Publications by authors named "Caroline Alberici Martins"

2 Publications

  • Page 1 of 1

Intracellular glutathione: a main factor in TEGDMA-induced cytotoxicity?

Dent Mater 2012 Apr 30;28(4):442-8. Epub 2011 Dec 30.

Department of Conservative/Preventive Dentistry and Periodontology, Hannover Medical School, Hannover, Germany.

Objective: To evaluate whether the reduction/prevention of triethylene glycol dimethacrylate (TEGDMA)-induced decrease of intracellular glutathione (GSH) protects human periodontal ligament fibroblasts (HPLF) against cell death.

Methods: HPLF were preincubated for 30 min with exogenous GSH and then treated with TEGDMA (2.5 mM) with/without GSH (0.5-2.5-5 mM) for the following incubation exposure types: 6h (GI); 6h followed by 18 h recovery time in presence (GII) or absence (GIII) of exogenous GSH; 24 h without recovery time (GIV). TEGDMA-cytotoxicity and intracellular glutathione were assessed by Hoechst 33342 and monobromobimane (MBBr) assays. Data were statistically analyzed with Bonferroni ANOVA (p<0.05).

Results: Preincubation with exogenous GSH increased the intracellular GSH-concentration. TEGDMA was cytotoxic at all treatment times except at 6h (GI) (94±7% of control). In GII the treatment with TEGDMA alone (59±7%) showed no different results to cultures exposed to TEGDMA and GSH. Exogenous GSH had no effect on the TEGDMA-induced cytotoxicity also in the GIII and GIV. Thus, a combined incubation with GSH did not prevent the cytotoxicity of TEGDMA, despite of a significant increase of intracellular GSH-concentration in the presence of exogenously supplied GSH.

Significance: The glutathione-decreasing effect of TEGDMA is not the major cause of TEGDMA-induced cytotoxicity, indicating more complex mechanisms, which are causative for TEGDMA-cytotoxicity in HPLF.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.dental.2011.11.022DOI Listing
April 2012

Immunohistochemical detection of factors related to cellular proliferation and apoptosis in radicular and dentigerous cysts.

J Endod 2011 Jan;37(1):36-9

Postgraduate Program of the Federal University of Santa Catarina, Florianopolis, Santa Catarina, Brazil.

Introduction: This study proposed to investigate aspects of cell proliferation and death in the epithelium of radicular (RCs) and dentigerous (DCs) cysts.

Methods: Serial sections of 17 RCs and 9 DCs were prepared for immunohistochemical detection of caspase-3, Bcl-2, and Ki-67 antigens.

Results: Caspase-3 was detected mainly in the suprabasal and superficial epithelial cells of RCs and DCs, whereas Ki-67 was detected predominantly in the basal layer. Both markers had significant expression in hyperplastic epithelium related to an intense inflammation in the capsule. Immunoreactivity for Bcl-2 was restricted to the basal layer and was significantly higher in atrophic epithelium of DCs than that of RCs.

Conclusions: These results suggest that epithelial proliferation is balanced by apoptosis and that the presence of inflammation inhibits the Bcl-2 expression. DCs and RCs have different formation mechanisms but have similar biological behavior in the presence of intense inflammatory infiltrate.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.joen.2010.09.010DOI Listing
January 2011
-->