Maternal oral exposure to low-dose BPA accelerates the onset of puberty by promoting prepubertal Kiss1 expression in the AVPV nucleus of female offspring.

As the incidence of precocious puberty has risen in recent years and the age at puberty onset is younger, children may be at increased risk for health consequences associated with the early onset of puberty. Bisphenol A (BPA) is recognized as an endocrine disruptor chemical that is reported to induce precocious puberty. The effect of BPA exposure modes, times, and doses (especially low dose) were controversial. In the present study, we evaluated the potential effects of maternal exposure to low-dose BPA on the hypothalamus, particularly on the arcuate (ARC) nucleus and anteroventral periventricular (AVPV) nucleus during peri-puberty in offspring of BPA-treated rats. Pregnant rats were exposed to corn oil vehicle, 0.05 mg·kg-1·day-1 BPA, or 5 mg·kg-1·day-1 from gestation day 1 (GD1) to postnatal day 21 (PND21) by daily gavage. Body weight (BW), vaginal opening (VO), ovarian follicular luteinization, and relevant hormone concentrations were measured; hypothalamic Kiss1 and GnRH1 levels by western immunoblot analysis were also assessed as indices of puberty onset. During or after exposure, low-dose BPA restricted BW after birth (at PND1 and PND5), and subsequently accelerated puberty onset by promoting the expression of prepubertal Kiss1 and GnRH1 in the AVPV nucleus on PND30, leading to advanced VO, an elevation in LH and FSH concentrations (on PND30). We also noted increased BW on PND30 and PND35. Maternal oral exposure to low-dose BPA altered the BW curve during the neonatal and peripubertal periods, and subsequently accelerated puberty onset by promoting prepubertal Kiss1 expression in the AVPV nucleus.

Auxin alleviates cadmium toxicity by increasing vacuolar compartmentalization and decreasing long-distance translocation of cadmium in Poa pratensis.

Kentucky bluegrass (Poa pratensis L.) hyperaccumulates cadmium (Cd) and exhibits a hypertolerance. Thus, it has potential for the phytoremediation of Cd-containing soil. Auxin signaling is involved in the response to Cd stress. However, the mechanisms of auxin-mediated detoxification and Cd translocation in plants remain unclear. This study aimed to investigate the effects of exogenous application of indole-3-acetic acid (IAA) on the Cd translocation, subcellular Cd distribution, chemical forms of Cd, and transcriptional regulation of Kentucky bluegrass. The results showed that the exogenous application of IAA increased the amount of organelle-bound Cd and vacuole-compartmentalized Cd in root cells, reduced the Cd concentration in the leaf tissues (epidermis, mesophyll, and vascular bundle) and root tissues (rhizodermis and cortex) but increased in the stele, and alleviate Cd-induced leaf chlorosis and growth inhibition. The expression of genes associated with Cd transporters (ABCs, ZIPs, NASs, OPTs, and YSLs), phosphatases, oxalate decarboxylases and lignin biosynthesis were significantly regulated by exogenous IAA under Cd stress. A positive regulation of phosphatases and oxalate decarboxylases genes related to an increase in phosphate- and oxalate-bound Cd, as well as a decrease in pectate- and protein-bound Cd and inorganic Cd, thereby contributing to a decrease in Cd phytotoxicity. The significant regulation of Cd transporters associated with decreasing the long-distance translocation of Cd, and the activation of lignin biosynthesis may contribute to the development of root endodermal barriers and increase the deposition of undissolved Cd phosphates and oxalate-bound Cd in the stele. These results revealed the important role of auxin in Cd detoxification and translocation in Kentucky bluegrass and they provide a theoretical basis for the phytoremediation of Cd-containing soil.

Bisphenol A exposure advances puberty onset by changing Kiss1 expression firstly in arcuate nucleus at juvenile period in female rats.

Bisphenol A (BPA) is ubiquitous in the environment and its adverse effects on precocious puberty have been reported. But its mechanism is not clear. In the present study, the potential effects of BPA on endocrine functions of hypothalamus, especially in the arcuate (ARC) nucleus and anteroventral periventricular (AVPe) nucleus, were studied from postnatal day 15 (PND15) to PND35 in female Sprague-Dawley (SD) rats. Neonatal rats were exposed to 0.5 mg·kg-1·day-1 BPA or corn oil vehicle from PND1 to PND14 via intramuscular injection. From PND20 to PND 25, BPA caused enrichment of H3K4me2 and H3K4me3 at Kiss1 promoter, concurrent with elevated gene expressions of Kiss1 and GnRH1 in ARC and strikingly increased serum E2 levels in BPA group on PND25. Until PND30, BPA induced obviously overexpression of Kiss1 and GnRH1 in AVPe nucleus. Subsequently, the vagina opening and first ovulation had occurred earlier in rats with BPA exposure in respect to vehicle by PND35. In this study, it is suggested that the effects of BPA on precocious puberty may be due to its action to activate Kiss1 gene in ARC during the juvenile period (from PND20 to PND25) firstly, subsequently to evoke the AVPe neurons, resulting in precocious puberty in the end.