiations can have destructive effects on ovary and uterus, affecting several reproduction parameters in females, such as folliculogenesis, oocyte morphology, and differentiation, hormones, reproductive cycle, and could lead to DNA damage. These effects may lead to subfertility and infertility due to increased free radical load and oxidative stress in the ovaries and uterus generated by these radiations. However, the effect of non-ionizing radiation on human gamete vis-à-vis female fertility is still poorly understood. Also, the findings of a whole-body EMR exposure in the same animal do not anticipate the results of a local EMR exposure. As a result, the outcomes of whole-body EMR exposure in animals cannot be directly compared to the outcomes of local EMR exposure in humans while using cell phones. Unfortunately, specific frequency and SAR value that causes impairment in the reproductive parameters and the exact mechanism of EMR action are not known so far. Moreover, further investigations are required to elucidate the role of EMR from mobile phones, Wi-Fi, and other devices in female fertility. Lastly, it is the need of the hour to understand the exact mechanism of EMR action on female fertility, establish safe exposure limits, and overcome the radiation effects.
Increasing cannabis use and importance as an environmental contaminant mixture and associated risks to exposed biota: A review
Published in Critical Reviews in Environmental Science and Technology, 2022
Emily K. C. Kennedy, Genevieve A. Perono, Dion B. Nemez, Alison C. Holloway, Philippe J. Thomas, Robert Letcher, Chris Marvin, Jorg Stetefeld, Jake Stout, Oliver Peters, Vince Palace, Gregg Tomy
Investigation into the effects of increased cannabis usage on the aquatic environment is a relatively new field of research. By consequence, there are many potential toxicological mechanisms of action that have yet to be explored in aquatic organisms. Endocrine disrupting chemicals are known to adversely affect wild fathead minnow populations (Kidd et al., 2007) and, based on research conducted in other species, cannabinoids and their metabolites have the potential to interfere with a variety of endocrine-related systems. There is evidence that endocannabinoids are involved in many processes related to female and male reproduction. The ECS is expressed across reproductive cells and tissues including the testis, prostate, sperm, ovary, uterus, placenta, and hypothalamic-pituitary-gonadal (HPG) axis; influencing signals mediated by sex hormones like estrogen, androgen and progesterone (Battista et al., 2012; Dobovišek et al., 2016; Gammon et al., 2005; Schuel et al., 2002; Walker et al., 2019). The complex interplay between endogenous endocannabinoids and their receptors are critical for normal reproductive function; these processes, including spermatogenesis, oogenesis, embryonic development, placentation, fertility, and folliculogenesis, may be perturbed in the presence of exogenous ligands such as Δ9-THC and CBD (Amoako et al., 2013; El-Talatini et al., 2009; Grimaldi et al., 2009; Maia et al., 2019; Walker et al., 2019). Additionally, other hormones such as glucocorticoids can modulate the HPG axis (Reviewed in: (Geraghty & Kaufer, 2015), and cannabinoids have been shown to influence glucocorticoid receptor (GR)-mediated signaling making it plausible that cannabinoids can adversely affect reproductive behavior and physiology via GR (Eldridge et al., 1991; Natale et al., 2020; Whirledge & Cidlowski, 2010).
Toxic and carcinogenic effects of hexavalent chromium in mammalian cells in vivo and in vitro: a recent update
Published in Journal of Environmental Science and Health, Part C, 2022
Shehnaz Islam, Sreejata Kamila, Ansuman Chattopadhyay
Exposure to high concentrations of Cr (VI) in drinking water (≥250 ppm) is reported to decrease ovarian follicle counts and increase follicular atresia in mice. However, a lower environmentally relevant concentration of Cr (VI) (0.1–150 ppm) did not induce ovarian toxicity in B6C3F1 mice even after 90 days exposure through drinking water.111 Persistent hexavalent chromium exposure, on the other hand, impaired the pubertal development and ovarian histoarchitecture in Wistar rat offspring.98 Exposure of 25 ppm potassium dichromate through drinking water in pregnant rats resulted in early reproductive senescence due to increase in the levels of apoptosis in germ cells and breakdown in advancing germ cell cyst in the F1 offsprings.100 The study also demonstrated that gestational exposure to Cr (VI) increased Cr concentration in the placenta, accelerated apoptosis of the germ cells through the up-regulation of p53/p27-Bax-caspase-3 proteins and increased co-localization of p53-SOD-2. Prenatal exposure to Cr (VI) in rats decreased pregnancy outcomes and reduced litter size throughout age, while Cr (IV) exposure through lactation increased follicular atresia.100 Primordial follicle numbers within the ovary are important determinants of the lifetime follicle reserve and folliculogenesis. Accelerated breakdown of germ cell cyst (GCC), advanced assembly of the primordial follicle, transition in primary follicle and downregulation of p-AKT, p-ERK, and XIAP proteins were also observed after exposure to Cr (VI).100 Treatment of Sprague-Dawley rats with 5, 10, 25, 50, 100, and 200 ppm of Cr (VI) resulted in an increase of follicular atresia and follicular cell apoptosis, along with depletion of steroid hormones like estradiol (E2), testosterone (T), and progesterone (P4) in a dose-dependent manner.102