To encourage the applicability of nano-adsorbent materials for heavy metal ion removal from seawater and limit any potential side effects for marine organisms, an ecotoxicological evaluation based on a biological effect-based approach is presented. ZnCl2 (10 mg L−1) contaminated artificial seawater (ASW) was treated with newly developed eco-friendly cellulose-based nanosponges (CNS) (1.25 g L−1 for 2 h), and the cellular and tissue responses of marine mussel Mytilus galloprovincialis were measured before and after CNS treatment. A control group (ASW only) and a negative control group (CNS in ASW) were also tested. Methods: A significant recovery of Zn-induced damages in circulating immune and gill cells and mantle edges was observed in mussels exposed after CNS treatment. Genetic and chromosomal damages reversed to control levels in mussels’ gill cells (DNA integrity level, nuclear abnormalities and apoptotic cells) and hemocytes (micronuclei), in which a recovery of lysosomal membrane stability (LMS) was also observed. Damage to syphons, loss of cilia by mantle edge epithelial cells and an increase in mucous cells in ZnCl2-exposed mussels were absent in specimens after CNS treatment, in which the mantle histology resembled that of the controls. No effects were observed in mussels exposed to CNS alone. As further proof of CNS’ ability to remove Zn(II) from ASW, a significant reduction of >90% of Zn levels in ASW after CNS treatment was observed (from 6.006 to 0.510 mg L−1). Ecotoxicological evaluation confirmed the ability of CNS to remove Zn from ASW by showing a full recovery of Zn-induced toxicological responses to the levels of mussels exposed to ASW only (controls). An effect-based approach was thus proven to be useful in order to further support the environmentally safe (ecosafety) application of CNS for heavy metal removal from seawater.
Objective: Patients with obstructive sleep apnea syndrome exhibit accelerated vascular aging and renal damage. Aim of the study was to investigate whether vascular dysfunction is a feature of obstructive sleep apnea syndrome per se or instead related to the presence of traditional cardiovascular risk factors.Methods: Forty patients with moderate-severe obstructive sleep apnea syndrome (20 with, 20 without traditional risk factors) and 20 matched healthy controls were enrolled. Renal vasodilating capacity, endothelium-dependent vasodilation in the brachial artery, carotid-femoral pulse wave velocity and carotid stiffness were measured. Oxidative stress, endothelial biomarkers and leukocyte adhesion molecule levels were also evaluated.Results: Apneic patients without traditional cardiovascular risk factors presented reduced endothelium-dependent vasodilation (3.7 AE 2.1 versus 6.1 AE 3.0%, P < 0.05), increased serum E-selectin (49.8 AE 11.5 versus 38.9 AE 17.9 ng/ml, P < 0.05), and impaired renal vasodilating capacity (6.0 AE 4.3 versus 10.4 AE 6.1%, P < 0.05), as compared to healthy controls. Endothelial NO synthase expression was reduced (0.0133 versus 0.0221 Â 10 6 copies/mg RNA, P < 0.05), whereas oxidative stress parameters and leukocyte adhesion molecules were similar to controls. Patients with obstructive sleep apnea syndrome and traditional risk factors also exhibit increased aortic and carotid stiffness, increased renal resistive index and intima-media thickness, and reduced expression of the endothelial progenitor cell marker CD34: however, these parameters were similar to those of healthy controls in patients with isolated obstructive sleep apnea syndrome.Conclusion: Obstructive sleep apnea syndrome is characterized by endothelial dysfunction and activation and impaired renal vasodilating capacity even in the absence of traditional cardiovascular risk factors, possibly due to reduced endothelial NO synthase expression.
Although amorphous silica is used in food products, cosmetics and paints and as vector for drug delivery, data on its potential health hazard are limited. The aim of this study was to investigate the cytotoxic and genotoxic potential of silica particles of different sizes (250 and 500nm) and structures (dense and mesoporous). Dense silica (DS) spheres were prepared by sol-gel synthesis, mesoporous silica particles (MCM-41) were prepared using hexadecyltrimethyl ammonium bromide as a structure-directing agent and tetraethylorthosilicate as silica source. Particles were accurately characterised by dynamic light scattering, nitrogen adsorption, X-ray diffraction and field emission scanning electron microscopy. Murine macrophages (RAW264.7) and human epithelial lung (A549) cell lines were selected for investigation. Genotoxicity was evaluated by Comet assay and micronucleus test. Cytotoxicity was tested by the trypan blue method. Cells were treated with 0, 5, 10, 20, 40 and 80 µg/cm(2) of different silica powders for 4 and 24 h. The intracellular localisation of silica was investigated by transmission electron microscopy. Amorphous particles penetrated into the cells, being compartmentalised within endocytic vacuoles. DS and MCM-41 particles induced cytotoxic and genotoxic effects in A549 and RAW264.7 although to different extent in the two cell lines. A549 were resistant in terms of cell viability, but showed a generalised induction of DNA strand breaks. RAW264.7 were susceptible to amorphous silica exposure, exhibiting both cytotoxic and genotoxic responses as DNA strand breaks and chromosomal alterations. The cytotoxic response of RAW264.7 was particularly relevant after MCM-41 exposure. The genotoxicity of amorphous silica highlights the need for a proper assessment of its potential hazard for human health.
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