RESUMEN
When applied in the same concentration to tomato plants, cadmium sulfate (CdSO4) and zinc sulfate (ZnSO4) were transported from soil to roots and from roots to shoots more readily than their nano counterparts: cadmium sulfide quantum dots (CdS QD) and zinc sulfide quantum dots (ZnS QD). Compared to the CdS QD, he higher rate of transport of CdSO4 resulted in a greater negative effect on growth, chlorophyll content, antioxidant properties, lipid peroxidation and activation of antioxidant defence systems. Although ZnSO4 was transported more rapidly than ZnS QD, the overall effect of Zn addition was positive (increase in total plant mass, stem length, antioxidant content and decrease in lipid peroxidation). However, these effects were more pronounced in the case of ZnS QD, suggesting that the mechanisms underpinning the activity of ZnS QD and ZnSO4 were different. Thus, the risk of phytotoxicity and food chain transfer of the two elements depended on their form (salt or nanoform), and consequently their effects on plants' growth and physiology were different.
This work elucidates the mechanisms underlying the responses of CdS QD and ZnS QD in contrast to those of their corresponding salts on tomato plants. Our results showed that faster transport from roots to leaves in the case of salts in respect to the nanoform augment their detrimental impact on tomato's antioxidant properties and growth and make the nanoform of both a better alternative for crop application either as fertilizers or as pesticides.
Asunto(s)
Compuestos de Cadmio , Puntos Cuánticos , Solanum lycopersicum , Sulfuros , Antioxidantes , Clorofila , Sales (Química) , Biodegradación AmbientalRESUMEN
The article describes: growth phenotypes of the four plant species (Noccaea caerulescens, Thlaspi perfoliatum, Arabidopsis halleri, Arabidopsis thaliana) before and after the treatment with ionic and nanoscale Zn and Cd (Fig. 1); the method of synthesis and characterization of ZnS QDs and CdS QDs (Fig. 2); the genetic characterization (performed with molecular markers) of the four plant species, their relative genecological relation (Fig. 3); a conceptual workflow designed to detect the amount of ionic Zn and Cd in the original solution/suspension used for the treatment (Fig. 4); the determination of Zn and Cd in the treatment soils after 30 days from supplement of ionic and nanoscale Zn and Cd (Fig. 5); the effect of the treatment on root elongation (Fig. 6); a workflow of a novel analytical method designed to detect the ionic and nanoscale Zn and Cd in the plant tissues after digestion with three different methods (Fig. 7); a reconstruction experiments with an exsiccated powder of plant tissue spiked with the same amount of Zn in the ionic and nanoscale forms (Fig. 8); a TEM-EDX analysis on these powdered plant tissues after removal of all soluble (ionic) Zn to show the presence of Zn in a non soluble form (nanoscale) (Fig. 9); the calculation of Bioconcentration Factor (BCF) and Translocation Factor (TF) and their ratios (Table 1); all data of the "spiking" experiments (Tables 2 and 3).
RESUMEN
The data included in this paper are associated with a research article entitled 'Differences in toxicity, mitochondrial function and miRNome in human cells exposed in vitro to Cd as CdS quantum dots or ionic Cd' [1]. The article concerns the use of miRNAs as biomarkers for engineered nanomaterials (ENMs) risk assessment. Two different type of human cells, HepG2 and THP-1, were exposed to different forms of Cadmium: nanoscale, as CdS quantum dots (CdS QDs), and ionic, as CdSO4 8/3 -hydrate (Cd(II)). The cells were treated with sub-toxic doses of CdS QDs; 3 µg ml-1 in HepG2 and 6.4 µg ml-1 and 50 µg ml-1 in THP-1, as well as equivalent cadmium doses as Cd(II). In this dataset, changes in expression levels of miRNAs are reported. In addition, GO enrichment analyses of target genes of miRNAs modulated by Cd stress, network analysis of the microRNome and an in silico pathway analysis are also reported. These data enhance and also summarize much of the data independently presented in the research article and therefore, must be considered as supplementary.
RESUMEN
Cadmium is toxic to humans, although Cd-based quantum dots exerts less toxicity. Human hepatocellular carcinoma cells (HepG2) and macrophages (THP-1) were exposed to ionic Cd, Cd(II), and cadmium sulfide quantum dots (CdS QDs), and cell viability, cell integrity, Cd accumulation, mitochondrial function and miRNome profile were evaluated. Cell-type and Cd form-specific responses were found: CdS QDs affected cell viability more in HepG2 than in THP-1; respective IC20 values were â¼3 and â¼50⯵g ml-1. In both cell types, Cd(II) exerted greater effects on viability. Mitochondrial membrane function in HepG2 cells was reduced 70 % with 40⯵g ml-1 CdS QDs but was totally inhibited by Cd(II) at corresponding amounts. In THP-1 cells, CdS QDs has less effect on mitochondrial function; 50⯵g ml-1 CdS QDs or equivalent Cd(II) caused 30 % reduction or total inhibition, respectively. The different in vitro effects of CdS QDs were unrelated to Cd uptake, which was greater in THP-1 cells. For both cell types, changes in the expression of miRNAs (miR-222, miR-181a, miR-142-3p, miR-15) were found with CdS QDs, which may be used as biomarkers of hazard nanomaterial exposure. The cell-specific miRNome profiles were indicative of a more conservative autophagic response in THP-1 and as apoptosis as in HepG2.
Asunto(s)
Compuestos de Cadmio/toxicidad , Cadmio/toxicidad , Mitocondrias/efectos de los fármacos , Puntos Cuánticos/toxicidad , Sulfuros/toxicidad , Supervivencia Celular/efectos de los fármacos , Células Hep G2 , Humanos , Potencial de la Membrana Mitocondrial/efectos de los fármacos , MicroARNs/metabolismo , Mitocondrias/fisiología , Células THP-1RESUMEN
The data included in this paper are associated with the research article entitled "Markers for toxicity to HepG2 exposed to cadmium sulphide quantum dots; damage to mitochondria" (Paesano et al.) [1]. The article concerns the cytotoxic and genotoxic effects of CdS QDs in HepG2 cells and the mechanisms involved. In this dataset, changes in expression levels of candidate genes are reported, together with details concerning synthesis and properties of CdS QDs, additional information obtained through literature survey, measures of the mitochondrial membrane potential and the glutathione redox state.
RESUMEN
Interaction of living organisms with quantum dots (QDs) is certainly more focused on environment and occupational exposure associated with production and release or disposal. Here, the transcription of genes involved in mitochondrial organization and function in HepG2 cells exposed to cadmium sulphide (CdS) QDs has been profiled to highlight biomarkers of exposure and effect to be tested for other cadmium based QDs. At low concentrations, exposure to CdS QDs induced only minor damage to nuclear DNA, and none to mitochondrial DNA. However, the stress caused an increase in the production of reactive oxygen species (ROS), which triggered the mitochondria-mediated intrinsic apoptotic pathway involving a cascade of transcriptomic events, finally prompting the activation of a rescue pathway. The transcriptomic analysis confirmed the involvement in the response to CdS QDs of genes related to apoptosis (AIFM2 and APAF1), oxidative stress response (OXR1 and AOX1) and autophagy (ATG3 and ATG7), as potential biomarkers. Other possible biomarkers specific for mitochondria function were LONP1 and HSPD1.