Effects triggered by platinum nanoparticles on primary keratinocytes

The platinum (Pt)-group elements (PGEs) represent a new kind of environmental pollutant and a new hazard for human health. Since their introduction as vehicle-exhaust catalysts, their emissions into the environment have grown considerably compared with their low natural concentration in the earth crust. PGE emissions from vehicle catalysts can be also in the form of nanometer-sized particles (Pt nanoparticles [PtNPs]). These elements, both in their metallic form or as ions solubilized in biological media, are now recognized as potent allergens and sensitizers. Human skin is always exposed to toxic particles; therefore, in the present study we addressed the question of whether polyvinylpyrrolidone-coated PtNPs may have any negative effects on skin cells, including predominantly epidermal keratinocytes. In this study, PtNPs of two sizes were used: 5.8 nm and 57 nm, in concentrations of 6.25, 12.5, and 25 μg/mL. Both types of NPs were protected with polyvinylpyrrolidone. Primary keratinocytes were treated for 24 and 48 hours, then cytotoxicity, genotoxicity, morphology, metabolic activity, and changes in the activation of signaling pathways were investigated in PtNP-treated cells. We found that PtNPs trigger toxic effects on primary keratinocytes, decreasing cell metabolism, but these changes have no effects on cell viability or migration. Moreover, smaller NPs exhibited more deleterious effect on DNA stability than the big ones. Analyzing activation of caspases, we found changes in activity of caspase 9 and caspase 3/7 triggered mainly by smaller NPs. Changes were not so significant in the case of larger nanoparticles. Importantly, we found that PtNPs have antibacterial properties, as is the case with silver NPs (AgNPs). In comparison to our previous study regarding the effects of AgNPs on cell biology, we found that PtNPs do not exhibit such deleterious effects on primary keratinocytes as AgNPs and that they also can be used as potential antibacterial agents, especially in the treatment of Escherichia coli, representing a group of Gram-negative species

Metal toxicokinetics and metal-driven damage to the gut of the ground beetle Pterostichus oblongopunctatus

Toxicokinetics makes up the background for predicting concentrations of chemicals in organisms and, thus, ecological risk assessment. However, physiological and toxicological mechanisms behind toxicokinetics of particular chemicals are purely understood. The commonly used one-compartment model has been challenged recently, showing that in the case of metals it does not describe the pattern observed in terrestrial invertebrates exposed to highly contaminated food. We hypothesised that the main mechanism shaping toxicokinetics of metals in invertebrates at high exposure concentrations in food is the cellular damage to the gut epithelial cells. Gut damage should result in decreased metal assimilation rate, while shedding the dead cells - in increased elimination rate. We performed a typical toxicokinetic experiment, feeding the ground beetles Pterostichus oblongopunctatus food contaminated with Cd, Ni or Zn at 40 mM kg(−1) for 28 days, followed by a depuration period of 14 days on uncontaminated food. The male beetles were sampled throughout the experiment for body metal concentrations and histopathological examinations of the midgut. All metals exhibited a complex pattern of internal concentrations over time, with an initial rapid increase followed by a decrease and fluctuating concentrations during further metal exposure. Histopathological studies showed massive damage to the midgut epithelium, with marked differences between the metals. Cd appeared the most toxic and caused immediate midgut cell degeneration. The effects of Ni were more gradual and pronounced after at least 1 week of exposure. Zn also caused extensive degeneration in the gut epithelium but its effects were the weakest among the studied metals