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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.

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.

Contamination from microplastics is a growing concern around the globe that materialized over the last few decades. Road dust is one of the main contributors of microplastics in an urban environment and presence of microplastics can be a major detriment to health of urban population. The present study focuses on the presence, quantification, and identification of microplastics in the ambient air. Coarse (PM10) and fine (PM2.5) particulates from urban and rural sites of Nagpur, India is collected using high volume air samplers for weekdays and weekends for a period of 24 h. Samples are collected in Polytetrafluoroethylene filter papers and are analyzed using a stereomicroscope, fluorescence microscopic study, and Fourier transform infrared spectroscopy (FTIR) analysis. Fluorescence microscopy is conducted using Nile Red staining for analyzing the presence of microplastics and studying its shapes and colors. An average total abundance ranging from 50 to 120 particles/day is observed. Fibers are the dominant shape, and transparent/white is the dominant color observed in all four sites. FTIR analysis is conducted for identification of the chemical composition of particles in Attenuated Reflectance mode. The polymers identified in the region are low-density polyethylene, rayon, rubber fiber, polystyrene, polyaniline, polyolefin, and chlorinated polyvinyl chloride. This research identified significant contamination of the study region from microplastics and highlights the necessity of performing a comprehensive health risk analysis of the study region to examine the impact of microplastics on urban health.

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.

Globally, exposure to ambient fine particulate matter (PM

Objective Garden cress (Lepidium sativum L.) is an important herb in traditional medicine used to improve production of breast milk in women and semen in men. In the present research the authors evaluated its ability to destroy leukemic cancer (Jurkat E6-1) cells, using the alkaloid extract of this plant. Methods Constituents of the alkaloid extract were analyzed by gas chromatography–mass spectrometry (GC–MS) and their cytotoxicity in leukemic cancer cells and healthy peripheral blood mononuclear cells (PBMCs) was assessed. Cell death via apoptosis was confirmed by DNA laddering, caspase-3 activity, annexin V-fluorescein isothiocyanate and mitochondrial toxicity assays. The specific course of gene activation in treated cells was determined through quantitative polymerase chain reaction (qPCR). Results GC–MS analysis identified six alkaloids and proto-alkaloids, namely, benzyl isothiocyanate (1), 2-ethoxy-4H-3,1-benzoxazin-4-one (2), (4R)-2-(2-aminophenyl)-4-phenyloxazoline (3), 5-acetyl-1,2-dihydro-6-methyl-2-oxo-4-phenyl-3-pyridinecarbonitrile (4), benzo[b][1,8]-naphthyridin-5(10H)-one,2,4,7-trimethyl (5) and 1,4-diaminoanthraquinone (6), in the alkaloid extract of L. sativum. Of these, compound 1 was previously identified in the seeds of L. sativum. Exposure to the alkaloid extract caused death of Jurkat E6-1 cells, with median lethal concentration (LC50) of 75.25 µg/mL. However, the alkaloid extract also showed a nontoxic and proliferative (1.6-fold) effect in healthy PBMCs. Further experiments performed with Jurkat cells at LC50 and sub-LC50 doses demonstrated DNA fragmentation, activation of caspase-3 and time-dependant phosphatidylserine translocation (apoptosis) from inner to outer cell membranes. Cell toxicity and assessment of adenosine triphosphate level, together with using qPCR to evaluate expression profile of major apoptosis genes, revealed that apoptosis may be induced by disruption in the mitochondrial outer membrane potential, through activation of extrinsic and intrinsic apoptosis pathways in Jurkat cells. Conclusion The ability of the alkaloid extract of L. sativum seeds to induce apoptosis indicates a potential pharmacological use in cancer chemotherapy. The separation of individual active compounds and further in-depth exploration of the molecular mechanism of apoptosis may lead to novel chemotherapeutic compounds in our future antineoplastic research.

Emissions (mainly leachates and landfill gases) from solid waste facilities are laden with mixtures of dangerous xenobiotics implicated with significant increase in various pathophysiological disorders including cancer, and eventual mortality of exposed wildlife and humans. However, the molecular mechanisms of solid waste leachates induce pathophysiological disorders and cell death are still largely unknown. Although, evolving evidence implicated generation of reactive oxygen species and oxidative stress as the possible mechanism. Recent scientific reports are linking reactive oxygen species and mitochondrial dysfunctions as the player mechanism in pathophysiological disorder and apoptosis induced by xenobiotics in solid waste leachates. This systematic review presents an explicit discussion of recent scientific findings on the structural and functional alterations in mitochondria induced by solid waste leachates as the molecular mechanisms plausibly responsible for the pathophysiological disorders, cancer and cell death reported in landfill toxicology and epidemiological studies. This review aims to increase scientific understanding on solid waste leachate induced mitochondria dysfunctions as the key player in molecular mechanisms of solid waste induced toxicity. The findings in this review were mainly from using primary cells, cell lines, Drosophila and fish. Whether the findings will similarly be observed in mammalian test systems in vivo and particularly in exposed humans, remained to be investigated. Improvement in technological advancements, enforcement of legislation and regulations, and creation of sophisticated health surveillance against exposure to solid waste leachates, will expectedly mitigate human exposure to solid waste emissions and contamination of the environment.

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.

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.

Global burden of disease estimates reveal that people in Nigeria are living shorter lifespan than the regional or global average life expectancy. Ambient air pollution is a top risk factor responsible for the reduced longevity. But, the magnitude of the loss or the gains in longevity accruing from the pollution reductions, which are capable of driving mitigation interventions in Nigeria, remain unknown. Thus, we estimate the loss, and the gains in longevity resulting from ambient PM2.5 pollution reductions at the local sub-national level using life table approach. Surface average PM2.5 concentration datasets covering Nigeria with spatial resolution of ∼1 km were obtained from the global gridded concentration fields, and combined with ∼1 km gridded population of the world (GPWv4), and global administrative unit layers (GAUL) for territorial boundaries classification. We estimate the loss or gains in longevity using population-weighted average pollution level and baseline mortality data for cardiopulmonary disease and lung cancer in adults ≥25 years and for respiratory infection in children under 5. As at 2015, there are six "highly polluted", thirty "polluted" and one "moderately polluted" States in Nigeria. People residing in these States lose ∼3.8-4.0, 3.0-3.6 and 2.7 years of life expectancy, respectively, due to the pollution exposure. But, assuming interventions achieve global air quality guideline of 10 μg/m3, longevity would increase by 2.6-2.9, 1.9-2.5 and 1.6 years for people in the State-categories, respectively. The longevity gains are indeed high, but to achieve them, mitigation interventions should target emission sources having the highest population exposures.

National estimates of the health and economic burdens of exposure to ambient fine particulate matter (PM2.5) in India reveal substantial impacts. This information, often lacking at the local level, can justify and drive mitigation interventions. Here, we assess the health and economic gains resulting from attainment of WHO guidelines for PM2.5 concentrations – including interim target 2 (IT-2), interim target 3 (IT-3), and the WHO air quality guideline (AQG) – in Nagpur district to inform policy decision making for mitigation. We conducted a detailed assessment of concentrations of PM2.5 in 9 areas, covering urban, peri-urban and rural environments, from February 2013 to June 2014. We used a combination of hazard and survival analyses based on the life table method to calculate attributed annual number of premature deaths and disability-adjusted life years (DALYs) for five health outcomes linked to PM2.5 exposure: acute lower respiratory infection for children

The occurrence of drastic climate changes is a consolidated knowledge. These events have an effect on land modification and alteration of precipitation level. The changes of geophysical factors are indicted to lead to biodiversity decline and a loss of functionality of ecosystems. The human quality of life and health is clearly affected by these environmental changes. The combination of climate changes with environmental pollution, due to human activities, has become a critical factor for a sustainable development and to human quality of life. The air pollution, foremost associate with mankind activities, is a global menace for whole environment and, in particular, for human well-being. The air pollutants have been classified into two main classes: biotic and abiotic. The first group contains different elements as pollen, virus and bacteria. The second group contains physical and chemical pollutants as radioactivity or organic compounds. Taking their origin into account the air pollutants are classified as primary and secondary. The primary air pollutants are those generated by a natural events or anthropic activities

Micro(nano)-plastics (MP/NPs) ubiquity in the environment constitutes the global environmental and toxicological related issues of the 21st century. MP/NPs are now constantly observed in all components of the environment including many human consumer products; sea food, milk, beer, honey, bottle and tap water, salts, tea, drinks, and in human faeces and placenta. However, the potential health impacts in wildlife and humans are still poorly understood. This critical review provides comprehensive information on the ubiquity of MP/NPs in human consumer products, potential exposure route, uptake and translocation in the body and the associated pathophysiological effects. It also presents insight into the possible mechanisms that can lead to initiation and progression of cancer pathogenesis in the body. The possible mechanisms of MP/NPs induced cancer formation are centered on individual and or interactive effects of reactive oxygen species, induction of oxidative stress, genome instability, and chronic inflammation. This provides a strong evidence for a mechanistic approach to MP/NPs carcinogenic potentials. However, whether these mechanisms are realizable remained to be investigated in wildlife and human studies.

Environmental occurrence of CECs poses a great threat to both aquatic life and human health. The aim of this study was to optimize and validate SPE/LC-(ESI)MS-MS method for simultaneous quantitative monitoring of two sub-classes of CECs (pharmaceuticals and hormones) and to estimate the concentrations of select CECs in environmental water samples. For all the tested analytes, recoveries in laboratory reagent water were greater than 81%. Average percent (relative standard deviation) RSD of the analytes in recovery, repeatability, and reproducibility experiments were ≤ 10%. Determination coefficients (r2) of primidone, diclofenac, testosterone, and progesterone were estimated to be 0.9979, 0.9972, 0.9968, and 0.9962, respectively. Limits of detection (LOD) for primidone, diclofenac, testosterone, and progesterone were 4.63 ng/L, 5.36 ng/L, 0.55 ng/L, and 0.88 ng/L, respectively. Limits of quantification (LOQ) for primidone, diclofenac, testosterone, and progesterone were 14.72 ng/L, 17.06 ng/L, 1.766 ng/L, and 2.813 ng/L, respectively. Average recoveries in environmental water and wastewater samples were greater than 74% and RSD were ≤ 7%. Trace levels (68.33–125.70 ng/L) of primidone were detected in four environmental water samples, whereas diclofenac was not detected in any of the tested sample. Trace levels of progesterone were observed in two environmental samples (16.64 –203.73 ng/L), whereas testosterone was detected in STP inlet sample (178.16 ng/L).

In this study, the concentrations of MgSO4, salinity and light intensity were optimised for maximum biomass productivity and lipid content in Chlorella sp. Lipid synthesized at varied experimental conditions was also assessed in detail for biodiesel properties through FAME analysis. FAMEs mainly composed of C16:0, C16:1(9), C16:3(7, 10, 13), C18:0, C18:1(11), C18:2(9, 12), C18:3(9, 12, 15). The optimum biomass productivity (372.50mgL(-1)d(-1)) and lipid content (32.57%) was obtained at MgSO4-150ppm; salinity-12.5ppm, and light intensity-25μmolm(-2)s(-1). However, at this condition the cetane number, a major biodiesel property was not complying with worldwide biodiesel standard. Therefore, further optimisations were done to check the suitability of biodiesel fuel. The optimum biomass productivity (348.47mgL(-1)d(-1)) and lipid content (12.43%) with suitable biodiesel fuel properties was obtained at MgSO4-50ppm, salinity-25ppm and light intensity-100μmolm(-2)s(-1). The validation experiments confirmed the closeness of predicted and measured response values.

In the present study, effects of various cultivation conditions on biomass and lipid productivity, detail FAME signature, CO 2 biofixation and elemental composition of Chlorella sp. and Chlamydomonas sp. have been investigated. In Chlorella sp., N-depletion has enhanced the lipid productivity by 12.70–14.61%. In Chlamydomonas sp., though the lipid content has increased by 22–26% upon N-depletion, lipid productivity has not changed significantly due to concomitant decrease in biomass productivity by 18–25%. The presence of lipid was also confirmed by FTIR spectroscopic analysis of biomass. The characteristic bands observed at 1744.30 cm −1 ( Chlamydomonas sp.) and ( Chlorella sp.) were credited to lipids due to C–O mode of the side chain from ester carbonyl group. Extracted lipid was transesterified to FAMEs. Chlorella sp. at N-replete indoor condition has produced the highest weight percentage of C16:0 (26.64%), C18:0 (3.77%) and C18:1 (27.94%). In Chlamydomonas sp., N-replete indoor condition has resulted in maximum content of MUFA (30.12%), LUFA (53.35%), second highest SFA (29.22%) and DUFA (23.23%). Inverse relationship was observed between MUFA and PUFA at all cultivation conditions. In both the microalgae, C16:0, C18:1 (9), C18:2 (9, 12), C18:3 (9, 12, 15) were identified as the major FAMEs which are suitable to be used as biodiesel components.

Present study reports the identification of genomic and proteomic signatures of endosulfan exposure in hepatocellular carcinoma cells (HepG2). HepG2 cells were exposed to sublethal concentration (15μM) of endosulfan for 24h. DNA microarray and MALDI-TOF-MS analyses revealed that endosulfan induced significant alterations in the expression level of genes and proteins involved in multiple cellular pathways (apoptosis, transcription, immune/inflammatory response, carbohydrate metabolism, etc.). Furthermore, downregulation of PHLDA gene, upregulation of ACIN1 protein and caspase-3 activation in exposed cells indicated that endosulfan can trigger apoptotic cascade in hepatocellular carcinoma cells. In total 135 transcripts and 19 proteins were differentially expressed. This study presents an integrated approach to identify the alteration of biological/cellular pathways in HepG2 cells upon endosulfan exposure.

Polymorphisms in DNA repair and multidrug resistance genes might contribute to interindividual and interethnic differences in DNA repair capacity and drug disposition respectively. In the present study, we determined the allele and genotype frequencies of four single nucleotide polymorphisms (SNPs) located in the DNA repair genes, XRCC1, XRCC3, XPD, OGG1, namely XRCC1 Arg399Gln, XRCC3 Thr241Met, XPD Lys751Gln, and OGG1 Ser326Cys, respectively and two SNPs located in the multidrug resistance gene, ABCB1, namely ABCB1 C3435T and ABCB1 C1236T, in 33-35 healthy and unrelated Sindhi individuals, residing in the Vidarbha region of Central India and compared them with the Maharashtrian population from the same geographical region and some other HapMap populations from the HapMap database. The study findings reveal that the Indian Sindhis are closely related to the Maharashtrians as well as Utah residents with Northern and Western European ancestry and Gujarati Indians in Houston, Texas in the HapMap database.

Exposure to PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) can elicit several types of cancer and non-cancer effects. Previous studies reported substantial burdens of PAH-induced lung cancer, but the burdens of other cancer types and non-cancer effects remain unknown. Thus, we estimate the cancer and non-cancer burden of disease, in disability-adjusted life years (DALYs), attributable to ambient PM2.5-bound PAHs exposure in Nagpur district, India, using risk-based approach. We measured thirteen PAHs in airborne PM2.5 sampled from nine sites covering urban, peri-urban and rural areas, from February 2013 to June 2014. We converted PAHs concentrations to benzo[a]pyrene equivalence (B[a]Peq) for cancer and non-cancer effects using relative potency factors, and relative toxicity factors derived from quantitative structure-activity relationships, respectively. We calculated time-weighted exposure to B[a]Peq, averaged over 30 years, and adjusted for early-life susceptibility to cancer. We estimated the DALYs/year using B[a]Peq exposure levels, published toxicity data, and severity of the diseases from Global Burden of Disease 2016 database. The annual average concentration of total PM2.5-bound PAHs was 458 ± 246 ng/m3 and resulted in 49,500 DALYs/year (0.011 DALYs/person/year). The PAH-related DALYs followed this order: developmental (mostly cardiovascular) impairments (55.1%) > cancer (26.5%) or lung cancer (23.1%) > immunological impairments (18.0%) > reproductive abnormalities (0.4%).

The present communication dealt with cytotoxic and free radical scavenging potential of tertiary and quaternary alkaloid extracts of Tribulus terrestris fruits. Tertiary and quaternary alkaloid extracts were found to be cytotoxic to leukemic cells (Jurkat E6-1) with LC50 values of 100 and 42 µg/ml, respectively. Compared to the control, reactive oxygen species and reactive nitrogen species were significantly reduced in the cells treated with lower concentrations of tertiary and quaternary alkaloid extracts. Cells treated with tertiary alkaloid extract demonstrated significantly elevated levels of peroxidise, catalase and superoxide dismutase-like activities, whereas cells treated with quaternary alkaloid extracts showed insignificant elevations of the tested enzyme activities, compared to the control cells. The antioxidant activity of tertiary alkaloid (100 µg/ml) extract was 46.78 and 14.92 µg/ml of ascorbic acid equivalent as estimated in ferric reducing antioxidant potential and total antioxidant assays. Quaternary alkaloid extract displayed an IC50 value of 159 µg/ml in the nitric oxide mitigation assay. Cells treated with quaternary alkaloid extracts showed 1.4-fold increase in superoxide dismutase-like activity compared to the control cells. These results suggest that tertiary and quaternary alkaloid extracts possessed cytotoxic and free radical scavenging potential against leukemic cells.

Environmental pollution presents the most unfortunate by-product of human civilization, which is threatening not only humans themselves but also the ecosystem. Pollution can take different forms such as air, water, soil, noise, light, heavy metal, and organic pollutions, but the effects are generally devastating. Among the different effects of pollution, mutagenic and genotoxic effects are long known. These effects are of utmost concern as they can lead to deadly diseases including cancer and can also be passed through future generations, affecting population gene pool and structures. With this realization, several short-term and long-term studies have been carried out to develop databases of mutagenic pollutants. With the developments in mutagenicity testing protocols, new mutagens are regularly being identified. The current chapter highlights the need to include genotoxicity and mutagenicity testing requirements in routine pollution monitoring programs, which are currently based mainly on chemical determination of pollutants.

Renewable, carbon neutral, economically viable alternative fuels are urgently needed to turn away the consequences of climate change. Photosynthetic capability of microalgae with respect to CO2 fixation at various CO2 partial pressures generated by CO2 generating buffer (KHCO3/K2CO3), increases in biodiesel precursors using IR-CO2 sensor and modern LED lights-based modern two tier flask photobioreactor has been studied. Chlorella vulgaris and Scenesdesmus obliquus were found to produce 37.11% and 32.23% of palmitic acid (C16:0) and 30.88% and 39.73% of octadecenoic acid (C18:1) of total fatty acid methyl esters (FAMEs) respectively at 7.5% of CO2 partial pressure, under the optimal values for growth. Carbon dioxide fixation rate, efficiency of conversion of biomass to calorific value and biodiesel precursors were also estimated.

The present study demonstrates apoptosis-inducing potential and mechanism of action of Tribulus terristris alkaloid extract in Jurkat E6-1 cancer cell line. Liquid Chromatography-Mass Spectrometry and High Resolution-Mass Spectrometry analysis identified the presence of four N-feruloyltyramine derivatives, namely trans-N-feruloyl-3-hydroxytyramine (1), trans-N-coumaroyltyramine (2), trans-N-feruloyltyramine (3) and trans-N-feruloyl-3-ethoxytyramine (4) in the alkaloid extract. Compounds 2 and 3 have not been yet reported in the alkaloid extract of T. terristris. In silico analysis revealed therapeutic potential of N-feruloyltyramine derivatives and strong binding efficiency to both chains of Tumor Necrosis Factor Receptor 1. Treatment of alkaloids extract to Jurkat E6-1 clone induced dose-dependent cytotoxicity (LC50 140.4 μg mL−1). Jurkat cells treated with alkaloids extract at sub-lethal concentration showed DNA fragmentation, enhancement in caspase-3 activity and phosphatidylserine translocation (apoptosis indicator) compared to control cells. Gene expression analysis using Human Apoptosis RT2 Profiler PCR Array analysis upon alkaloid treatment was found to significantly alter expression of critical genes such as TNFR1, FADD, AIFM, CASP8, TP53, DFFA and NFKB1. These genes are predicted to mediate apoptotic cell death via both intrinsic and extrinsic apoptosis pathway. In summary, we report the identification of new N-feruloyltyramine derivatives from alkaloid extract of T. terristris fruit with probable anti-leukemic and pharmacological potential., Graphical abstract Image 1

Global burden of disease estimates reveal that people in Nigeria are living shorter lifespan than the regional or global average life expectancy. Ambient air pollution is a top risk factor responsible for the reduced longevity. But, the magnitude of the loss or the gains in longevity accruing from the pollution reductions, which are capable of driving mitigation interventions in Nigeria, remain unknown. Thus, we estimate the loss, and the gains in longevity resulting from ambient PM

In the present study, we attempt to shed light on the underlying molecular mechanism of the anticancer activity of pterostilbene (PTS) in HepG2 cells through the proteomic approach. PTS was found to induce apoptosis by altering the expression of apoptotic genes and the G2/M phase of cell cycle arrest. Further, the 2-DE map showed the expression of 72 differentially regulated proteins in PTS-treated HepG2 cells, of which 8 spots with >2 fold up- or down-regulated level were identified by MALDI-TOF analysis, which has a regulatory role in apoptosis. These findings for the first time offer valuable insights into the mechanism of apoptotis by PTS in HepG2 cells.

Anthropogenic activities have substantially increased the level of greenhouse gases (GHGs) in the atmosphere and are contributing significantly to the global warming. Carbon dioxide (CO2 ) is one of the major GHGs which plays a key role in the climate change. Various approaches and methodologies are under investigation to address CO2 capture and sequestration worldwide. Carbonic anhydrase (CA) mediated CO2 sequestration is one of the promising options. Therefore, the present review elaborates recent developments in CA, its immobilization and bioreactor methodologies towards CO2 sequestration using the CA enzyme. The promises and challenges associated with the efficient utilization of CA for CO2 sequestration and scale up from flask to lab-scale bioreactor are critically discussed. Finally, the current review also recommends the possible future needs and directions to utilize CA for CO2 sequestration.

Present study describes the induction of carbonic anhydrase (CA) activity in Chlamydomonas sp. in presence of calcium carbonate. Results indicated that calcium carbonate increased the activity of extracellular CA enzyme by 14-fold compared to culture grown at 3 % CO2, and by fourfold compared to the culture grown at 0.03 % CO2. CA was purified by gel exclusion followed by ion exchange chromatography. Molecular weight of the purified CA was found to be approximately 28 kDa. The enzyme showed optimum stability in the pH range of 8.0–9.0 and temperature of 35 °C. CA activity was inhibited with Hg2+ and Pb2+, while Zn2+ was found to accelerate its activity. Purified CA was employed for carbonation reaction with CO2 and the calcite produced was characterized by scanning electron microscope and X-ray diffraction. The enhancement in CA activity was found to be reliable, convenient, and may be employed for CO2 sequestration using whole cells or immobilized bioreactor systems.

Inhalable particulate matter (PM10), comprising fine and thoracic coarse particulate matter (PM2.5 and PM10-2.5, respectively), is emitted from several sources. The sources includes construction and agricultural activities, transportation, industrial processes, power plants, wildfires, household solid cookfuels and suspensions or re-suspensions from unpaved roads, mining and natural sources. Previous studies, specifically from developed countries and China have shown that PM10 may contain several dangerous organic chemicals (DOCCs). However, very little is known about PM10 in developing countries. Therefore is study seeks to identify the DOCCs in airborne PM10 in Nagpur district, India. We collected 24-hr ambient PM10 samples from urban, peri-urban and rural areas of the district during wintertime (January, 2013). The DOCCs in the PM10 were identified by gas chromatography-mass spectrometry. The results revealed that polycyclic aromatic hydrocarbons (PAHs), chlorinated hydrocarbons, dioxins, furans, phthalate esters, aldehydes, ketones, phenols and organic acids are major DOCCs in the PM10. Quantitative analysis of thirteen individual PAHs in the PM10 revealed concentrations that greatly exceeded health-based guideline. This suggests that prolong inhalation of such PM10 may pose adverse risk to health of the population.

Aegle marmelos (Indian Bael) is a tree which belongs to the family of Rutaceae. It holds a prominent position in both Indian medicine and Indian culture. We have screened various fractions of Aegle marmelos extracts for their anticancer properties using in vitro cell models. Gas chromatography-Mass spectrometry (GC-MS) was employed to analyze the biomolecules present in the Aegle marmelos extract. Jurkat and human neuroblastoma (IMR-32) cells were treated with different concentrations of the fractionated Aegle marmelos extracts. Flow cytometric analysis revealed that optimal concentration (50ug/ml) of beta caryophyllene and caryophyllene oxide fractions of Aegle marmelos extract can induce apoptosis in Jurkat cell line. cDNA expression profiling of pro-apoptotic and anti-apoptotic genes was carried out using real time PCR (RT-PCR). Down-regulation of anti-apoptotic genes (bcl-2, mdm2, cox2 and cmyb) and up-regulation of pro-apoptotic genes (bax, bak1, caspase-8, caspase-9 and ATM) in Jurkat and IMR-32 cells treated with the beta caryophyllene and caryophyllene oxide fractions of Aegle marmelos extract revealed the insights of the downstream apoptotic mechanism. Furthermore, in-silico approach was employed to understand the upstream target involved in the induction of apoptosis by the beta caryophyllene and caryophyllene oxide fractions of Aegle marmelos extract. Herein, we report that beta caryophyllene and caryophyllene oxide isolated from Aegle marmelos can act as potent anti-inflammatory agents and modulators of a newly established therapeutic target,15-lipoxygenase (15-LOX). Beta caryophyllene and caryophyllene oxide can induce apoptosis in lymphoma and neuroblastoma cells via modulation of 15-LOX (up-stream target) followed by the down-regulation of anti-apoptotic and up-regulation of pro-apoptotic genes. © 2014 Bentham Science Publishers.

Manganese is an essential trace element however elevated environmental and occupational exposure to this element has been correlated with neurotoxicity symptoms clinically identical to idiopathic Parkinson's disease. In the present study we chronically exposed human neuroblastoma SH-SY5Y cells to manganese (100 μM) and carried out expression profiling of miRNAs known to modulate neuronal differentiation and neurodegeneration. The miRNA PCR array results reveal alterations in expression levels of miRNAs, which have previously been associated with the regulation of synaptic transmission and apoptosis. The expressions of miR-7 and miR-433 significantly reduced upon manganese exposure. By in silico homology analysis we identified SNCA and FGF-20as targets of miR-7 and miR-433. We demonstrate an inverse correlation in expression levels where reduction in these two miRNAs causes increases in SNCA and FGF-20. Transient transfection of SH-SY5Y cells with miR-7 and miR-433 mimics resulted in down regulation of SNCA and FGF-20 mRNA levels. Our study is the first to uncover the potential link between manganese exposure, altered miRNA expression and parkinsonism: manganese exposure causes overexpression of SNCA and FGF-20 by diminishing miR-7 and miR-433 levels. These miRNAs may be considered critical for protection from manganese induced neurotoxic mechanism and hence as potential therapeutic targets.