In vitro cytotoxicity of chemical preservatives on human fibroblast cells
Preservatives are widely used substances that are commonly added to various cosmetic and pharmaceutical products to prevent or inhibit microbial growth. In this study, we compared the in vitro cytotoxicity of different types of currently used preservatives, including methylparaben, imidazolidinyl ur...
| Autores: | , , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión publicada |
| Fecha de publicación: | 2018 |
| País: | Brasil |
| Institución: | Universidade Federal de São Paulo (UNIFESP) |
| Repositorio: | Repositório Institucional da UNIFESP |
| Idioma: | inglés |
| OAI Identifier: | oai:repositorio.unifesp.br:11600/54312 |
| Acceso en línea: | http://dx.doi.org/10.1590/s2175-97902018000100031 https://repositorio.unifesp.br/handle/11600/54312 |
| Access Level: | acceso abierto |
| Palabra clave: | Preservatives Pharmaceutical/chemistry Fibroblasts/cytotoxicity Cell death/drag effects Cosmetics/additives |
| Sumario: | Preservatives are widely used substances that are commonly added to various cosmetic and pharmaceutical products to prevent or inhibit microbial growth. In this study, we compared the in vitro cytotoxicity of different types of currently used preservatives, including methylparaben, imidazolidinyl urea (IMU), and sodium benzoate, using the human newborn fibroblast cell line CCD 1072Sk. Of the tested preservatives, only IMU induced a reduction in cell viability, as shown using the MIT assay and propidium iodide staining (IMU > methylparaben > sodium benzoate). IMU was shown to promote homeostatic alterations potentially related to the initiation of programed cell death, such as decreased mitochondrial membrane potential and caspase-3 activation, in the treated cells Methylparaben and sodium benzoate were shown to have a very low cytotoxic activity. Taken together, our results suggest that IMU induces programed cell death in human fibroblasts by a canonical intrinsic pathway via mitochondrial perturbation and subsequent release of proapoptotic factors. |
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