Polyol-based Synthesis of Praseodymium Oxide Nanoparticles

A series of well-crystallized praseodymium oxide (Pr6O11) nanoparticles are synthesized via a highly scalable process from praseodymium nitrate. Praseodymium hydroxide is synthesized through a modified polyol process and subsequent calcination in air at 600°C for 2 h to transform the precursor material into Pr6O11 nanoparticles. A complete characterization of a specific sample by SEM, HRTEM, and X-ray diffraction (XRD) demonstrates that Pr6O11 nanoparticles form elementary blocks with a calculated size of 118 nm, containing slightly agglomerated nanocrystalline particles with a polycrystalline face-centred cubic phase and an individual size of around 10 nm. Particles can be easily dispersed in water through ultrasonification. Particles display a BET Specific Surface Area (SSA; 8.75 m² g-1) with a nitrogen adsorption-desorption isotherm of type II and a helium density of powders (d = 5.66 g cm-3)

Advances in Carcinogenic Metal Toxicity and Potential Molecular Markers

Metal compounds such as arsenic, cadmium, chromium, cobalt, lead, mercury, and nickel are classified as carcinogens affecting human health through occupational and environmental exposure. However, the underlying mechanisms involved in tumor formation are not well clarified. Interference of metal homeostasis may result in oxidative stress which represents an imbalance between production of free radicals and the system’s ability to readily detoxify reactive intermediates. This event consequently causes DNA damage, lipid peroxidation, protein modification, and possibly symptomatic effects for various diseases including cancer. This review discusses predominant modes of action and numerous molecular markers. Attention is paid to metal-induced generation of free radicals, the phenomenon of oxidative stress, damage to DNA, lipid, and proteins, responsive signal transduction pathways with major roles in cell growth and development, and roles of antioxidant enzymatic and DNA repair systems. Interaction of non-enzymatic antioxidants (carotenoids, flavonoids, glutathione, selenium, vitamin C, vitamin E, and others) with cellular oxidative stress markers (catalase, glutathione peroxidase, and superoxide dismutase) as well as certain regulatory factors, including AP-1, NF-κB, Ref-1, and p53 is also reviewed. Dysregulation of protective pathways, including cellular antioxidant network against free radicals as well as DNA repair deficiency is related to oncogenic stimulation. These observations provide evidence that emerging oxidative stress-responsive regulatory factors and DNA repair proteins are putative predictive factors for tumor initiation and progression

Effect of Cr(V) on reproductive organ morphology and sperm parameters: An experimental study in mice

BACKGROUND: Cr(V) species are formed during the intracellular reduction of Cr(VI), a ubiquitous environmental pollutant. In this study, the acute toxicity of a physiologically stable Cr(V) compound, [Cr(V)-BT](2- )(BT = bis(hydroxyethyl)aminotris(hydroxymethyl)methane) was investigated in the male reproductive system of sexually mature 60-day-old male ICR-CD1 mice. METHODS: Eight-week-old animals were subcutaneously injected daily with a dose of ca 8 μmol of Cr/mouse, during 5 days. The control group was injected with 0.5 mL of BT buffer. Testis and epididymis morphology was evaluated using light and transmission electron microscopy. Epididymal sperm counts, motility and acrosome integrity were also assayed using standard methods. RESULTS: Seminiferous epithelium abnormalities were detected in the Cr(V)-BT experimental group, including intraepithelial vacuolation, and remarkable degeneration of Sertoli cells, spermatocytes and spermatids. The premature release of germ cells into the tubular lumen was also evident. Histological evaluation of epididymal compartments revealed apparently normal features. However, the epididymal epithelium presented vacuolation. [Cr(V)-BT](2- )induced a reduction in sperm acrosome integrity. However, sperm motility and density were not significantly affected. CONCLUSION: This in vivo study using a Cr(V) compound, provides evidence for the potential reproductive hazards caused on male reproductive system by species containing chromium in intermediate oxidation states

The Werner Syndrome Protein Suppresses Telomeric Instability Caused by Chromium (VI) Induced DNA Replication Stress

Telomeres protect the chromosome ends and consist of guanine-rich repeats coated by specialized proteins. Critically short telomeres are associated with disease, aging and cancer. Defects in telomere replication can lead to telomere loss, which can be prevented by telomerase-mediated telomere elongation or activities of the Werner syndrome helicase/exonuclease protein (WRN). Both telomerase and WRN attenuate cytotoxicity induced by the environmental carcinogen hexavalent chromium (Cr(VI)), which promotes replication stress and DNA polymerase arrest. However, it is not known whether Cr(VI)-induced replication stress impacts telomere integrity. Here we report that Cr(VI) exposure of human fibroblasts induced telomeric damage as indicated by phosphorylated H2AX (γH2AX) at telomeric foci. The induced γH2AX foci occurred in S-phase cells, which is indicative of replication fork stalling or collapse. Telomere fluorescence in situ hybridization (FISH) of metaphase chromosomes revealed that Cr(VI) exposure induced an increase in telomere loss and sister chromatid fusions that were rescued by telomerase activity. Human cells depleted for WRN protein exhibited a delayed reduction in telomeric and non-telomeric damage, indicated by γH2AX foci, during recovery from Cr(VI) exposure, consistent with WRN roles in repairing damaged replication forks. Telomere FISH of chromosome spreads revealed that WRN protects against Cr(VI)-induced telomere loss and downstream chromosome fusions, but does not prevent chromosome fusions that retain telomere sequence at the fusion point. Our studies indicate that environmentally induced replication stress leads to telomere loss and aberrations that are suppressed by telomerase-mediated telomere elongation or WRN functions in replication fork restoration

Cancer effects of formaldehyde: a proposal for an indoor air guideline value

Formaldehyde is a ubiquitous indoor air pollutant that is classified as “Carcinogenic to humans (Group 1)” (IARC, Formaldehyde, 2-butoxyethanol and 1-tert-butoxypropanol-2-ol. IARC monographs on the evaluation of carcinogenic risks to humans, vol 88. World Health Organization, Lyon, pp 39–325, 2006). For nasal cancer in rats, the exposure–response relationship is highly non-linear, supporting a no-observed-adverse-effect level (NOAEL) that allows setting a guideline value. Epidemiological studies reported no increased incidence of nasopharyngeal cancer in humans below a mean level of 1 ppm and peak levels below 4 ppm, consistent with results from rat studies. Rat studies indicate that cytotoxicity-induced cell proliferation (NOAEL at 1 ppm) is a key mechanism in development of nasal cancer. However, the linear unit risk approach that is based on conservative (“worst-case”) considerations is also used for risk characterization of formaldehyde exposures. Lymphohematopoietic malignancies are not observed consistently in animal studies and if caused by formaldehyde in humans, they are high-dose phenomenons with non-linear exposure–response relationships. Apparently, these diseases are not reported in epidemiological studies at peak exposures below 2 ppm and average exposures below 0.5 ppm. At the similar airborne exposure levels in rodents, the nasal cancer effect is much more prominent than lymphohematopoietic malignancies. Thus, prevention of nasal cancer is considered to prevent lymphohematopoietic malignancies. Departing from the rat studies, the guideline value of the WHO (Air quality guidelines for Europe, 2nd edn. World Health Organization, Regional Office for Europe, Copenhagen, pp 87–91, 2000), 0.08 ppm (0.1 mg m−3) formaldehyde, is considered preventive of carcinogenic effects in compliance with epidemiological findings

Phytoremediation of heavy metal-contaminated sites: Eco-environmental concerns, field studies, sustainability issues and future prospects

Environmental contamination due to heavy metals (HMs) is of serious ecotoxicological concern worldwide because of their increasing use at industries. Due to non-biodegradable and persistent nature, HMs cause serious soil/water pollution and severe health hazards in living beings upon exposure. HMs can be genotoxic, carcinogenic, mutagenic, and teratogenic in nature even at low concentration. They may also act as endocrine disruptors and induce developmental as well as neurological disorders and thus, their removal from our natural environment is crucial for the rehabilitation of contaminated sites. To cope with HM pollution, phytoremediation has emerged as a low-cost and eco-sustainable solution to conventional physico-chemical cleanup methods that require high capital investment and labor alter soil properties and disturb soil microflora. Phytoremediation is a green technology wherein plants and associated microbes are used to remediate HM-contaminated sites to safeguard the environment and protect public health. Hence, in view of the above, the present paper aims to examine the feasibility of phytoremediation as a sustainable remediation technology for the management of metals-contaminated sites. Therefore, this paper provides an in-depth review on both the conventional and novel phytoremediation approaches, evaluate their efficacy to remove toxic metals from our natural environment, explore current scientific progresses, field experiences and sustainability issues and revise world over trends in phytoremediation research for its wider recognition and public acceptance as a sustainable remediation technology for the management of contaminated sites in 21st century