L-carnitine is a small essential molecule indispensable in fatty acid metabolism and required in several biological pathways regulating cellular homeostasis. Despite considerable progress in understanding of L-carnitine biosynthesis and metabolism, very few data are reported concerning the protective role of L-carnitine from oxidative stress-induced DNA damage that is known to be a factor in cell transformation and tumourigenesis. In order to detect the capability of L-carnitine to protect mammalian cells from oxidative stress-induced chromosomal effects, we analysed chromosome aberrations in mitotic CHO cells, which represent an appropriate cytogenetic model to study compounds that enhance cell protection against externally induced DNA damage. We chose H2O2 as an inducer of oxidative stress. Our results demonstrate for the first time a marked and reproducible reduction of H2O2-induced chromosome damage involving an L-carnitine-mediated capacity to buffer intracellular formation of reactive oxygen species (ROS). Furthermore, by studying the mitotic index and cell cycle progression, we also demonstrated that this protective effect is highly specific, since L-carnitine itself was not able to prevent the inhibition of cell growth caused by H2O2.
L-carnitine protects mammalian cells from chromosome aberrations but not from inhibition of cell proliferation induced by hydrogen peroxide
LIOI, Maria Brigida;
2005-01-01
Abstract
L-carnitine is a small essential molecule indispensable in fatty acid metabolism and required in several biological pathways regulating cellular homeostasis. Despite considerable progress in understanding of L-carnitine biosynthesis and metabolism, very few data are reported concerning the protective role of L-carnitine from oxidative stress-induced DNA damage that is known to be a factor in cell transformation and tumourigenesis. In order to detect the capability of L-carnitine to protect mammalian cells from oxidative stress-induced chromosomal effects, we analysed chromosome aberrations in mitotic CHO cells, which represent an appropriate cytogenetic model to study compounds that enhance cell protection against externally induced DNA damage. We chose H2O2 as an inducer of oxidative stress. Our results demonstrate for the first time a marked and reproducible reduction of H2O2-induced chromosome damage involving an L-carnitine-mediated capacity to buffer intracellular formation of reactive oxygen species (ROS). Furthermore, by studying the mitotic index and cell cycle progression, we also demonstrated that this protective effect is highly specific, since L-carnitine itself was not able to prevent the inhibition of cell growth caused by H2O2.File | Dimensione | Formato | |
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