Corrosion susceptibility of titanium covered by dental cements.

OBJECTIVES: The aim of this study is to determine the influence of acidic fluorinated cements (as glass ionomer (GI) cements) on the passivation of titanium, using electrochemical investigations. METHODS: We realized experimental electrodes that associate titanium and dental cements. Polarization resistance of titanium electrodes has been determined for uncovered metal and electrodes covered with three dental cements. Student's t-tests proved the reproducibility. We also compared successive voltammograms for uncovered titanium and GI covered titanium. RESULTS: Correct passivation was observed with zinc eugenate, but fluorinated GI or zinc phosphate coverage increased the corrosion susceptibility. SIGNIFICANCE: However there is no evidence of titanium depassivation when covered with cement. No clinical contraindication can be held.

The vestigial locus of Drosophila melanogaster is involved in resistance to inhibitors of dTMP synthesis.

The vestigal (vg) gene encodes a nuclear protein which plays a major role in the formation of the wing of Drosophila. Resistance or sensitivity to aminopterin, an inhibitor of the dihydrofolate reductase enzyme in D. melanogaster, seems to be associated with a specific alteration in vg gene function. Wild-type and vg mutant strains selected for growth on increasing concentrations of aminopterin display changes in physiological and biochemical parameters such as viability on normal and aminopterin-containing media, duration of development, wing phenotype, dihydrofolate reductase activity, and cross-resistance to fluorodeoxyuridine (FUdR) and to methotrexate. Our results indicate that the mechanisms of resistance differ in the wild-type and mutant strains. The vg83b27 mutant, in which the major part of intron 2 of the vg gene is deleted, is associated with a high rate of resistance to FUdR, an inhibitor of thymidylate synthetase. Moreover, vg83b27/vgBG heterozygotes, which are wild type when grown on normal medium, display a strong vg phenotype when grown on aminopterin. Our results indicate a role for the vestigial locus in mediating resistance to inhibitors of dTMP synthesis.

Vestigial mutants of Drosophila melanogaster live better in the presence of aminopterin: increased level of dihydrofolate reductase in a mutant.

Vestigial (vg) mutants of Drosophila melanogaster are characterized by atrophied wings. In this paper we show that: (1) aminopterin an inhibitor of dihydrofolate reductase (DHFR) and fluorodeoxyuridine (FUdR), an inhibitor of thymidylate synthetase induce nicks in the wings of wild-type flies and phenocopies of the vg mutant phenotype when vg/+ and vgB/+ flies are reared on these substances (vgB is a deficiency of the vg locus). Only thymidine and thymidylate can rescue the flies from the effect of aminopterin. We propose that the vg phenotype is due to a decrease in the dTMP pool in the wings. (2) Mutant vg strains yield more offspring on medium containing aminopterin than on normal medium. The resistance of vg larvae to the inhibitor seems specific to the gene. This is the first case of aminopterin resistance in living eucaryotes. In contrast sensitivity of the vg larvae to FUdR is observed. (3) An increase in the activity and amount of DHFR is observed in mutant strains as compared with the wild-type flies. Our data suggest that the vg+ gene is a regulatory gene acting on the DHFR gene or a structural gene involved in the same metabolic pathway.

Inhibitors of thymidylate synthesis increase whereas thymidine decreases meiotic recombination in Drosophila melanogaster.

We have demonstrated the effect of different media on meiotic recombination in Drosophila melanogaster. Recombination is more frequent when the medium is deprived of bases, nucleosides and nucleotides. We have shown that two inhibitors of thymidylate (dTMP) synthesis - aminopterin inhibiting dihydrofolate reductase (DHFR) and fluorodeoxyuridine (FUdR) inhibiting thymidylate synthetase - result in a significant increase in meiotic recombination in the yellow/white region on the X chromosome of Drosophila melanogaster. Moreover the addition of thymidine to the richest medium significantly lowers normal recombination. Such studies represent a powerful tool for future studies on the mechanism of meiotic recombination.

Dihydrofolate reductase activity and resistance to aminopterin in various species of Drosophila.

The aim of our work was to compare the mechanisms of resistance to aminopterin, inhibitor of the dihydrofolate reductase enzyme, between different Drosophila species and those described for cultured cells. Moreover we compared the systematic species divisions based on morphological traits and those based on a molecular approach. For this purpose, the effect of aminopterin on viability and wing phenotype was studied in different Drosophila species. Dihydrofolate reductase was measured in adult flies. We found an important dihydrofolate reductase activity in the melanogaster sub-group compared to the other species studies. Wing effect was observed only in this sub-group. The effects of aminopterin on the wing phenotype were very similar to the phenotype of rudimentary mutants. Both deplete the pyrimidine pool and it has been shown by the studies of the structural genes of the nucleotide pyrimidine pathway that the wing tissue is very sensitive to every pertubation of this metabolism. The D. ananassae species was found to be fully resistant at the concentrations of the inhibitor tested. No or very little dihydrofolate reductase activity was detected. The binding of the enzyme to the inhibitor was comparable to that found in the Oregon strain of D. melanogaster. The purine and pyrimidine salvage pathways were investigated and the D. ananassae species displayed an important thymidine kinase activity. The D. ananassae flies were sensitive on Sang medium compared to the Oregon flies but were able to use exogenous bases or nucleosides more efficiently.(ABSTRACT TRUNCATED AT 250 WORDS)

[Study of the effect of 2 inhibitors of nucleotide synthesis, aminopterin and fluorodeoxyuridine, on wild type strains and vestigial mutants in Drosophila melanogaster]. / Etude de l'effet de deux inhibiteurs de la synthèse des nucléotides l'aminoptérine et la fluorodésoxyuridine sur des souches sauvage et mutantes vestigial chez Drosophila melanogaster.

Two inhibitors of nucleotide metabolism, aminopterin and FUdR, were tested on a wild type strain, on two mutant strains: vg and vgnp, and on a vg strain with the wild type genetic background. Without inhibitors, a lengthening of the developing time was observed for the mutant strains compared to the wild type. With aminopterin, larval mortality and lengthening of developing time are significantly higher in the wild type than in the mutant strains. Mutant strains seemed to be resistant to low concentrations of FUdR. The hypothesis of a perturbed pyrimidine metabolism in the mutants seems to be confirmed.