Cytotoxic response of two cell lines exposed in vitro to four endodontic sealers

Aim: To investigate the cytotoxicity of four endodontic sealers with different bases – Epiphany (EPH), AH Plus (AHP), Sealer 26 (S26) and Endofill (ENF) – on human foreskin fibroblasts (HFF) and mouse macrophages (J774/G8). Methods: Cells were placed in direct contact with freshly prepared endodontic sealers in polypropylene tubes. The cells were incubated for 24, 48 and 72 h. Cytotoxicity was assessed using the MTT assay (cell viability) and Griess reagent (NO release). Results: On the HFF cultures, EPH showed the lowest viability levels of all four sealers at 24 h (p<0.05), but over time (72h), EPH lessened its toxic levels in a similar pattern as the other three materials (p>0.05). The viability of all four sealers on the macrophage cultures showed no statistically significant difference over time, except between EPH and AHP at 72 h (p<0.05). Although uniformity was not detected in macrophage and fibroblast release of NO in response to sealers over time, a trend of increased NO levels for EPH (p<0.05) was observed. Conclusions: The response pattern varied depending on time and type of cell line used for analysis, although the results indicate a higher cytotoxicity for EPH in short-term tests

Cytotoxic response of two cell lines exposed in vitro to four endodontic sealers

investigate the cytotoxicity of four endodontic sealers with different bases Epiphany (EPH), AH Plus (AHP), Sealer 26 (S26) and Endofill (ENF) on human foreskin fibroblasts (HFF) and mouse macrophages (J774/G8). Methods: Cells were placed in direct contact with freshly prepared endodontic sealers in polypropylene tubes. The cells were incubated for 24, 48 and 72 h. Cytotoxicity was assessed using the MTT assay (cell viability) and Griess reagent (NO release). Results: On the HFF cultures, EPH showed the lowest viability levels of all four sealers at 24 h (p0.05). The viability of all four sealers on the macrophage cultures showed no statistically significant difference over time, except between EPH and AHP at 72 h (p<0.05). Although uniformity was not detected in macrophage and fibroblast release of NO in response to sealers over time, a trend of increased NO levels for EPH (p<0.05) was observed. Conclusions: The response pattern varied depending on time and type of cell line used for analysis, although the results indicate a higher cytotoxicity for EPH in short-term tests

Papel do óxido nítrico no desenvolvimento de lesões cardíacas na fase aguda da infecção experimental pelo Trypanosoma cruzi Role of nitric oxide in the development of cardiac lesions during the acute phase of experimental infection by Trypanosoma cruzi

A doença de Chagas é causada pelo Trypanosoma cruzi e o coração é o órgão mais acometido. O óxido nítrico apresenta importante ação anti-Trypanosoma, porém, com pouca evidência de seu papel no mecanismo de lesão tecidual. O objetivo deste estudo foi analisar a contribuição do óxido nítrico no desenvolvimento da inflamação e da fibrose cardíaca na fase aguda da infecção experimental por cepas Y e Colombiana do Trypanosoma cruzi. A inflamação foi significativamente maior nos animais infectados pela cepa Colombiana, comparada com os infectados com a cepa Y, tanto nos animais C57BL/6 (3,98x1,87%; p=0,004) quanto nos animais C57BL/6 deficientes na sintase do óxido nítrico induzível (3,99x2,4%; p=0,013). O parasitismo cardíaco dos animais C57BL/6 deficientes na sintase do óxido nítrico induzível infectados pela cepa Colombiana foi significativamente maior que o destes mesmos animais infectados com a cepa Y (2,78x0,17 ninhos/mm²; p=0,004) assim como, os animais C57BL/6 infectados com a cepa Colombiana (2,78x1,33 ninhos/mm²; p=0,006) ou cepa Y (2,78x0,53 ninhos/mm²; p=0,005). Os dados reforçam o papel do óxido nítrico no controle do parasitismo e sugerem seu papel na proteção tecidual, controlando a inflamação e potencialmente diminuindo lesões cardíacas durante a fase aguda na doença de Chagas experimental.<br>Chagas disease is caused by Trypanosoma cruzi and the heart is the organ most affected. Nitric oxide has notable anti-Trypanosoma action, but with little evidence regarding its role in the mechanism for tissue injury. The objective of this study was to analyze the contribution of nitric oxide towards the development of inflammation and cardiac fibrosis during the acute phase of experimental infection by Y and Colombian strains of Trypanosoma cruzi. The inflammation was significantly more intense in animals infected with the Colombian strain, compared with those infected with the Y strain, both in C57BL/6 animals (3.98 vs 1.87%; p = 0.004) and in C57BL/6 animals deficient in inducible nitric oxide synthase (3.99 vs 2.4%; p = 0.013). The cardiac parasite load in inducible nitric oxide synthase-deficient C57BL/6 animals infected with the Colombian strain was significantly greater than in those infected with the Y strain (2.78 vs. 0.17 nests/mm²; p = 0.004), and also significantly greater than in the C57BL/6 infected with both the Colombian strain (2.78 vs 1.33 nests/mm²; p = 0.006) and Y strains (2.78 vs 0.53 nests/mm²; p = 0.005). The data confirm that nitric oxide has a role in parasite load control and suggest that it has a role in tissue protection, through controlling inflammation and potentially reducing cardiac lesions during the acute phase of Chagas disease