ABSTRACT:Epidemiological studies have indicated that exposure of humans to inorganic arsenic in drinking water is associated with the occurrence of bladder cancer. The mechanisms by which arsenic induces this malignancy are still uncertain; however, arsenic metabolites are suspected to play a pivotal role. The aim of the present study was the investigation of uptake capabilities of human urothelial cells (UROtsa) compared with primary human hepatocytes (phH) as well as the intracellular distribution of the arsenic species. Additionally, we were interested in the cyto-and genotoxic potential (comet assay, radical generation) of the different arsenic compounds in these two cell types. Our results show that UROtsa cells accumulate higher amounts of the arsenic species than the phH. Differential centrifugation revealed that the arsenic compounds are preferentially distributed into nuclei and ribosomes. After 24-h exposure, arsenic is mainly found in the ribosomes of UROtsa cells and in the nuclei and mitochondria of phH. In contrast to the pentavalent arsenic species, the trivalent species induced a 4-to 5-fold increase of DNA damage in hepatocytes. Radical generation, measured by thiobarbituric acid reactive substances, was more pronounced in hepatocytes than in urothelial cells. In summary, the uptake of arsenic compounds appears to be highly dependent upon cell type and arsenic species. The nonmethylating urothelial cells accumulate higher amounts of arsenic species than the methylating hepatocytes. However, cyto-and genotoxic effects are more distinct in hepatocytes. Further studies are needed to define the implications of the observed accumulation in cellular organelles for the carcinogenic activity of arsenic.The association between arsenic exposure and urinary bladder cancer, typically transitional cell carcinomas, has been observed in the same endemic areas of the world in which skin cancer populations have been identified (Chiou et al., 1995). In addition to bladder and skin cancer, chronic arsenic exposure causes several malignant and nonmalignant human diseases [for review, see Tseng (2007) (Challenger, 1945) consists of a series of reductions and oxidative methylations. In the sequence of reactions, the ϩ5 oxidative arsenic species are always formed before the analogous ϩ3 arsenic species.Recently, Hayakawa et al. (2005) proposed a new metabolic pathway for arsenic biotransformation in which the ϩ3 arsenic species are formed before the respective ϩ5 species. The trivalent metabolites are oxidized by hydrogen peroxide or other agents to the pentavalent species, which are considered end products of arsenic metabolism.It is generally accepted that the ϩ3 methylated arsenic species are more cyto-and genotoxic (e.g., Styblo et al., 2000;Mass et al., 2001;Aposhian et al., 2003;Kligerman et al., 2003;Dopp et al., 2004) and are more potent enzyme inhibitors (e.g., Styblo et al., 1997aStyblo et al., , 2002Schuliga et al., 2002;Chang et al., 2003) than the pentavalent counThis work was kindly supported by the Ge...

The aim of this study was to determine the effects of 38% silver diamine fluoride (SDF) on carious lesions of human deciduous teeth. Ten extracted deciduous incisors with caries were collected and treated with SDF. After the treatment, the teeth were sectioned through the center of the carious lesion. The extent of sliver precipitation was examined using quantitative backscattered electron scanning electron microscopy (qBSE-SEM), energy-dispersive X-ray spectroscopy (EDX), and micro-computed tomography (micro-CT). The qBSE-SEM images revealed that the silver particles could penetrate through the pellicle complex, along with the rod sheaths into the demineralized enamel rods and the dentinal tubules, and form silver-enriched barriers surrounding the carious lesions at depths up to 2,490.2 μm (mean 744.7 ± 448.7 μm) within the dentinal tubules of the carious lesions, but less likely in the sound enamel. The EDX spectrum analysis revealed that carbon, oxygen, phosphorus, chlorine, silver, and calcium were the main elements detected in the lesions treated with SDF. Additionally, sodium, magnesium, aluminum, silicon, zinc, sulfur, and fluorine were detected as the minor elements within the SDF precipitation “zone.” The micro-CT analysis further showed that in the deep cavitated lesions, the silver precipitation could be observed in the pulp chamber. These findings provide new evidence defining the SDF mode of action for arresting caries and suggest that the application of a highly concentrated SDF solution on deciduous teeth should be used with caution for various carious lesions.

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Background.-As silver diamine fluoride (SDF) gains popularity for caries arrest, the authors aimed to investigate the content of fluoride and silver in 38% SDF produced for the US market and its short-term stability. Methods.-Five samples of 38% SDF were evaluated when the bottle was first opened, and at 7 and 28 days. Fluoride concentrations were determined with a fluoride ion-selective electrode, and silver concentrations were determined with a simultaneous inductively coupled plasma mass spectrometer. pH was measured with a pH probe. Weight and volume of individual drops were measured. Results.-At day 0, 40% of individual measured values were above the expected fluoride concentration, and at day 28, 93% were above the expected fluoride concentration (P = .005). At day 0, 19% of individual measured values were below the lowest expected silver concentration, and at day 28, 93% were below (P < .001). Acidity (pH 10) was consistent over the 3 periods. Mean (standard deviation) weight of a drop was 40 (4.0) milligrams, and mean (standard deviation) volume was 32.55 (1.89) microliters, 30% more than the reported value of 25 μL. Conclusion.-Over 28 days, the product pH is stable, whereas the fluoride content tends to increase and the silver content tends to decrease. Drops were larger than expected when dispensed from the bottle.