Introduction Recently, increases in impedance coupled with diminished hearing of CI patients have been related to corrosion of platinum electrode contacts. In this study, potential Pt nanoparticle toxicity was investigated in cultures of the organ of Corti cell line (HEI-OC1) and of spiral ganglion neurons (SGN) dissociated from postnatal rats.
Methods Both cell types were exposed to Pt nanoparticles (Pt-NP, 3 nm) with varying concentrations. The biological activity of the HEI-OC1 cells was quantitatively determined by the resazurin assay. The survival rate and the neurite outgrowth following exposure to Pt-NP were quantified by using anti-neurofilament antibodies. Transmission (TEM) and scanning electron microscopy (SEM) were used to characterize changings in morphology and mitochondrial damage of the HEI-OC1 cells exposed to 100 µg/ml Pt-NP.
Results Growth and metabolic activity of the HEI-OC1 cells were reduced between 75 und 150 µg/ml of the Pt-NP. SEM and TEM imaging revealed Pt-NP triggered discrete morphological changings and apoptosis signalling as well as increased autophagosomal-lysosomal compartment in surviving cells following exposure to 100 µg/ml Pt-NP. In contrast, Pt-NP did not induce any cytotoxicity in SGN. Instead, the neurite outgrowth was supported by the Pt-NP from 20 µg/ml of the Pt-NP up.
Conclusions Pt-NP at concentrations between 75-150 µg/ml induced not only apoptosis in the HEI-OC1 cells, but also cellular repair mechanism as shown by SEM and TEM imaging. The SGN cultived in Pt-NP supplemented medium did not demonstrate any cytotoxicity, but support of neurite outgrowth. SEM and immunocytochemistry will be used to characterize the morphology and composition of the primary spiral ganglion cell population following Pt-NP exposure.
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