Adsorptive Removal of Arsenic and Mercury from Aqueous Solutions by Eucalyptus Leaves

The study is a first-time investigation into the use of Eucalyptus leaves as a low-cost herbal adsorbent for the removal of arsenic (As) and mercury (Hg) from aqueous solutions. The adsorption capacity and efficiency were studied under various operating conditions within the framework of response surface methodology (RSM) by implementing a four-factor, five-level Box–Wilson central composite design (CCD). A pH range of 3–9, contact time (t) of 5–90 min, initial heavy metal (As or Hg) concentration (C 0) of 0.5–3.875 mg/L, and adsorbent dose (m) of 0.5–2.5 g/L were studied for the optimization and modeling of the process. The adsorption mechanism and the relevant characteristic parameters were investigated by four two-parameter (Langmuir, Freundlich, Temkin, and Dubinin–Radushkevich) isotherm models and four kinetic models (Lagergren’s pseudo-first order (PFO), Ho and McKay’s pseudo-second order (PSO), Weber–Morris intraparticle diffusion, and modified Freundlich). The new nonlinear regression-based empirical equations, which were derived within the scope of the study, showed that it might be possible to obtain a removal efficiency for As and Hg above 94% at the optimum conditions of the present process-related variables (pH = 6.0, t = 47.5 min, C 0 = 2.75 mg/L, and m = 1.5 mg/L). Based on the Langmuir isotherm model, the maximum adsorption or uptake capacity of As and Hg was determined as 84.03 and 129.87 mg/g, respectively. The results of the kinetic modeling indicated that the adsorption kinetics of As and Hg were very well described by Lagergren’s PFO kinetic model (R 2 = 0.978) and the modified Freundlich kinetic model (R 2 = 0.984), respectively. The findings of this study clearly concluded that the Persian Eucalyptus leaves demonstrated a higher performance compared to several other reported adsorbents used for the removal of heavy metals from the aqueous environment.Funding Information The authors would like to thank Tehran University of Medical Sciences for financial support.Scopu

Lipopolysaccharide- And lipoteichoic acid-mediated pro-inflammatory cytokine production and modulation of TLR2, TLR4 and MyD88 expression in human endometrial cells

Background: Toll-like receptor (TLR)-mediated inflammatory processes are supposed to be involved in pathophysiology of spontaneous abortion and preterm labor. Here, we investigated functional responses of human endometrial stromal cells (ESCs) and whole endometrial cells (WECs) to lipopolysaccharide (LPS) and lipoteichoic acid (LTA). Methods: Endometrial tissues were obtained from 15 cycling women who underwent laparoscopic tubal ligation. Modulation of TLR2, TLR4 and MyD88 expression and production of pro-inflammatory cytokines by WECs and ESCs in response to LPS and LTA were assessed. Results: WECs and ESCs expressed significant levels of TLR4 and MyD88 transcripts but, unlike WECs, ESCs failed to express TLR2 gene. Regardless of positive results of Western blotting, ESCs did not express TLR4 at their surface as judged by flow cytometry. Immunofluorescent staining revealed intracellular localization of TLR4 with predominant perinuclear pattern. LPS stimulation marginally increased TLR4 gene expression in both cell types, whereas such treatment significantly upregulated MyD88 gene expression after 8 hr (p<0.05). At the protein level, however, LPS activation significantly increased TLR4 expression by ESCs (p<0.05). LTA stimulation of WECs was accompanied with non-significant increase of TLR2 and MyD88 transcripts. LPS and LTA stimulation of WECs caused significant production of IL-6 and IL-8 in a dosedependent manner (p<0.05). Similarly, ESCs produced significant amounts of IL-6, IL-8 and also TNF-α in response to LPS activation (p<0.05). Conclusion: Our results provided further evidence of initiation of inflammatory processes following endometrial TLR activation by bacterial components which could potentially be harmful to developing fetus

Placental Kisspeptins Differentially Modulate Vital Parameters of Estrogen Receptor-Positive and -Negative Breast Cancer Cells.

Kisspeptins (KPs) are major regulators of trophoblast and cancer invasion. Thus far, limited and conflicting data are available on KP-mediated modulation of breast cancer (BC) metastasis; mostly based on synthetic KP-10, the most active fragment of KP. Here, we report for the first time comprehensive functional effects of term placental KPs on proliferation, adhesion, Matrigel invasion, motility, MMP activity and pro-inflammatory cytokine production in MDA-MB-231 (estrogen receptor-negative) and MCF-7 (estrogen receptor-positive). KPs were expressed at high level by term placental syncytiotrophoblasts and released in soluble form. Placental explant conditioned medium containing KPs (CM) significantly reduced proliferation of both cell types compared to CM without (w/o) KP (CM-w/o KP) in a dose- and time-dependent manner. In MDA-MB-231 cells, placental KPs significantly reduced adhesive properties, while increased MMP9 and MMP2 activity and stimulated invasion. Increased invasiveness of MDA-MB-231 cells after CM treatment was inhibited by KP receptor antagonist, P-234. CM significantly reduced motility of MCF-7 cells at all time points (2-30 hr), while it stimulated motility of MDA-MB-231 cells. These effects were reversed by P-234. Co-treatment with selective ER modulators, Tamoxifen and Raloxifene, inhibited the effect of CM on motility of MCF-7 cells. The level of IL-6 in supernatant of MCF-7 cells treated with CM was higher compared to those treated with CM-w/o KP. Both cell types produced more IL-8 after treatment with CM compared to those treated with CM-w/o KP. Taken together, our observations suggest that placental KPs differentially modulate vital parameters of estrogen receptor-positive and -negative BC cells possibly through modulation of pro-inflammatory cytokine production

The impact of particulate matters on apoptosis in various organs: Mechanistic and therapeutic perspectives

Ecological air contamination is the non-homogenous suspension of insoluble particles into gas or/and liquid fluids known as particulate matter (PM). It has been discovered that exposure to PM can cause serious cellular defects, followed by tissue damage known as cellular stress. Apoptosis is a homeostatic and regulated phenomenon associated with distinguished physiological actions inclusive of organ and tissue generation, aging, and development. Moreover, it has been proposed that the deregulation of apoptotic performs an active role in the occurrence of many disorders, such as autoimmune disease, neurodegenerative, and malignant, in the human population. Recent studies have shown that PMs mainly modulate multiple signaling pathways involved in apoptosis, including MAPK, PI3K/Akt, JAK/STAT, NFκB, Endoplasmic Stress, and ATM/P53, leading to apoptosis dysregulation and apoptosis-related pathological conditions. Here, the recently published data concerning the effect of PM on the apoptosis of various organs, with a particular focus on the importance of apoptosis as a component in PM-induced toxicity and human disease development, is carefully discussed. Moreover, the review also highlighted the various therapeutic approaches, including small molecules, miRNA replacement therapy, vitamins, and PDRN, for treating diseases caused by PM toxicity. Notably, researchers have considered medicinal herbs a potential treatment for PM-induced toxicity due to their fewer side effects. So, in the final section, we analyzed the performance of some natural products for inhibition and intervention of apoptosis arising from PM-induced toxicity

Effect of term placental kisspeptins on proliferation of MDA-MB-231 and MCF-7 breast cancer cells.

<p>MDA-MB-231 (A) and MCF7 (B) cells were treated with different media as indicated in the figure for 24, 48 and 72 hr. All treatments were performed in six replicas. The extent of proliferation was measured by Propidium Iodide (PI) fluorometric assay. Significant differences were analyzed by Kruskal-Wallis test with a Dunnett’s posthoc test. Different dilutions from 1:2 to 1:8 were tested. CM: Term placenta conditioned medium containing KP, CM-w/o KP: KP-free CM, anti-KP: anti-Kp-54/Kp-145 antibody, Rb Ig: Rabbit immunoglobulin, Medium: Culture medium alone, KP: Kisspeptin. Results are representative of 7 term placentas. * CM <i>vs</i>. CM-w/o KP(p<0.05–0.01 for MDA-MB-231 and p<0.05–0.001 for MCF-7), φ CM <i>vs</i>. medium (p<0.01–0.001 for MDA-MB-231 and p<0.05–0.01 for MCF-7), β CM <i>vs</i>. CM+anti-KP-10 (p<0.05–0.01 for MDA-MB-231 and p<0.05 for MCF-7), Φ CM-w/o KP <i>vs</i>. medium (p<0.05–0.001 for MDA-MB-231 and p<0.05 for MCF-7), ψ KP-10 <i>vs</i>. medium (p<0.05–0.01 for MDA-MB-231 and p<0.05–0.01 for MCF-7).</p

Effect of term placental kisspeptins on adhesion of MDA-MB-231 and MCF-7 breast cancer cells.

<p>MDA-MB-231 (A) and MCF-7 (B) cells were treated with different media as indicated in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0153684#pone.0153684.g003" target="_blank">Fig 3</a> for 150 min and their adhesion to fibronectin-coated plates was assessed by a colorimetric assay. Different dilutions from 1:2 to 1:8 were tested. CM: Term placenta conditioned medium containing KP, CM-w/o KP: KP-free CM, anti-KP: anti-Kp-54/Kp-145 antibody, Rb Ig: Rabbit immunoglobulin, Medium: Culture medium alone, KP: Kisspeptin. Results are representative of 11 term placentas. * CM <i>vs</i>. CM-w/o KP(p<0.05 for MDA-MB-231).</p

Effect of term placental kisspeptins on invasiveness of MDA-MB-231 and MCF-7 breast cancer cells.

<p>MDA-MB-231 (A) and MCF-7 (B) cells were treated with supernatants of cultured term placental explants containing KP (CM), CM plus 1 μM KISS1R antagonist; P-234, KP-free CM (CM-w/o KP), KP-10 or culture medium alone and their invasion toward chemo attractant (FCS) through Matrigel-coated filters was investigated. Invading cells was enumerated in 50 random fields (Ab and Bb) and expressed as percentage of corresponding controls (Aa and Ba). C) Gelatin zymographic analysis for matrix metalloproteinase (MMP) expression. MDA-MB-231 cells treated with CM released higher amounts of MMP2 and MMP9 compared to those treated with either CM-w/o KP. In parallel, cells treated with KP-10 showed slightly higher MMP9 activity in comparison to cultured in medium alone. Cells treated with Phorbol 12-myristate 13-acetate (PMA) served as positive control. CM failed to express detectable levels of MMP2 and MMP9. Results of two (denoted by numbers) out of four samples are shown. KP: Kisspeptin, MW: Molecular weight.</p

Effect of term placental kisspeptins on motility of MDA-MB-231 and MCF-7 breast cancer cells.

<p>MDA-MB-231 (A) and MCF-7 (B) cells were treated with supernatants of cultured term placental explants containing KP (CM), KP-free CM (CM-w/o KP), KP-10 or culture medium alone and their migration toward scratch was monitored during a period of 30 hr. Representative photographs are shown in Aa (MDA-MB-231) and Ba (MCF-7). Percent of reduction in scratched areas at each time point compared to initial time point was measured and analyzed using Image J software (Ab for MDA-MB-231 and Bb for MCF-7). Treatment with P-234 reversed the effect of CM on motility of MDA-MB-231 (Ac) and MCF-7 (Bc). Co-treatment with selective ER modulators inhibited the effect of CM on motility of MCF-7 cells (Bc). * CM <i>vs</i>. CM-w/o KP (p<0.05–0.001 for MDA-MB-231 and p<0.05–0.001), φ CM <i>vs</i>. medium (p<0.01–0.001 for MDA-MB-231 and p<0.001–0.0001 for MCF-7), ψ KP-10 <i>vs</i>. medium (p<0.05–0.01 for MDA-MB-231 and p<0.01–0.0001 for MCF-7),? CM <i>vs</i>. CM-w/o KP and CM+P-234 (p<0.05),? CM-w/o KP, CM+P-234, CM+100 nm Tam and CM+1 nm Ral <i>vs</i>. CM (p<0.05). Results are representative of 4 term placentas. Tam: Tamoxifen, Ral: Raloxifene.</p

Kisspeptin expression by human term placenta.

<p>A) Sections of human term (TP) and first trimester (FTP) placenta were double stained with anti-Kp-54/Kp-145 and anti-CK7, a syncytiotrophoblast (STB) marker. Nuclei were counterstained with DAPI. Kisspeptin was mainly localized to apical and basal surfaces of the STBs. B) Isolated cytotrophoblasts failed to express KISS1. A contaminating positive cell, most probably a STB, has been shown by white arrow. In negative control slides, primary antibody was substituted by non-immune rabbit sera. C) Western blotting of FTP and TP (from three placentas denotes as TP1-3). Lysates were probed with anti-Kp-54/Kp-145 antibody. The antibody produced one prominent band at ~15–16 kDa, which is in good agreement with the calculated MW for Kp-145 (15.391 kDa). With purified Kp-10, anti-Kp-54/Kp-145 produced a single band at about 1.5 kDa, which is in good agreement with the theoretical MW for Kp-10-13. β-actin served as loading control. D) Western blotting of conditioned medium (CM) collected from cultured term placental explants at different time points (1–72 hr). KP was released from placental explants in as early as 1 hr after initiation of culture, peaked at 4–6 hr and then progressively decreased until 72 hr. No KISS1-specific band was observed after KP removal (CM-w/o KP) by immuno precipitation. E) RT-PCR analysis of KISS1expression in total RNA freshly isolated from TP (representative experiment). β-actin served as loading control. No amplification controls (NAC) always were shown to be negative. The presence of KPs in CM was also confirmed by capture ELISA using two fold serially-diluted CMs. The results showed a positive correlation between CM concentration and OD (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0153684#pone.0153684.g001" target="_blank">Fig 1F</a>). Results are representative of 11 term and 3 first trimester placentas. KPs: Kisspeptin, CK7: Cytokeratin 7, TP: Term placenta, FTP: First trimester placenta, NC: Negative control. Scale bar: A; 100 μm, B; 50μm.</p