Human Reproduction Functions: Evaluation with Radiobioassay
Fuad S. Ashkar, Lelio G. Colombetti in Radiobioassays, 2019
Of further interest is another prolactin-releasing hormone, TRH. If an antiserum to TRF is given in rats both TSH and prolactin levels in the circulation drop.34 Conversely, a TRF bolus given i.v. in the human increases the circulating levels of both prolactin and thyroid hormones. Prolactin shows a diurnal pattern of release highest during nighttime sleeping hours and lowest during the daytime waking hours.35 This pattern occurs in both males and females of all ages. Phenothiazines, methyldopa, and reserpine interfere with dopamine metabolism and augment circulating dopamine levels. These are dopamine agonists. Of clinical significance is the data showing that estrogens increase prolactin secretion and release. Birth control pills, especially the sequential type, correlate with higher levels of circulating prolactin.36 Progesterone can also cause an elevation of prolactin secretion in vivo. Glucocorticoids decrease prolactin secretion.
Prolactin
George H. Gass, Harold M. Kaplan in Handbook of Endocrinology, 2020
A great deal of progress has been made regarding the regulation of prolactin secretion by the hypothalamus. The identity of the prolactin-releasing hormone, if one exists, and a complete uderstanding of paracrine and autocrine regulation of prolactin secretion within the pituitary gland need to be established.
Breastfeeding
Alison Edwards in Postnatal and Neonatal Midwifery Skills, 2020
Prolactin-releasing hormone (from the hypothalamus) stimulates prolactin (from the anterior pituitary) production which in turn stimulates the acini cells of the breasts to produce milk. Prolactin release peaks towards the end of feeds.
Effects of atrazine on fish, amphibians, and reptiles: update of the analysis based on quantitative weight of evidence
Published in Critical Reviews in Toxicology, 2019
Mark L. Hanson, Keith R. Solomon, Glen J. Van Der Kraak, Richard A. Brian
In studies on reptiles (Russart and Rhen 2016), eggs (stage 20) of snapping turtles (Chelydra serpentina) were exposed to concentrations equivalent to 2 and 40 μg atrazine/L (of egg). Exposures were not measured so penetration into the egg was not confirmed. Only responses in gene expression in the hypothalamus were reported. No effects were observed on any of the measured genes in embryos tested 24-h after treatment. One week after treatment, expressions of several genes (androgen receptor, proopiomelanocortin, kisspeptin receptor, aromatase, prodynorphin) were significantly increased but only at 2 and not at 40 μg atrazine/L. The only gene (prolactin releasing hormone) tested six months after exposure was significantly increased at 2 but not at 40 μg atrazine/L. No apical endpoints were reported so it is not possible to judge relevance. The lack of a consistent concentration-response and complete lack of effect of relatively large dose of estradiol (0.5 μg/egg) on any of these genes raises questions about the conduct and validity of the study. As no measures of exposure were reported, a mix-up of the 2 μg atrazine/L and estradiol treatments cannot be ruled out.
Atrazine neural and reproductive toxicity
Published in Toxin Reviews, 2022
Hamidreza Sadeghnia, Sara Shahba, Alireza Ebrahimzadeh-Bideskan, Shabnam Mohammadi, Amir Mohammad Malvandi, Abbas Mohammadipour
Some studies showed a delay in crabs' ovarian growth with reduction in vitellogenin protein after atrazine treatment (Silveyra et al. 2017, 2020). A study by Papoulias showed that the number of mature oocytes was lower in atrazine exposed Japanese medaka ovaries (Papoulias et al. 2014). Wirbisky et al. (2016b) showed that follicular atresia induced by atrazine is also associated with progesterone level elevation (Wirbisky et al. 2016b). Atrazine increases adenylate cyclase-activating peptide 1 (ADCYAP1) in zebrafish ovarian tissue, which causes elevation of the progesterone level (Wirbisky et al. 2016b). On the other hand, it is demonstrated that higher progesterone levels inhibit ovarian follicle development and can lead to follicular atresia (Telfer et al. 1991). Reduction in egg production by fathead fish was observed previously after atrazine exposure (Tillitt et al. 2010). Since atrazine decreases the expression of zona pellucida glycoprotein 3.1 (zp3.1) (Richter et al. 2016), the decrease in egg production after atrazine exposure may result from downregulation of genes required for reproduction such as zp3.1. According to the current evidence, another effect of atrazine on the female reproductive system is through the hypothalamic-pituitary-ovarian axis. It is well documented that this herbicide decreases the expression of gonadotropin-releasing hormone (GnRH) in the hypothalamus, luteinizing hormone (LH) in the pituitary, and FSH in the ovary (Qin et al. 2015). A previous study also reported that some essential hypothalamic genes in turtle, including kisspeptin receptor 1 (Kiss1R), pro-opiomelanocortin (POMC), CYP19A1, prodynorphin (PDYN) and prolactin-releasing hormone (PRLH) expression, are altered by atrazine, evidencing the adverse effects of this herbicide on both hypothalamic-pituitary-gonadal and hypothalamic-pituitary-adrenal axes (Russart and Rhen 2016).
Related Knowledge Centers
- Estrogen
- Leukemia Inhibitory Factor
- Oxytocin
- Vasoactive Intestinal Peptide
- Prostaglandin
- Dopamine
- Prolactin
- Thyrotropin-Releasing Hormone
- Hypothalamic–Pituitary–Prolactin Axis