The stability of CuO nanoparticles (NPs) is expected to play a key role in the environmental risk assessment of nanotoxicity in aquatic systems. In this study, the effect of alginate (model polysaccharides) on the stability of CuO NPs in various environmentally relevant ionic strength conditions was investigated by using time-resolved dynamic light scattering. Significant aggregation of CuO NPs was observed in the presence of both monovalent and divalent cations. The critical coagulation concentrations (CCC) were 54.5 and 2.9 mM for NaNO3 and Ca(NO3)2, respectively. The presence of alginate slowed nano-CuO aggregation rates over the entire NaNO3 concentration range due to the combined electrostatic and steric effect. High concentrations of Ca2+ (>6 mM) resulted in stronger adsorption of alginate onto CuO NPs; however, enhanced aggregation of CuO NPs occurred simultaneously under the same conditions. Spectroscopic analysis revealed that the bridging interaction of alginate with Ca2+ might be an important mechanism for the enhanced aggregation. Furthermore, significant coagulation of the alginate molecules was observed in solutions of high Ca2+ concentrations, indicating a hetero-aggregation mechanism between the alginate-covered CuO NPs and the unabsorbed alginate. These results suggested a different aggregation mechanism of NPs might co-exist in aqueous systems enriched with natural organic matter, which should be taken into consideration in future studies.
It has become increasingly apparent that global manganese (Mn) pollution to air and water is a significant threat to human health. Despite this recognition, research is only beginning to comprehend the detrimental effects of exposure. Mn, while essential, is particularly harmful to the central nervous system, and overexposure is symptomatic of several neurological disorders. At-risk populations have been identified, but it is still unclear whether typical exposure levels have any long-term consequences. Those at an elevated risk have diminished intellectual function, learning and memory, and mental development. While the overall mechanism of toxicity is undetermined, Mn has been found to induce oxidative stress, exacerbate mitochondrial dysfunction, dysregulate autophagy, and promote apoptosis, ultimately enhancing neurodegeneration. Extrapolation of this in vitro and in vivo data to humans is difficult. There is a definite need to correlate epidemiological studies with causative effects. It is imperative that research efforts endure, so threats are appropriately identified and exposure properly regulated. 相似文献