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Manganese (Mn) is an essential trace element required for many physiological functions including proper biochemical and cellular functioning of the central nervous system (CNS). However, exposure to excess level of Mn through occupational settings or from environmental sources has been associated with neurotoxicity. The cellular and molecular mechanism of Mn-induced neurotoxicity remains unclear. In the current study, we investigated the effects of 30-day exposure to a sub-lethal concentration of Mn (100 μM) in human neuroblastoma cells (SH-SY5Y) using transcriptomic approach. Microarray analysis revealed differential expression of 1057 transcripts in Mn-exposed SH-SY5Y cells as compared to control cells. Gene functional annotation cluster analysis exhibited that the differentially expressed genes were associated with several biological pathways. Specifically, genes involved in neuronal pathways including neuron differentiation and development, regulation of neurogenesis, synaptic transmission, and neuronal cell death (apoptosis) were found to be significantly altered. KEGG pathway analysis showed upregulation of p53 signaling pathways and neuroactive ligand-receptor interaction pathways, and downregulation of neurotrophin signaling pathway. On the basis of the gene expression profile, possible molecular mechanisms underlying Mn-induced neuronal toxicity were predicted.

Microplastics are considered to be ubiquitous and widespread emerging contaminants. They are persistent in the nature and pose considerable harm to the environment. Their omnipresence is documented in almost all aquatic habitats, several atmospheric and terrestrial environments, and also in human consumables. The objective of this review is to provide an overview of the environmental prevalence of the microplastics in all environmental compartments, and their possible adverse impacts. It also presents review of the studies conducted in India and the epitome of potential mitigation measures. The need and direction of future research are highlighted. The review will help in determining the exposure levels, environmental consequences, and risk estimations, and will guide the researchers and policymakers.

Manganese is a vital nutrient and is maintained at an optimal level (2.5–5 mg/day) in human body. Chronic exposure to manganese is associated with neurotoxicity and correlated with the development of various neurological disorders such as Parkinson’s disease. Oxidative stress mediated apoptotic cell death has been well established mechanism in manganese induced toxicity. Oxidative stress has a potential to alter the epigenetic mechanism of gene regulation. Epigenetic insight of manganese neurotoxicity in context of its correlation with the development of parkinsonism is poorly understood. Parkinson’s disease is characterized by the α-synuclein aggregation in the form of Lewy bodies in neuronal cells. Recent findings illustrate that manganese can cause overexpression of α-synuclein. α-Synuclein acts epigenetically via interaction with histone proteins in regulating apoptosis. α-Synuclein also causes global DNA hypomethylation through sequestration of DNA methyltransferase in cytoplasm. An individual genetic difference may also have an influence on epigenetic susceptibility to manganese neurotoxicity and the development of Parkinson’s disease. This review presents the current state of findings in relation to role of epigenetic mechanism in manganese induced neurotoxicity, with a special emphasis on the development of Parkinson’s disease.

Landfill soil leachates, containing myriad of xenobiotics, increase genotoxic and cytotoxic stress–induced cell death. However, the underlying mechanism involved in the elimination of the damaged cells is yet to be fully elucidated. This study investigated the apoptotic processes induced in lymphoma (Jurkat) cells by landfill soil leachates from Olusosun (OSL, Nigeria) and Nagpur (NPL, India). Jurkat was incubated with sub-lethal concentrations of OSL and NPL for 24 h and analyzed for DNA fragmentation and apoptosis using agarose gel electrophoresis and Hoechst 33258–PI staining, respectively. Complementary DNA expression profiling of some pro-apoptotic and anti-apoptotic genes regulating apoptosis was also analyzed using real-time PCR (RT-PCR) method. Agarose gel electrophoresis revealed DNA fragmentations in OSL and NPL–treated cells. Hoecsht-33258 – Propidium Iodide (PI) based apoptotic analysis confirmed apoptotic cell death in exposed Jurkat. RT-PCR analysis revealed different fold changes in the pro- and anti-apoptotic genes in OSL and NPL–treated Jurkat. There was significant increase in fold change of the up-regulated genes; apoptosis inducing factor mitochondrion-associated 2 (AIFM2), Fas-associated death domain (FADD), Caspase-2, Caspase-6, BH3 interacting domain death agonist (BID), tumor suppressor (p53), and BCL2 associated agonist of cell death (BAD) and down-regulation of apoptosis inhibitor 5 (API5). Results suggest that OSL and NPL elicited genotoxic stress–related apoptosis in Jurkat. The dysregulation in the expression of genes involved in apoptotic processes in wildlife and human exposed to landfill emissions may increase aetiology of various pathological diseases including cancer.

The increase in the atmospheric concentrations of one of the vital green house gasses, carbon dioxide, due to anthropogenic interventions has led to several undesirable consequences such as global warming and related changes. In the global effort to combat the predicted disaster, several CO₂ capture and storage technologies are being deliberated. One of the most promising biological carbon dioxide sequestration technologies is the enzyme catalyzed carbon dioxide sequestration into bicarbonates which was endeavored in this study with a purified C. freundii SW3 β-carbonic anhydrase (CA). An extensive screening process for biological sequestration using CA has been defined. Six bacteria with high CA activity were screened out of 102 colonies based on plate assay and presence of CA in these bacteria was further emphasized by activity staining and Western blot. The identity of selected bacteria was confirmed by 16S rDNA analysis. CA was purified to homogeneity from C. freundii SW3 by subsequent gel filtration and ion exchange chromatography which resulted in a 24 kDa polypeptide and this is in accordance with the Western blot results. The effect of host on metal ions, cations and anions which influence activity of the enzyme in sequestration studies suggests that mercury and HCO₃ ⁻ ion almost completely inhibit the enzyme whereas sulfate ion and zinc enhances carbonic anhydrase activity. Calcium carbonate deposition was observed in calcium chloride solution saturated with carbon dioxide catalyzed by purified enzyme and whereas a sharp decrease in calcium carbonate formation has been noted in purified enzyme samples inhibited by EDTA and acetazolamide.

Fluorosis is caused by excess of fluoride intake over a long period of time. Aberrant change in the Runt-related transcription factor 2 (RUNX2) mediated signaling cascade is one of the decisive steps during the pathogenesis of fluorosis. Up to date, role of fluoride on the epigenetic alterations is not studied. In the present study, global expression profiling of short noncoding RNAs, in particular miRNAs and snoRNAs, was carried out in sodium fluoride (NaF) treated human osteosarcoma (HOS) cells to understand their possible role in the development of fluorosis. qPCR and in silico hybridization revealed that miR-124 and miR-155 can be directly involved in the transcriptional regulation of Runt-related transcription factor 2 (RUNX2) and receptor activator of nuclear factor κ-B ligand (RANKL) genes. Compared to control, C/D box analysis revealed marked elevation in the number of UG dinucleotides and D-box sequences in NaF exposed HOS cells. Herein, we report miR-124 and miR-155 as the new possible players involved in the development of fluorosis. We show that the alterations in UG dinucleotides and D-box sequences of snoRNAs could be due to NaF exposure.

To rank pollutants in two Nigerian water supply schemes according to their effect on human health using a risk-based approach. Hazardous pollutants in drinking-water in the study area were identified from a literature search and selected pollutants were monitored from April 2010 to December 2011 in catchments, treatment works and consumer taps. The disease burden due to each pollutant was estimated in disability-adjusted life years (DALYs) using data on the pollutant's concentration, exposure to the pollutant, the severity of its health effects and the consumer population. The pollutants identified were microbial organisms, cadmium, cobalt, chromium, copper, iron, manganese, nickel, lead and zinc. All were detected in the catchments but only cadmium, cobalt, chromium, manganese and lead exceeded World Health Organization (WHO) guideline values after water treatment. Post-treatment contamination was observed. The estimated disease burden was greatest for chromium in both schemes, followed in decreasing order by cadmium, lead, manganese and cobalt. The total disease burden of all pollutants in the two schemes was 46 000 and 9500 DALYs per year or 0.14 and 0.088 DALYs per person per year, respectively, much higher than the WHO reference level of 1 × 10(-6) DALYs per person per year. For each metal, the disease burden exceeded the reference level and was comparable with that due to microbial contamination reported elsewhere in Africa. The estimated disease burden of metal contamination of two Nigerian water supply systems was high. It could best be reduced by protection of water catchment and pretreatment by electrocoagulation.

Microplastics (MPs) are ubiquitous pollutants that affect various environmental matrices, including air, water, soil, food, and beverages. In India, there is limited research on microplastics in bottled drinking water, which is a significant route of MP exposure to the human body. To date, the data on the occurrence of MPs in national and local bottled water brands have not been studied and compared. Therefore, the current study focuses on the contamination of MPs in bottled water from different national and local brands procured from the market of Nagpur, India. The MPs were observed in all the analyzed samples. It was observed that the local bottled water showed higher MP contamination compared to national bottled water, with MP concentrations of 212 ± 100 MPs/L and 72 ± 36 MPs/L, respectively. The MPs were identified and characterized using microscopic and attenuated total reflectance–fourier transform infrared spectroscopy (ATR–FTIR) analysis, revealing that the dominant MP particles were fragments (71%), followed by fibers (23%), and others (6%). Among the observed particles, 50% of particles were black colored, followed by transparent (16%), red (13%), orange (8%), green (3%), blue (5%), and yellow (5%). The predominant polymer types were polyethylene (PE) and polyethylene terephthalate (PET). Overall, the pollution load indices suggested a moderate level of contamination in bottled water samples. Furthermore, the estimated annual human exposure to MPs was calculated as 5186 ± 3751 p/kg–bw/year for children and 1482 ± 1072 p/kg–bw/year for adults, making it a significant route of human exposure to MPs.

Carbonic anhydrase enzyme, one of the fastest known enzymes, remains largely unexplored in prokaryotes when compared to its mammalian counterparts despite its ubiquity. In this study, the enzyme has been purified from Bacillus subtilis SA3 using sequential Sephadex G-75 chromatography, DEAE cellulose chromatography, and sepharose-4B-L-tyrosinesulphanilamide affinity chromatography and characterized to provide additional insights into its properties. The apparent molecular mass of carbonic anhydrase obtained by SDS-PAGE was found to be approximately 37 kDa. Isoelectric focusing of the purified enzyme revealed an isoelectric point (pI) of around 6.1 when compared with marker. The presence of metal ions such as Zn 2+ , Co 2+ , Cu 2+ , Fe 3+ , Mg 2+ , and anion SO 4 − increased enzyme activity while strong inhibition was observed in the presence of Hg 2+ , Cl − , HCO 3 − , and metal chelator EDTA. The optimum pH and temperature for the enzyme were found to be 8.3 and 37°C, respectively. Enzyme kinetics with p-nitrophenyl acetate as substrate at pH 8.3 and 37°C determined the V max and K m values of the enzyme to be 714.28 μmol/mg protein/min and 9.09 mM, respectively. The K i value for acetazolamide was 0.22 mM, compared to 0.099 mM for sulphanilamide. The results from N-terminal amino acid sequencing imply the purified protein is a putative beta-carbonic anhydrase with close similarities to CAs from plants, microorganisms.

Sewage treatment plant (STP) acts as a potential source of microplastic contamination in the environment. The presence of microplastics in the sewage treatment plant is reported over the globe in varying concentrations. Hence, the current study is intended to evaluate the presence and abundance of microplastics occurring in sewage treatment plants in India. The samples were processed through digestion and density separation, followed by microscopic and polymer identification through Fourier transform infrared spectroscopy. Also, different wastewater parameters were studied to analyze their influence. High microplastic concentrations were detected in the influent (1860 ± 265 MPs/L), which reduced by > 90%, to around 148 ± 51 MPs/L in the effluent. The concentration of microplastics in sewage sludge was 830 MPs/kg. The prominent plastic types identified include low-density polyethylene, polypropylene, polyurethane, polyvinyl chloride, and rayon. The smaller particles prevail in the effluent, releasing around 30 billion particles per day to the environment. This suggests that the current STP is efficient in removing the majority of the particles, but considerations are needed to avoid the ecological risks associated.