Mitochondria are critical targets in the hepatotoxicity of cadmium (Cd). Abnormal mitochondrial dynamics have been increasingly implicated in mitochondrial dysfunction in pathophysiological conditions. Therefore, our study aimed to investigate the effects and underlying mechanism of Cd on mitochondrial dynamics during hepatotoxicity. In the L02 liver cell lines, 12 μM cadmium chloride (CdCl2) exposure induced excessive mitochondrial fragmentation as early as 3 h post-treatment with Cd, which preceded the mitochondrial dysfunction such as reactive oxygen species (ROS) overproduction, mitochondrial membrane potential (ΔΨm) loss and ATP reduction. Concurrent to mitochondrial fragmentation, CdCl2 treatment increased the protein levels of dynamin-related protein (Drp1) and promoted the recruitment of Drp1 into mitochondria. Strikingly, mitochondrial fragmentation also occurred in the liver tissue of rats exposed to CdCl2, accompanied by enhanced recruitment of Drp1 into mitochondria. Moreover, in L02 cells, Drp1 silencing could effectively reverse Cd-induced mitochondrial fragmentation and mitochondrial dysfunction. Furthermore, the increased expression and mitochondrial recruitment of Drp1 were tightly related to the disturbance of calcium homeostasis, which could be prevented by both chelating [Ca2+]i and inhibiting [Ca2+]m uptake. Overall, our study indicated that Cd induced Drp1-dependent mitochondrial fragmentation by disturbing calcium homeostasis to promote hepatotoxicity. Manipulation of Drp1 may be the potential avenue for developing novel strategies to protect against cadmium-induced hepatotoxicity.

The oral microbiome consists of a planktonic microbiome residing in saliva and an adhering microbiome (the biofilm adhering to oral hard and soft tissues). Here we hypothesized that possible differences in microbial composition of the planktonic and adhering oral microbiome on teeth can be related to the forces by which different bacterial species are attracted to the tooth surface. The relative presence of 7 oral bacterial species in saliva and biofilm collected from 10 healthy human volunteers was determined twice in each volunteer by denaturinggradient-gel electrophoresis. Analysis of both microbiomes showed complete separation of the planktonic from the adhering oral microbiome. Next, adhesion forces of corresponding bacterial strains with salivacoated enamel surfaces were measured by atomic force microscopy. Species that were found predominantly in the adhering microbiome had significantly higher adhesion forces to saliva-coated enamel (-0.60 to -1.05 nN) than did species mostly present in the planktonic microbiome (-0.40 to -0.55 nN). It is concluded that differences in composition of the planktonic and the adhering oral microbiome are due to small differences in the forces by which strains adhere to saliva-coated enamel, providing an important step in understanding site-and material-specific differences in the composition of biofilms in the oral cavity.