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 IC values were ~3 and ~50 ?g ml. In both cell types, Cd(II) exerted greater effects on viability. Mitochondrial membrane function in HepG2 cells was reduced 70 % with 40 ?g ml 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 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.
Differences in toxicity, mitochondrial function and miRNome in human cells exposed in vitro to Cd as CdS quantum dots or ionic Cd
Zappettini A;Villani M;
2020
Abstract
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 IC values were ~3 and ~50 ?g ml. In both cell types, Cd(II) exerted greater effects on viability. Mitochondrial membrane function in HepG2 cells was reduced 70 % with 40 ?g ml 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 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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.