Toxic effects of chromium on the aquatic cyanobacterium Oscillatoria sp and removal of chromium by biosorption

“Chromium” is a non-essential metal for microorganisms and plants and a serious pollutant in diverse environment conditions. The hexavalent form of the metal Cr (IV) is considered to be more toxic than relatively harmless Cr(III) form. Certain microorganisms in the environment are able to tolerate high levels of Cr due to their resistance mechanism. In the present work we report the toxic effect of chromium on Oscillatoria sp and the removal of hexavalent using the cyanobacterium Oscillatoria sp., by biosorption method. Oscillatoria sp., was grown in BG-11 medium containing different concentration of Cr. Effect of Cr on cellular metabolism was studied by estimating the amount of chlorophyll a, carotenoids,  c. phycocyanin, allophycocyanin, sugars, free amino acids and proteins at various metal concentration. An increase in metal concentration caused a decrease in the growth of the Oscillatoria sp., and also decreased the cellular contents like chlorophyll a, carotenoids, c.phycocyanin, allophycocyanin, sugars, free amino acids and proteins. Biosorption of chromium by Oscillatoria sp., was carried out using living cells, heat killed cells and pre-treated cells. Results showed that high amount of metal were adsorbed by heat killed and living cells of Oscillatoria sp. The experimental conditions used in the present work are simple and have low operational cost. The proposed biosorption method is economically feasible and eco-friendly in nature

Seaweed extract as a biostimulant for legume crop, green gram

The aim of this research is to investigate the effect of seaweed extracts obtained from the marine green algae, Ulva lactuca Linnaeus, Caulerpa scalpelliformis (R. Brown ex Turner) C. Agardh, brown algae Sargassum plagiophyllum C. Agardh, Turbinaria conoides (J. Agardh) Kutzing, Padina tetrastromatica Hauck, Dictyota dichotama (Hudson) J. V. Lamouroux on the stimulate germination, growth parameters of the Vigna radiata. The present study reveals the seeds germination, fresh weight and dry weight of shoots and roots. These results suggested that seaweed extracts stronger induce seed germination and growth parameters

Hydrogenolysis of sorbitol over Ni, Pt and Ru supported on SBA-15

Hydrogenolysis of sorbitol (15% aqueous solution) has been carried out in a batch reactor over Ni (6 wt%), Pt (1 wt%) and Ru (1 wt%) supported on SBA-15 and carbon coated SBA-15 (SBA-15(C)). For comparison, the three metals have also been supported on activated carbon (AC). The catalysts are characterized by XRD, N2 and H2 adsorption measurements. Addition of Ca(OH)2 to the reaction mixture increases conversion and selectivity for the dihydroxy compounds, 1,2-propanediol (PD) and ethylene glycol (EG). Based on yield of dihydric alcohols (PD+EG), the performance of the catalysts at 220 °C and 60 bar in the presence of Ca(OH)2 is in the order: Ru-AC ~ Ru-SBA-15(C) > Ru-SBA-15 ~ Ni-SBA-15, the yields being 40, 39, 31 and 29 wt%, respectively

Sodium-coupled Monocarboxylate Transporters in Normal Tissues and in Cancer

SLC5A8 and SLC5A12 are sodium-coupled monocarboxylate transporters (SMCTs), the former being a high-affinity type and the latter a low-affinity type. Both transport a variety of monocarboxylates in a Na+-coupled manner. They are expressed in the gastrointestinal tract, kidney, thyroid, brain, and retina. SLC5A8 is localized to the apical membrane of epithelial cells lining the intestinal tract and proximal tubule. In the brain and retina, its expression is restricted to neurons and the retinal pigment epithelium. The physiologic functions of SLC5A8 include absorption of short-chain fatty acids in the colon and small intestine, reabsorption of lactate and pyruvate in the kidney, and cellular uptake of lactate and ketone bodies in neurons. It also transports the B-complex vitamin nicotinate. SLC5A12 is also localized to the apical membrane of epithelial cells lining the intestinal tract and proximal tubule. In the brain and retina, its expression is restricted to astrocytes and Müller cells. SLC5A8 also functions as a tumor suppressor; its expression is silenced in tumors of colon, thyroid, stomach, kidney, and brain. The tumor-suppressive function is related to its ability to mediate concentrative uptake of butyrate, propionate, and pyruvate, all of which are inhibitors of histone deacetylases. SLC5A8 can also transport a variety of pharmacologically relevant monocarboxylates, including salicylates, benzoate, and γ-hydroxybutyrate. Non-steroidal anti-inflammatory drugs such as ibuprofen, ketoprofen, and fenoprofen, also interact with SLC5A8. These drugs are not transportable substrates for SLC5A8, but instead function as blockers of the transporter. Relatively less is known on the role of SLC5A12 in drug transport

Primary tumor-induced immunity eradicates disseminated tumor cells in syngeneic mouse model

WOS: 000462721900029PubMed ID: 30926774Although clinically apparent metastasis is associated with late stages of cancer development, micro-metastatic dissemination may be an early event. However, the fate of these early disseminated tumor cells (DTC) remains elusive. We show that despite their capacity to disseminate into secondary organs, 4T1 tumor models develop overt metastasis while EMT6-tumor bearing mice clear DTCs shed from primary tumors as well as those introduced by intravenous (IV) injection. Following the surgical resection of primary EMT6 tumors, mice do not develop detectable metastasis and reject IV-injected tumor cells. In contrast, these cells readily grow and metastasize in immuno-deficient athymic or Rag2(-/- )mice, an effect mimicked by CD8(+) T-cell depletion in immunocompetent mice. Furthermore, recombinant G-CSF or adoptive transfer of granulocytic-MDSCs isolated from 4T1 tumor-bearing mice, induce metastasis by suppressing CD8(+) T-cells in EMT6-primed mice. Our studies support the concept of immune surveillance providing molecular insights into the immune mechanisms during tumor progression.Georgia Cancer Center; Forbes Institute research fund; Bridge Fund by Augusta University Research Inc.; American Cancer Society Institutional fundWe gratefully acknowledge the generous help from Flow Cytometry, Genomics Core facilities, and Labaratory of Animal Services. We thank Drs. Rafi Ahmed and Paulo C. Rodriguez for insightful discussions and comments, Dr. Iskander Asm for for helping with and training of our staff on the tail vein injections. This work was supported by start up funds to H.K. by Georgia Cancer Center. Additional research fundings to H.K. provided by American Cancer Society Institutional fund, Forbes Institute research fund, and Bridge Fund by Augusta University Research Inc

Molecular targets for the protodynamic action of cis-urocanic acid in human bladder carcinoma cells

<p>Abstract</p> <p>Background</p> <p>cis-urocanic acid (cis-UCA) is an endogenous amino acid metabolite capable of transporting protons from the mildly acidic extracellular medium into the cell cytosol. The resulting intracellular acidification suppresses many cellular activities. The current study was aimed at characterizing the molecular mechanisms underlying cis-UCA-mediated cytotoxicity in cultured cancer cells.</p> <p>Methods</p> <p>5367 bladder carcinoma cells were left untreated or treated with cis-UCA. Cell death was assessed by measuring caspase-3 activity, mitochondrial membrane polarization, formation and release of cytoplasmic histone-associated DNA fragments, and cellular permeabilization. Cell viability and metabolic activity were monitored by colorimetric assays. Nuclear labelling was used to quantify the effects of cis-UCA on cell cycle. The activity of the ERK and JNK signalling pathways was studied by immunoblotting with specific antibodies. Phosphatase activity in cis-UCA-treated cells was determined by assay kits measuring absorbance resulting from the dephosphorylation of an artificial substrate. All statistical analyses were performed using the two-way Student's t-test (p < 0.05).</p> <p>Results</p> <p>Here we report that treatment of the 5637 human bladder carcinoma cells with 2% cis-UCA induces both apoptotic and necrotic cell death. In addition, metabolic activity of the 5637 cells is rapidly impaired, and the cells arrest in cell cycle in response to cis-UCA. Importantly, we show that cis-UCA promotes the ERK and JNK signalling pathways by efficiently inhibiting the activity of serine/threonine and tyrosine phosphatases.</p> <p>Conclusions</p> <p>Our studies elucidate how cis-UCA modulates several cellular processes, thereby inhibiting the proliferation and survival of bladder carcinoma cells. These anti-cancer effects make cis-UCA a potential candidate for the treatment of non-muscle invasive bladder carcinoma.</p

Characterization and Optical Properties of the Single Crystalline SnS Nanowire Arrays

The SnS nanowire arrays have been successfully synthesized by the template-assisted pulsed electrochemical deposition in the porous anodized aluminum oxide template. The investigation results showed that the as-synthesized nanowires are single crystalline structures and they have a highly preferential orientation. The ordered SnS nanowire arrays are uniform with a diameter of 50 nm and a length up to several tens of micrometers. The synthesized SnS nanowires exhibit strong absorption in visible and near-infrared spectral region and the direct energy gapEgof SnS nanowires is 1.59 eV

Deferiprone: Pan-selective Histone Lysine Demethylase Inhibition Activity and Structure Activity Relationship Study

Deferiprone (DFP) is a hydroxypyridinone-derived iron chelator currently in clinical use for iron chelation therapy. DFP has also been known to elicit antiproliferative activities, yet the mechanism of this effect has remained elusive. We herein report that DFP chelates the Fe 2+ ion at the active sites of selected iron-dependent histone lysine demethylases (KDMs), resulting in pan inhibition of a subfamily of KDMs. Specifically, DFP inhibits the demethylase activities of six KDMs - 2A, 2B, 5C, 6A, 7A and 7B - with low micromolar IC 50 s while considerably less active or inactive against eleven KDMs - 1A, 3A, 3B, 4A-E, 5A, 5B and 6B. The KDM that is most sensitive to DFP, KDM6A, has an IC 50 that is between 7- and 70-fold lower than the iron binding equivalence concentrations at which DFP inhibits ribonucleotide reductase (RNR) activities and/or reduces the labile intracellular zinc ion pool. In breast cancer cell lines, DFP potently inhibits the demethylation of H3K4me3 and H3K27me3, two chromatin posttranslational marks that are subject to removal by several KDM subfamilies which are inhibited by DFP in cell-free assay. These data strongly suggest that DFP derives its anti-proliferative activity largely from the inhibition of a sub-set of KDMs. The docked poses adopted by DFP at the KDM active sites enabled identification of new DFP-based KDM inhibitors which are more cytotoxic to cancer cell lines. We also found that a cohort of these agents inhibited HP1-mediated gene silencing and one lead compound potently inhibited breast tumor growth in murine xenograft models. Overall, this study identified a new chemical scaffold capable of inhibiting KDM enzymes, globally changing histone modification profiles, and with specific anti-tumor activities

Key stages in mammary gland development - Involution: apoptosis and tissue remodelling that convert the mammary gland from milk factory to a quiescent organ

Involution of the mammary gland is an essential process that removes the milk-producing epithelial cells when they become redundant at weaning. It is a two-step process that involves the death of the secretory epithelium and its replacement by adipo-cytes. During the first phase, remodelling is inhibited and apoptotic cells can be seen in the lumena of the alveoli. In the second phase, apoptosis is accompanied by remodelling of the surrounding stroma and re-differentiation of the adipocytes. Considerable effort has been directed towards understanding the molecular mechanisms of the involution process and this has resulted in the identification of the principal signalling pathways involved

Myocardial infarction risk and tamoxifen therapy for breast cancer

Tamoxifen prevents recurrence after breast cancer and breast cancer among high-risk women, and may prevent myocardial infarction (MI). To assess the impact of tamoxifen on MI risk, we conducted a case–control study of first MI after breast cancer nested among women diagnosed with breast cancer, while enrolled in a health maintenance organisation from 1980 to 2000. We obtained information on breast cancer treatment and MI risk factors through medical record reviews and interviews. Data were analysed using conditional logistic regression. Of 11 045 women with breast cancer, 134 met MI criteria and were matched to two MI-free control subjects on year of birth and breast cancer diagnosis. After adjusting for smoking, hypertension and diabetes, tamoxifen was unassociated with MI (odds ratio (OR)=1.2, 95% confidence interval (CI)=0.7–1.9). Duration, cumulative dose and recency of use were not associated with MI. Radiation therapy was associated with MI (OR=2.0, 95% CI=1.1–3.5), an association that varied slightly but not statistically significantly by tamoxifen use (radiation with tamoxifen, OR=2.0, 95% CI=0.9–4.4; radiation without tamoxifen, OR=2.9, 95% CI=1.2–7.5). Tamoxifen treatment for breast cancer does not appear to increase or decrease MI risk, although radiation therapy appears to increase MI risk