Chironomus riparius exposure to fullerene-contaminated sediment results in oxidative stress and may impact life cycle parameters.

A key component of understanding the potential environmental risks of fullerenes (C60) is their potential effects on benthic invertebrates. Using the sediment dwelling invertebrate Chironomus riparius we explored the effects of acute (12h and 24h) and chronic (10d, 15d, and 28d) exposures of sediment associated fullerenes. The aims of this study were to assess the impact of exposure to C60 in the sediment top layer ((0.025, 0.18 and 0.48) C60 mg/cm2) on larval growth, oxidative stress and emergence rates and to quantify larval body burdens in similarly exposed organisms. Oxidative stress localization was observed in the tissues next to the microvilli and exoskeleton through a method for identifying oxidative stress reactions generated by reactive oxygen species. Rapid intake of fullerenes was shown in acute experiments, whereas body residues decreased after chronic exposure. Transmission electron microscopy analysis revealed oxidative damage and structural changes in cells located between the lipid droplets and next to the microvilli layer in fullerene exposed samples. Fullerene associated sediments also caused changes in the emergence rate of males and females, suggesting that the cellular interactions described above or other effects from the fullerenes may influence reproduction rates.

Structural domains involved in human cytomegalovirus glycoprotein B-mediated cell-cell fusion.

A novel fusion assay was established to determine fusion activity with cocultivated human foreskin fibroblasts of stable transfectants derived from human astrocytoma cells (U373) expressing authentic or mutagenized human cytomegalovirus glycoprotein B (HCMV gB; gpUL55). Compared to transfectants expressing authentic HCMV gB, those expressing gB forms with a deletion of hydrophobic domain 1 (hd1; aa 714-747) or with deletions of specific segments in the cytoplasmic tail (aa 811-825 and 871-906) exhibited significantly reduced heterologous fusogenicity. HCMV gB-specific monoclonal antibodies (MAbs) as well as MAb against cellular annexin II prevented fusion of the transfectant expressing authentic gB. Comparable surface exposure of HCMV gB or its derivatives was demonstrated in all transfectants by FACS analysis. Our observations are compatible with the notion that indigenous fusion activity of HCMV gB depends on the extracellular hd1 domain and on the conformation of the cytoplasmic tail.