Jon Dahl - Academia.edu (original) (raw)

Papers by Jon Dahl

Den norske tannlegeforenings Tidende

European Journal of Oral Sciences, 2021

The purpose of the study was to measure the cement thickness obtained when ceramic rods were lute... more The purpose of the study was to measure the cement thickness obtained when ceramic rods were luted to dentin and to analyze the relation between cement thickness and the previously published tensile bond strength of similar test specimens. In addition, the ISO standard 4049:2019 method was used to determine the film thickness of the used cements. Zirconia (n = 100) and lithium disilicate (n = 50) rods were cemented to bovine dentin using one of five different resin‐based cements. The ceramic‐dentin test specimens were cut into two slices and the cement thickness was measured using a scanning electron microscope and compared to the bond strength values of similar specimens already published. The mean cement thickness recorded for ceramic rods cemented to dentin was in the range 20–40 μm, which was larger than the cement film thickness found by the ISO method. The cement film thickness determined according to ISO standard methods did not concur with the results obtained when cementing...

Mutation Research/Environmental Mutagenesis and Related Subjects, 1988

Toxicology Letters, 1990

The irreversible binding of o,p'-DDD was examined in isolated lung cells, in lung microsomes and ... more The irreversible binding of o,p'-DDD was examined in isolated lung cells, in lung microsomes and in vivo in male New Zealand White rabbits. Non-ciliated bronchiolar (Clara) cells had the highest capacity to bind o,p'-DDD, followed by alveolar type II cells. A fraction of mixed unidentified lung cells was also able to bind o,p'-DDD while no binding was observed in alveolar macrophages. The activation of o,p'-DDD was shown to be mediated by cytochrome P-450 in both lung microsomes and isolated lung cells. In vivo, the binding was preferentially localized in the lung alveolar and bronchiolar regions. The binding of o,p'-DDD observed in vivo may thus be caused by the capacity of several cell types to activate o,p'-DDD.

Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 2011

Journal of Biomedical Materials Research Part A, 2010

Methacrylate monomers that are found to leach from cured resin‐based dental materials induce biol... more Methacrylate monomers that are found to leach from cured resin‐based dental materials induce biological effects in vitro. The underlying mechanisms have not been fully elucidated although involvement of increased cellular reactive oxygen species (ROS) and DNA‐damage has been suggested. In this in vitro study we have elucidated the impact of a commonly used methacrylate monomer, HEMA, on the level and oxidation state of cellular glutathione, intracellular ROS level, as well as the formation of complex between HEMA and glutathione. HEMA exposure rapidly led to increased level of ROS and reduced level of GSH (reduced form of glutathione). Antioxidants effectively counteracted the ROS increase, but had no effect on the GSH depletion. No change in glutathione‐disulphide (GSSG; oxidized form of glutathione) concentration was detected in the HEMA treated cells, showing that oxidation of glutathione was not responsible for the reduced GSH concentration. Further we demonstrated spontaneous f...

Journal of Biomedical Materials Research Part A, 2011

The aim of this in vitro study was to investigate possible involvement of cytochrome P450 (CYP) e... more The aim of this in vitro study was to investigate possible involvement of cytochrome P450 (CYP) enzymes in modifying the toxic potential of 2-hydroxyethyl-methacrylate (HEMA). Primary cultures of CYP expressing rat alveolar type 2 cells were exposed to varying concentrations of HEMA. Nuclear translocation of aryl hydrocarbon receptor (AhR) after HEMA exposure (100 μM) was demonstrated by immunocytochemical staining. Using reverse transcriptase PCR, increased mRNA level of AhR-regulated genes encoding enzymes associated with detoxification of xenobiotics were found. Exposure to 1 mM HEMA rapidly (6 h) resulted in cells with an apoptotic like morphology as suggested by marked nuclear condensation. Cotreatment of the HEMA exposed cells with a CYP inhibitor (disulfiram) or an antioxidant (vitamin C) effectively rescued the cells from this fate. Despite this effect of vitamin C, no increased level of reactive oxygen species was observed in the HEMA exposed cells. Our results suggest that HEMA activates AhR regulated gene transcription and that CYP is involved in the formation of a highly reactive HEMA metabolite.

Archives of Toxicology, 1990

Lung, liver and kidney injury were studied in mice, rats and rabbits 48 h after termination of a ... more Lung, liver and kidney injury were studied in mice, rats and rabbits 48 h after termination of a 4 h inhalation exposure to bromobenzene vapour (250-3400 ppm). Light and electron microscopy of lung tissue revealed injury to Clara cells and adjacent epithelium in mouse bronchioli (bromobenzene concentration 250 ppm and 1000 ppm) and to Clara cells of rat bronchi and bronchioli (1000 ppm bromobenzene) and of rabbit bronchi (2500 ppm and 3400 ppm). Histological and clinicochemical indices of liver damage were found in the same animals, whereas kidney toxicity was observed in mice (two out of ten showed tubular necrosis and elevated concentration of plasma urea) and rats (all had elevated plasma concentrations of creatinine) exposed to 1000 ppm bromobenzene. Inhalation exposure thus produced less kidney injury than expected from previous studies with equimolar doses given intraperitoneally. The mouse was the most severely affected species, followed by the rat, and lastly the rabbit. The animal susceptibility could not be ranked according to the rate of 14C-bromobenzene covalent binding in lung or liver, but it was inversely related to the rate of N-demethylation of benzphetamine (indicative of P450IIB activity) in both lung and liver microsomal preparations. Differences in a P450 mediated detoxification could therefore be of importance in species variability to bromobenzene injury.

British Dental Journal, 2013

Snus er klassifisert av Verdens helseorganisasjons kreftforskningsinstitu på basis av epidemiolog... more Snus er klassifisert av Verdens helseorganisasjons kreftforskningsinstitu på basis av epidemiologiske og eksperimentelle studier som kreftfremkallende for mennesker (1). Derfor merkes snus med at det kan gi kreft. På bakgrunn av to svenske undersøkelser (2, 3) foreslår EU-kommisjonen at kreftadvarselen skal utgå. Vi viser i vår artikkel at det ikke er vitenskapelig grunnlag for å endre advarselsteksten.