Thimerosal-Derived Ethylmercury Is a Mitochondrial Toxin in Human Astrocytes: Possible Role of Fenton Chemistry in the Oxidation and Breakage of mtDNA
Figure 2
Colocalization of Mitotracker () and DCF (peroxide) fluorescence in normal human astrocytes. Thimerosal induces oxidative stress at the mitochondrial level. High resolution images of control NHAs and NHAs treated for 60 minutes with 14.4 M Thimerosal. (a) Mitotracker (red), ROS-induced DCF (green), and nuclear Hoechst staining (blue) of NHAs at × 60 in the absence (left) and presence (right) of 14.4 M Thimerosal. (b) Images of control and treated cells obtained at × 150 magnification. An orange-colored “horseshoe” shaped signal in the control cell consists of a network of mitochondria which is mirrored in the ROS-induced DCF image. The same is demonstrated in the treated cells by a “lightening bolt” shaped mitochondrial network. (c) Square outlines of the cells from (b) highlighting individual Mitotracker and ROS images, and their overlaid images. (d) Intensity profile of MT, DCF, and Hoechst along the two diagonal lines in (b) (with the MT signal × 4 in the Thimerosal treated image). Red: MT signal, blue: Hoechst signal, green: ROS-generated DCF, black: fit to the ROS signal, based on the amplitudinal changes of MT and Hoechst. The two simulations indicate that four times the amount of DCF is generated by mitochondria in the ethylmercury-treated cells, but background cytosolic rates of generation are the same.
