Early life environment and developmental immunotoxicity in inflammatory dysfunction and disease

Components of the innate immune system such as macrophages and dendritic cells are instrumental in determining the fate of immune responses and are, also, among the most sensitive targets of early life environmental alterations including developmental immunotoxicity (DIT). DIT can impede innate immune cell maturation, disrupt tissue microenvironment, alter immune responses to infectious challenges, and disrupt regulatory responses. Dysregulation of inflammation, such as that observed with DIT, has been linked with an increased risk of chronic inflammatory diseases in both children and adults. In this review, we discuss the relationship between early-life risk factors for innate immune modulation and promotion of dysregulated inflammation associated with chronic inflammatory disease. The health risks from DIT-associated inflammation may extend beyond primary immune dysfunction to include an elevated risk of several later-life, inflammatory-mediated diseases that target a wide range of physiological systems and organs. For this reason, determination of innate immune status should be an integral part of drug and chemical safety evaluation.     

Preconcentration of samarium with modified yeast cells for its determination by atomic emission spectroscopy

A chelating-modified biosorbent is produced by coupling of a dye, procion red, to yeast cells. The resulting modified cells have been characterized by Fourier transform infrared, elemental analysis and thermogravimetric analysis and studied for preconcentration and determination of trace Sm(III). The optimum pH value for sorption of the samarium ions is 6.2. The sorption capacity of functionalized modified yeast cells is 7.2 mg g^?1. Recovery was 99% when Sm(III) was eluted with an aqueous solution of 0.1 mol L^?1 ethylenediaminetetraacetic acid. Scatchard analysis suggested that binding sites were homogeneous. The equilibrium data were analyzed using Langmuir, Freundlich, Temkin, and Redlich–Peterson isotherm models, and the respective constants were determined as 1.0 (L mg^?1), 2.9 [(mg g^?1) (L mg^?1)^1/n], 2.4 × 10⁸ (L g^?1), and 30 (dm³ g^?1) at 20 °C. The method was applied for an Sm(III)-containing sample of ceramic industry effluent.     

Cytotoxicity of single-walled carbon nanotubes,multi-walled carbon nanotubes,and chrysotile to human lung epithelial cells

Carbon nanotubes (CNTs) have found numerous applications in various industries. Recently, adverse effects of these materials on human and animal cells in vitro have been reported. In the present study, the cytotoxicity of single-walled carbon nanotubes (SWCNTs), multi-walled carbon nanotubes (MWCNTs), and chrysotile asbestos in human lung epithelial cells has been studied using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The cells were exposed for 6 h and 24 h to between 0.97 and 1500 μg mL^?1 of CNTs and chrysotile fibers prepared in two culture media containing 5% serum and 0.5% dimethylsulfoxide. Dose–response curves were obtained to determine the nonobservable adverse effect concentration and the half-maximum inhibitory concentration (IC₅₀). The way of dispersion affects the cytotoxicity of CNTs. For MWCNT, the toxicological indexes were lower than for SWCNT. Chrysotile fibers were even less cytotoxic than CNTs. Therefore, workplace control measures are recommended as priority for occupational and environmental conditions.     

DNA fragmentation,apoptosis and cell cycle arrest induced by sodium arsenite in cultured murine Sertoli cells: prevention by curcumin

Arsenic is a significant environmental concern worldwide, primarily due to geo physiochemical contamination of drinking water, and a major public health hazard in both developing and developed countries. The present study was aimed to investigate ameliorative effects of curcumin (Cur) against sodium arsenite (SA)-induced toxicity in cultured murine Sertoli cells. The cells were treated with SA (5 μM) and Cur (5 μg/ml and 10 μg/ml) alone or in combination for 12 hr. The SA treatment decreased cell viability, produced oxidative stress, and induced apoptosis as reflected by reactive oxygen species (ROS) generation, loss of mitochondrial transmembrane potential, DNA fragmentation, and apoptotic cells. Moreover, the SA-induced cell cycle arrest in the cells is characterized by a rise in the number of cells in the sub G1 phase of the cell cycle. The Cur was found to be effective in reversing all these arsenic (As)-induced cellular events. Data suggest that Cur modulates As-mediated oxidative stress, apoptosis, DNA fragmentation, and cell cycle arrest through suppression of excessive ROS generation. Evidence indicates that Cur may emerge as a useful protective agent against As-induced Sertoli cells toxicity by inhibiting As-induced damage in testes.     

Cytotoxicity of benalaxyl,metalaxyl, and triadimefon on Chinese hamster ovary cells

The cytotoxicity of the fungicides benalaxyl, metalaxyl, and triadimefon was evaluated in vitro using the Chinese hamster ovary (CHO-K1) cell line. The midpoint cytotoxicity values of neutral red (NR) incorporation (NRI₅₀), total cellular protein content (TCP₅₀), and the methyl tetrazolium assay (MTT₅₀) were estimated. Benalaxyl was the most cytotoxic fungicide, followed by metalaxyl and triadimefon. Fetal calf serum (10%) caused a reduction in benalaxyl, metalaxyl, and triadimefon cytotoxicity by factors of 1.8, 1.3, and 1.3. The effects of sublethal concentrations (NRI₂₅) of the three fungicides on the glutathione redox cycle components glutathione S-transferase, glutathione reductase, glutathione peroxidase, and total glutathione content were studied. The ameliorative effects of extracellular glutathione (1 mmol L^?1), vitamin C (70 µmol L^?1), and vitamin E (30 µmol L^?1) were also investigated. The three antioxidants led to significant effects on the glutathione redox cycle components.     

Manufactured silver and gold nanoparticles-induced apoptosis by caspase-pathway in human cell lines

Abstract

Metallic nanoparticles have emerged as an important class of nanomaterials for a wide range of industrial and medical applications. Because of the intensive commercial applications, risk assessment of these nanoparticles is of great importance. In the present study, the human hepatoma and leukemia cells were used to characterize the apoptotic effects of silver nanoparticles (4.7 and 42?nm) and gold nanoparticles (30?nm). Apoptotic cells were identified by chromatin condensation and flow cytometry analysis, using Annexin V/PI, TUNEL and caspase activation assays. Flow cytometry analysis showed that the three metallic nanoparticles induced apoptotic cell death in a concentration and time dependent-manner. Moreover, the three nanoparticles induced activation of caspase-3 and -7 in hepatoma and leukemia cells. Apoptotic effects were stronger after exposure of both cell lines with 4.7?nm silver nanoparticles than those obtained with 42?nm silver and 30?nm gold nanoparticles. In conclusion, silver (4.7 and 42?nm) and gold (30?nm) nanoparticles induced apoptosis in hepatoma and leukemia cells via the caspase dependent pathway. The smaller silver nanoparticles (4.7?nm) had a greater ability to induce apoptosis in both cell lines.     

Green synthesis and characterization of metal ions-mixed titania for application in dye-sensitized solar cells

Abstract

The objective of the present study is to synthesize various metal ions mixed TiO₂ nanoparticles using a continuous hydrothermal synthesis pilot reactor for dye-sensitized solar cells (DSCs). In the pilot plant, aqueous solutions of the metal salts are mixed with a flow of supercritical water (450?°C and 24.1?MPa) in a confined jet mixer for continuous synthesis of metal ions-mixed nano-titania. Characterization of the particles was made using Brunauer–Emmett–Teller technique for specific surface area, powder X-ray diffraction analysis and transmission electron microscopy for identification and crystallite size, X-ray photoelectron spectroscopy for surface analysis and infrared spectroscopy for distinct group identification. Following the already existing procedures and using the titanates synthesized, dye-sensitized cells of 1?cm² area were assembled and their photovoltaic parameters were evaluated under standard test conditions. The power conversion efficiencies (η %) for 40?mol % Zn²⁺, 5?mol % Zr⁴⁺ and 10?mol % Zn⁴⁺ titania were obtained to be 4.8, 4.95 and 4.9, respectively. The promising efficiency results from a greener and large-scale production of nano-titania is a step forward towards commercializing DSC technology.     

Chromosome damage in individuals exposed to heavy metals†

Testing the mutagenic activity of environmental pollutants has become an important area of modern environmental science and prophylactic medicine. The most suitable method for short‐term mutagenicity testing on man, at present, are chromosome studies on somatic cells of exposed individuals. Mutation types analyzed by such studies are of high practical relevance as indicator system of genetic damage induced in man under in vivo conditions. A rather large series of such studies has been dedicated to the action of heavy metals on individuals contacted with these metals under therapeutic, ecological or occupational conditions or by intoxication. Lead, cadmium, chromium, nickel, mercury, zinc and other metals as well as their compounds have been under study. Analyses of that kind, of course, are hampered by difficulties with the distinct estimation of the actual load as well as unclear conditions of exposition, e.g. simultaneous exposition to different metals.

Results obtained till now arouse some suspicion of a direct or indirect mutagenic activity in man by certain chromium and platinum compounds, arsenic, mercury, and combinations of lead with other heavy metals (cadmium, zinc, arsenic, antimony, etc.). Life style, above all smoking habits, well may act comutagenic. In most cases, however, mutagenic activity of metals and metal compounds apparently is clearly superposed by their toxic activity. In specific cases, chromosome studies also may contribute to discover sources of ecological exposition and to monitor occupational load by heavy metals.     

DNA damage in mouse organs and in human sperm cells by bisphenol A

Abstract

The in vivo genotoxic potential of bisphenol A using the comet assay in mice and in human sperm cells in vitro without metabolizing enzymes was studied. Male mice were exposed by oral gavage to the following doses of bisphenol A (0 125, 250 and 500?mg/kg body weight). DNA damage was investigated in liver, kidney, testes, urinary bladder, colon and lungs cells. In testicular cells, a significant increase in DNA strand breaks was observed in the lowest, but not in the medium or highest dose groups. Histopathological investigation of the testicular samples did not show any treatment dose-related effects. No DNA strand breaks were observed in any of the other investigated tissues. In human sperm cells in vitro, bisphenol A did not induce DNA strand breaks.     

Alkylation of metals and the activity of metal‐alkyls†

The biochemical basis for resistance to metal ion toxicity is emerging though it is complicated by the different resistance mechanisms. Several strategies for resistance to toxic metal ions have been identified:

1. The development of energy driven efflux pumps which keep toxic element levels low in the interior of the cell. Such mechanisms have been described for Cd(II) and As(V).

2. Oxidation (e.g. AsO^2‐ to AsO₄ ^3‐) or reduction (e.g. Hg²⁺ to Hg⁰) can enzymatically and intracellularly convert a more toxic form of an element to a less toxic form.

3. The biosynthesis of intracellular polymers which serve as traps for the removal of metal ions from solution such as traps have been described for cadmium, calcium, nickel and copper.

4. The binding of metal ions to cell surfaces.

5. The precipitation of insoluble metal complexes (e.g. metal sulfides and metal oxides) at cell surfaces.

6. Biomethylation and transport through cell‐membranes by diffusion controlled processes.

In this short review I shall discuss the implications of biomethylation as a detoxification mechanism for microorganisms as well as for certain higher organisms.