Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis最新文献

In recent times, environmental pollution has been an alarming concern. This is increasing day-in-and-day-out, especially in the Asia-Pacific region due to the increasing population, urbanization, industrialization and inappropriate waste management measures. Pollution abatement is the need of the hour to sustain the biosphere in general and the human life in particular. A range of physical, chemical and biological strategies are commonly employed to remove pollutants from the contained water, soil and air. Physical, chemical or physicochemical remediation processes are commonly employed owing to their high efficiency, stability, recyclable property and low procurement cost as compared to metals, inorganic and organic materials. Materials of the later type include biocomposites, thin films, modified (bio)polymers, nanoparticles, nanofilters, sorbent like activated charcoal, and carbon nanotubes and nanosensors. Remediation mechanism largely follows sorption, degradation, oxidation, reduction, catalytic conversion, detection and microbial toxicity principles. This review details the mechanisms of action by these various remediating entities, their successful applications in pollution abatement, drawbacks and future prospects.HighlightsEnvironmental remediation using metals, inorganic and organic materials are discussed extensively.Major remediating approaches, viz., physical, physicochemical and chemical are elaborated citing latest references.The significance of biocomposites, biopolymers, polymers, thin films, nanoparticles, nanofilters, nanosensors and sorbents in remediation are highlighted.Pollutant removal from water, air and soil has been precisely discussed.A note on drawbacks, improvement and future prospects of remediating agents is presented.

Chromium VI (Cr (VI)) can cross cell membranes readily and causes the formation of Cr-DNA adducts, genomic damages, elevation of reactive oxygen species (ROS) and alteration of survival signaling pathways, as evidenced by the modulation in p53 signaling pathway. Mammals, including humans are exposed to Cr, including Cr (VI), frequently through inhalation, drinking water, and food. Several studies demonstrated that Cr (VI) induces cellular death through apoptosis and autophagy, genotoxicity, functional alteration of mitochondria, endocrine and reproductive impairments. In the present review, studies on deleterious effects of Cr (VI) exposure to mammalian cells (in vivo and in vitro) have been documented. Special attention is paid to the underlying molecular mechanism of Cr (VI) toxicity.

Hexavalent chromium (Cr(VI)) compounds are environmental and occupational lung carcinogens. The present study followed the chronic effect of Cr(VI) on the neoplastic transformation of BEAS-2B lung bronchial epithelial cells with or without deletion of Gene 33 (Mig6, EFFRI1), a multifunctional adaptor protein. We find that Gene 33-deleted cells exhibit increased anchorage-independent growth compared to control cells after transformed by 8-week but not 24-week Cr(VI) exposure. Gene 33-deleted cells show a higher level of cell proliferation and are more resistant to acute Cr(VI) toxicity compared to control cells after transformed by 8-week but not 24-week Cr(VI) exposure, despite that 24-week-transformed cells have increased resistance to acute Cr(VI) toxicity. However, Gene 33-deleted cells show increased migration after transformed by both 8-week and 24-week Cr(VI) exposures. Furthermore, only cells transformed by 24 weeks of Cr(VI) exposure can form subcutaneous tumors in nude mice. Although no significant difference in the size of tumors formed by the two cell types, there is a marked difference in the histological manifestation and more MMP3 expression in tumors from Gene 33-deleted cells. Our results demonstrate progressive neoplastic transformation of BEAS-2B cells and the adaptation of these cells to Gene 33 deletion during chronic exposure to Cr(VI).

The main environmental problem in urban areas, especially in Brazil, is the discharge of untreated sewage. The in vivo Drosophila melanogaster Somatic Mutation and Recombination Test (SMART) was used to assess the genotoxicity of surface waters from three different sites in the Tocantins River, Brazil. The in silico approach was used to search for known and predicted interactions between environmental chemicals found in our samples and Drosophila and human proteins. The genotoxicity tests were performed in standard (ST) and high bioactivation (HB) crosses with samples collected at two periods, the rainy and dry seasons. Mutant spot frequencies found in treatments with unprocessed water from the test sites were compared with the frequencies observed in negative controls. The collection points were represented as sites A, B and C along Tocantins River. Sites A and B are located in Porto Nacional City, whereas site C is located in Palmas City. Considering the rainy season collection, positive responses in the ST cross were observed for sites A and C (89.47% and 85% of recombination, respectively) and in the HB cross for sites A, B and C (88.24%, 84.21% and 82.35% of recombination, respectively). The positive results in the dry season were restricted to sites A and B (88.89% and 85.71% of recombination, respectively) in the HB cross. In accordance with in vivo and in silico results, we hypothesize that ribosomal proteins (RPs) in fruit fly and humans are depleted in cells exposed to heavy metal causing DNA damage and chromosome instability, increasing homologous recombination.

Purpose: To conduct a comprehensive meta-analysis investigating the association between polychlorinated biphenyl (PCB) exposure and serum thyroid hormone levels among adults. Methods: Eleven studies met inclusion criteria for analysis following systematic search of PubMed, Embase, and Scopus databases. Of these, 7 studies measured exposure by the total sum of PCB congeners (∑PCB), 1 study measured individual PCB congener levels, and 3 studies measured both ∑PCB levels and PCB congener levels. Correlation coefficients (r) were extracted from each study. Summary estimates were calculated for ∑PCB levels and PCB congeners reported by 2 or more studies: PCB 28, 52, 101, 105, 118, 138, 153, and 180, using random effects model. Results: Significant negative correlation was found between ∑PCBs and T3 (r: -0.09; 95% CI: -0.17, -0.02) and FT3 (r: -0.24; 95% CI: -0.36, -0.12). Congener-specific analysis found T3 to be negatively correlated with PCB-153 (r: -0.19; 95% CI: -0.34, -0.03) and PCB-180 (r: -0.14; 95% CI: -0.26, -0.01), whereas TSH was positively correlated with PCB-105 (r: 0.15; 95% CI: 0.02, 0.28). Conclusions: The present study is the first meta-analysis to investigate the association between PCB exposure and thyroid hormone dysfunction among adults. Results suggest a significant association between PCB exposure and thyroid hormone dysregulation.

In the present study, we have isolated endosulfan tolerant bacterial strains from the rhizosphere of plants growing in a pesticide-contaminated area. The tolerance capacities of these strains were tested up to 50,000 µg ml^-1 of endosulfan. It was found that out of nineteen, four strains (EAG-EC-12, EAG-EC-13, EAG-EC-14, and EAG-EC-15) were capable of surviving up to 50,000 µg ml^-1 endosulfan concentration in the media; thus, these four strains were selected for the characterization. Among four, two strains were identified as Serratia liquefaciens, while the other two strains were Bacillus sp. and Brevibacterium halotolerans. The result shows that growth of strain Serratia liquefaciens 1 and Serratia liquefaciens 2 in treated medium was statistically similar to that of control (cfu 6.8 × 10⁷) after 24 h, while strains Bacillus sp. and Brevibacterium halotolerans have shown growth significantly less than the control. The degradation potential of these strains was analyzed against 100 to 250 µg ml^-1 of endosulfan in a Minimal Broth Medium (MBM), and it was recorded that only 9, 2, 7, and 19% of endosulfan (100 µg ml^-1) remain after a 72 h incubation period of Bacillus sp., Serratia liquefaciens 1, Serratia liquefaciens 2, and Brevibacterium halotolerans, respectively. This endosulfan removal potential of studied strains was decreased with an increase in concentration of endosulfan.

Disruption of element homeostasis may contribute to increased susceptibility of men to cancer development. Whether environmental low-level metal exposure could contribute to the pathogenesis of testicular cancer is unknown. Comparison of the level of 18 elements in whole blood, serum and urine and parameters of oxidative stress/antioxidant status between men with testicular germ cell tumors (TGCT) and healthy men showed significant difference between the groups in most parameters. The results of linear discriminant analysis with a discrimination rate of 96% indicated whole blood Ca, Co, Cu, Fe, K, Mg, Na and Zn, serum Ca, Cu, Na and Ni, and urine Cd, Co, Fe and Mn being the strongest predictors of illness. TGCT patients had a significant increase in serum and blood Cu and decrease in serum Fe and blood Zn with cancer progression. Significantly higher concentrations of Al, As, Pb, and Ni in whole blood/serum of men with TGCT confirm the hypothesis that low-level environmental exposure to these elements may contribute to cancer development. Relationship between elements concentrations and treatment outcomes should be carefully monitored during cancer treatment since high concentrations of commonly used platinum-based chemotherapeutics may additionally disturb the homeostasis of elements.

Synaptic plasticity plays an important role in learning and memory in the developing hippocampus. However, the precise molecular mechanism in lead exposure models remains to be studied. UCP2, an inner mitochondrial anion carrier, regulates synaptic plasticity through uncoupling neurons. And hnRNP K, an RNA binding protein, plays a role in modulating the expression of transcripts coding synaptic plasticity. We aim to investigate whether lead exposure affects UCP2 and hnRNP K expression levels. The Sprague-Dawley rats were exposed to different lead acetate concentrations (0 g/l, 0.5 g/l, 2.0 g/l) during gestational and lactational periods. PC12 cells were also exposed to different lead acetate concentrations (0 μM, 1 μM and 100 μM). We found that the expression levels of UCP2 and hnRNP K had significant declines in the lead exposure rat hippocampus and PC12 cells. Furthermore, the up-regulation of hnRNP K expression level could reverse the expression level of UCP2 in lead exposure models. In conclusion, these results suggest that lead exposure can reduce the expression level of UCP2 which is mediated by decreasing the expression level of hnRNP K.

In 2007, dietary exposure to "scrap melamine' resulted in the death of a large number of cats and dogs, which was attributed to the formation of melamine cyanurate crystals in their kidneys. In this study, we investigated if changes in urinary pH could diminish the renal toxicity associated with exposure to combinations of melamine and cyanuric acid. Female Sprague-Dawley rats were treated for three days with suspensions of melamine and cyanuric acid at doses that were expected to induce renal toxicity. Dosing was then discontinued and the rats were treated for seven days with drinking water solutions (i.e., ammonium chloride and sodium bicarbonate) that would alter urinary pH. The urinary pH of rats administered ammonium chloride drinking water decreased from pH 6.0-6.2 to pH 5.1-5.2. This was accompanied by a decrease in the incidence of melamine cyanurate crystals in the kidneys and a decrease in the incidence of renal lesions. These data suggest that acidification of urine may help overcome the renal toxicities associated with the formation of melamine cyanurate crystals in the kidney.

Both microgravity and radiation exposure in the spaceflight environment have been identified as hazards to astronaut health and performance. Substantial study has been focused on understanding the biology and risks associated with prolonged exposure to microgravity, and the hazards presented by radiation from galactic cosmic rays (GCR) and solar particle events (SPEs) outside of low earth orbit (LEO). To date, the majority of the ground-based analogues (e.g., rodent or cell culture studies) that investigate the biology of and risks associated with spaceflight hazards will focus on an individual hazard in isolation. However, astronauts will face these challenges simultaneously Combined hazard studies are necessary for understanding the risks astronauts face as they travel outside of LEO, and are also critical for countermeasure development. The focus of this review is to describe biologic and functional outcomes from ground-based analogue models for microgravity and radiation, specifically highlighting the combined effects of radiation and reduced weight-bearing from rodent ground-based tail suspension via hind limb unloading (HLU) and partial weight-bearing (PWB) models, although in vitro and spaceflight results are discussed as appropriate. The review focuses on the skeletal, ocular, central nervous system (CNS), cardiovascular, and stem cells responses.