F. Morandini

TL;DR: In NRK-52E cell line the stress response is an early and metal-induced event that correlates well with the direct oxidative damage induced by mercury, and different chaperones are involved in the specific nephrotoxic mechanism of these environmental pollutants and work together for cell survival.

TL;DR: The results demonstrate that, in MDCK cells, inorganic Hg(2+) promotes the activation of specific detoxifying pathways that may, at least partly, depend on the activity of MRP transporters.

TL;DR: Results, proving that subcytotoxic HgCl(2) concentrations affect either the antioxidant defences of MDCK cells or their GJIC, indicate these critical functions as suitable biological targets of early mercury-induced tubular cell injury.

TL;DR: It is shown that, in proliferating NRK‐52E cell cultures, low concentrations of Pb(II) affect the cell adhesive ability and stimulate the disassembly of FAs, thus inhibiting the integrin‐activated signalling.

TL;DR: In vitro investigation of the mechanism(s) of the early nephrotoxic potential of mercury chloride (HgCl2), one of the most diffused and biologically active mercury ( Hg2+) compounds, indicates that MDCK cells represent a suitable in vitro model for the study of Hg neph rotations.