Influence of sawdust addition on the toxic effects of cadmium and copper oxide nanoparticles on Vigna radiata seeds.

Studies in the literature concern the toxicity of nanoparticles either in a Petri dish or in agar media-based tests. Therefore, for environmental relevance, individual and binary mixtures of metal oxide nanoparticles (M-NPs) cadmium oxide (CdO-NP) and copper oxide (CuO-NP) were tested in this study for their effect on Vigna radiata in soil with and without the addition of sawdust. Seed germination was 67% in 100 mg CuO-NP in soil without sawdust. Seeds failed to germinate in 100 mg CdO +100 mg CuO-NPs in soil without the addition of sawdust and germination was 83% at the same concentration in soil with sawdust. In sawdust added to soil, when compared with control (soil without M-NPs), the maximum reduction in shoot (82%) and root (80%) length and wet (61%) and dry (54%) weight of plant was recorded in CdO-NP treated soil. Similarly, compared with control (soil without sawdust and M-NPs), the percent reduction in shoot (61%) and root (70%) length and wet (44%) and dry (48%) weight was highest in CdO-NP treated soil not supplemented with sawdust. In a binary mixture test (CdO-NP + CuO-NP), the addition of sawdust promoted the above plant growth parameters compared with individual CdO-NP and CuO-NP tests. Cadmium (511 mg kg-1 for individual and 303 mg kg-1 for binary mixture tests) and Cu (953 mg kg-1 for individual and 2954 mg kg-1 for binary mixture tests) accumulation was higher in plants grown in soil without sawdust. The beneficial effect of sawdust addition was observed in seed germination, plant growth, and metal accumulation. With or without sawdust, the binary mixture of CdO and CuO was antagonistic. These results indicate that sawdust can prevent M-NP-induced toxicity and reduce metal accumulation in plant tissues.

The Expression and Contribution of SRCs with Preeclampsia Placenta.

The steroid hormones act by binding to their receptors and subsequently interacting with coactivators. Several classes of coactivators have been identified and shown to be essential in estradiol (E2) responsiveness. The major coregulators are the p160 steroid receptor coactivator (SRC) family. Although the function of SRCs in other organs has been well studied, it has not been thoroughly studied in the placenta. In addition, the correlation between preeclampsia (PE) and SRCs has not been examined previously. Therefore, we compared the expression patterns of SRCs in normal and PE placentas. In human PE placental tissues, SRC-1 mRNA, and protein levels were downregulated in the PE group. In addition, to assess the expression of SRCs in a PE environment, we used Reduced Uterine Perfusion Pressure (RUPP) model and placental cells were cultured in hypoxia condition. SRC-1 proteins were reduced in the placenta of PE-like rat RUPP model. Furthermore, SRCs proteins were significantly downregulated in hypoxia-grown placental cells. To examine the interaction between estrogen receptors (ERs) and SRC-1 protein, we performed co-immunoprecipitation. The interaction of SRC-1 with ERα was significantly stronger than that with ERß. In PE placenta, the interaction of both ERα and ERß with SRC-1 was stronger than that in normal placenta. In summary, our results demonstrate that expression levels of SRC-1, not SRC-2 and SRC-3, were decreased in hypoxia-induced PE placenta, which may further reduce the signaling of sex steroid hormones such as E2. The dysregulated signaling of E2 by SRC-1 expression could be associated with the PE placental symptoms of patients.

Pregnenolone sulfate regulates prolactin production in the rat pituitary.

Pregnenolone sulfate (PS) is a neuroactive steroid hormone produced in the brain. In this study, the effects of PS on synthesis and secretion of rat pituitary prolactin (PRL) were examined. To accomplish this, GH3 rat pituitary adenoma cells were treated with PS, which showed significantly increased mRNA and protein levels of PRL compared with the control. The mechanism of action responsible for the effects of PS on PRL synthesis and secretion was investigated by pretreating cells with inhibitors of traditional PRL- or the PS-related signaling pathway. PS-stimulated PRL transcription was significantly reduced by inhibitors of PKA, PKC and MAPK, but unchanged by GABAAR and NMDAR inhibitors. Western blotting analysis revealed that the total ERK1/2 level was upregulated in a time-dependent manner following PS treatment. An approximate 10% increase in GH3 cell proliferation was also observed in response to PS relative to the control. In the animal study, levels of PRL in the pituitary and in serum were elevated by PS. PS-stimulated PRL synthesis was also found to be associated with decreased expression of PRL target genes such as GNRH1, FSHB and LHB. These findings show that PS upregulates PRL synthesis and secretion in vivo and in vitro via MAPK signaling, suggesting that it has the potential for use as a therapeutic hormone to treat PRL-related disorders such as hypoprolactinemia and low milk supply.