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Muzamil Yaqub Want,1,2 Priya Yadav,1,3 Rakin Khan,1 Garima Chouhan,1,4 Mohammad Islamuddin,1,5 Sheka Yagub Aloyouni,6 Asoke P Chattopadhyay,7 Suliman Yousef AlOmar,8 Farhat Afrin1,9 1Parasite Immunology Laboratory, Department of Biotechnology, Jamia Hamdard (Hamdard University), New Delhi, 110062, India; 2Roswell Park Comprehensive Cancer Center, Buffalo, NY, 14263, USA; 3Department of Microbiology, University of Kalyani, Kalyani, West Bengal, 741235, India; 4Department of Biotechnology, School of Engineering and Technology, Sharda University, Greater Noida, Uttar Pradesh, 201306, India; 5Molecular Virology and Vaccinology Laboratory, Department of Biotechnology, Jamia Millia Islamia, New Delhi, 110025, India; 6Health Sciences Research Center, Princess Nourah Bint Abdulrahman University, Riyadh, 11671, Saudi Arabia; 7Department of Chemistry, University of Kalyani, Kalyani, West Bengal, 741235, India; 8Doping Research Chair, Department of Zoology, College of Science, King Saud University, Riyadh, 11451, Saudi Arabia; 9Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, Taibah University, Madina, 41477, Saudi ArabiaCorrespondence: Farhat Afrin; Suliman Yousef AlOmar Tel +91-7596846639; +966-500767717Email farhatafrin@gmail.com; syalomar@ksu.edu.saIntroduction: The current therapeutic armory for visceral leishmaniasis (VL) caused by Leishmania donovani complex is inadequate, coupled with serious limitations. Combination therapy has proved ineffective due to mounting resistance; however, the search for safe and effective drugs is desirable, in the absence of any vaccine. There is a growing interest in the application of nanoparticles for the therapeutic effectiveness of leishmaniasis. Aimed in this direction, we assessed the antileishmanial effect of gold nanoparticles (GNP) against L. donovani in vitro.Methods: GNP were synthesized and characterized for particle size by dynamic light scattering (DLS) and atomic force microscopy (AFM) and for optical properties by UV-visible spectroscopy. Cytotoxicity of GNP was measured by the MTT proliferation assay. The antileishmanial activity of the nanoparticles was evaluated against L. donovani promastigotes and macrophage-infected amastigotes in vitro.Results: GNP showed a strong SPR peak at 520 nm and mean particle size, polydispersity index (PDI), and zeta potential of 56.0 ± 10 nm, 0.3 ± 0.1 and − 27.0 ± 3 mV, respectively. The GNPs were smooth and spherical with a mean particle diameter of 20 ± 5 nm. Nanoparticles [1.2– 100 μM] did not reveal any cytotoxicity on RAW 264.7 murine macrophage cell line, but exerted significant activity against both promastigotes and amastigote stages of L. donovani with 50% inhibitory concentrations (IC50) of 18.4 ± 0.4 μM and 5.0 ± 0.3 μM, respectively. GNP showed significant antileishmanial activity with deformed morphology of parasites and the least number of surviving promastigotes after growth reversibility analysis.Conclusion: GNP may provide a platform to conjugate antileishmanial drugs onto the surface of nanoparticles to enhance their therapeutic effectiveness against VL. Further work is warranted, involving more in-depth mechanistic studies and in vivo investigations.Keywords: gold nanoparticles, surface plasmon resonance, visceral leishmaniasis L. donovani, promastigotes, amastigotes

Magnesium oxide nanoparticles (MgONP) are predominantly utilized in industrial products. This study was undertaken to elucidate the mechanisms underlying toxic effect of MgONP in human colon cancer (HT 29) cells over 48 hr period. Cytotoxicity was evaluated by using MTT and neutral red uptake assays. Data demonstrated that MgONP reduced cell viability in concentration- and time-dependent manner. MgONP induced oxidative stress by decreasing glutathione (GSH) concentrations and elevation of reactive oxygen species (ROS) and lipid peroxidation levels. Increased caspase-3 enzyme activity and greater condensed, damaged chromosome was observed following MgONP exposure in HT 29 cells. The level of interleukin-4 (IL-4), tumor necrosis factor (TNF-α), and DNA fragmentation were significantly higher in MgONP incubated cells. The results showed that MgONP-induced toxicity in HT 29 cells may be mediated through oxidative stress.

The effect of IL-1β on cytokine and chemokine production by human preadipocytes has been examined. Preadipocytes were incubated with IL-1β, and cytokine and chemokine release was measured at 24 h by protein arrays, while the expression of cytokine/chemokine genes was assessed by qPCR at 4 and 24 h. IL-1β stimulated the secretion of multiple cytokines/chemokines, including IL-6, IL-8, IL-10, IL-13, MCP-4, TNFα and IP-10. IL-10 was not released by un-stimulated preadipocytes, while IL-6 exhibited the greatest response to IL-1β (453-fold increase). IL-16 and IL-12p40 did not respond to IL-1β. qPCR demonstrated that IL-1β markedly stimulated CCL3, CSF3 and CXCL10 expression at 4 h (>900-fold mRNA increase). A time-course indicated that while CCL13 (encoding MCP-4) exhibited minimal basal expression in preadipocytes, expression increased progressively following differentiation. Human preadipocytes are highly sensitive to IL-1β, the cytokine stimulating a major inflammatory response in these cells similar to that in mature adipocytes.

Cadmium sulfide nanoparticles (CdSNP) are increasingly used in biological applications. This study was undertaken to understand the mechanisms underlying adverse effects of CdSNP using human lung adenocarcinoma epithelial (A549) cells. Cellular toxicity was evaluated by using 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide and neutral red assays. Results showed that CdSNP reduced mitochondrial function and induced lysosomal activity in concentration and time-dependent manner. CdSNP produced oxidative stress as evidenced by reduction of glutathione (GSH) levels and increase in reactive oxygen species and lipid peroxidation levels. Induction of caspase-3 enzymes and condensed, fragmented nuclei was observed in CdSNP-treated cells. Furthermore, the levels of interleukin-8, tumor growth factor and DNA fragmentation were significantly higher in CdSNP exposed cells. Data indicated that toxicity of CdSNP noted in A549 cells may be mediated through oxidative stress. This study warrants more comprehen...

Boswellia papyrifera and Boswellia carterii released from smoke contaminate indoor environment and consequently adversely affect humans as evidenced by respiratory disturbances. The aim of this study was to determine the effects of these plants on pathological and biochemical changes in vas deferens of albino rats. Animals were administered 4 g/kg body weight B. papyrifera and B. carterii daily for 120 days along with controls. Significant changes were observed in epithelial cell types and some cells showed signs of degeneration. The ultrastructural studies revealed marked changes in cytoplasmic organelles. Microvilli were missing and lysosomes were found in the cytoplasm. In addition, all treated groups plasma fructose and other biochemical parameters were decreased indicating reduced energy necessary for motility and contractility of spermatozoa. Many spermatozoa were disorganized and agglomerated. Data suggest that smoke from these plants adversely affects vas deferens.

The use of nanotechnology has seen an exponential growth in the areas of health care, consumer products, clothes, electronics, and sporting goods.1 This is due to the unique properties of nanomaterials (eg, chemical, mechanical, optical, magnetic, and biological), which make them desirable for commercial and medical applications.2,3 According to a recent survey, the number of nanotechnology-based consumer products available in the world market has crossed the 1000 mark.4 Thus, it is essential to assess the health hazards of nanomaterials in humans and other species.2 Metal nanoparticles exhibit unique properties in terms of optical, magnetic, and electrical activity.5 One of the most interesting chemical elements used as nanoparticles for biomedical applications is cobalt oxide nanoparticles (Co3O4NPs). Occupational exposure of cobalt can lead to various lung diseases, such as interstitial pneumonitis, fibrosis, and asthma.6 De Boeck et al7 reported the genotoxic potential of cobalt nanoparticles in humans. A synergistic effect of cobalt and tungsten carbide enhanced production of reactive oxygen species (ROS) and induced DNA fragmentation.8 In view of their possible risk for human health as nanotechnology products, the cytotoxic and genotoxic effects Co3O4NPs are of concern. ROS is an important factor in the apoptosis process as well as in DNA damage,9 oxidative stress-induced damage, and other cellular processes. However, the mechanisms involved in the toxicity of commercially important Co3O4NPs are poorly understood. Human hepatocarcinoma (HepG2) cells have been used as a surrogate for human hepatocytes and have found application in the study of nanoparticle cytotoxicity.10 Subsequently, measurement of ROS with 2,7-dichlorfluorescein-diacetate (DCFH-DA) was carried out to determine whether ROS generation could be a possible mechanism in the observed cytotoxicity of Co3O4NPs. In the presence of DNA damage or cellular stress, p53 protein triggers cell-cycle arrest to provide time for the damage to be repaired or for self-mediated apoptosis.11 Recent studies have shown that Co3O4NPs releases cobalt ions (Co2+) in the aqueous state. Therefore, we also investigated whether Co3O4NPs induce a cellular response in HepG2 cells, and if so, whether they produce toxicity by releasing soluble Co2+ or by exerting a toxic effect unique to Co3O4NPs. The present investigations were carried out to study the underlying mechanisms of cytotoxicity and genotoxicity induced by Co3O4NPs in human hepatoma cells through ROS generation and oxidative stress.