IADR Abstract Archives
SOD1 and SOD2 may compensate RNS in aged odontoblasts
Objectives: The increase of the reactive oxygen species (ROS) was considered to be a reason for aging of cells. The higher concentration of nitric oxide (NO) reacts with superoxide (O2-) to form peroxynitrite (ONOO-) inducing cell damage. The anti-oxidant enyzmes superoxide dismutase 1 (SOD1) and SOD2 inhibit ONOO- formation reacting with O2- promoting cell homeostasis. It is unknown, whether reactive nitrogen species (RNS) are accumulated in aged odontoblasts.
Methods: The decalcified frozen free-floating sections of the young and aged molars were incubated with antibodies against inducible nitric oxide synthase (iNOS), 3-nitrotyrosine (3-NT) (a marker for ONOO-), SOD1 and SOD2 using quantitative immunohistochemistry. The subcellular localizations of iNOS, 3-NT, SOD1 and SOD2 in young and aged odontoblasts were examined by double immunofluorescence incubations.
Results: In comparison to the young odontoblasts, aged odontoblasts revealed higher staining intensities for SOD1 and SOD2 but low staining intensities for iNOS and 3-NT. SOD1, SOD2, iNOS and 3-NT were detected in cytoplasm of young and aged odontoblasts, while iNOS and 3-NT were detected in nucleus of a small number of young odontoblasts.
Conclusions: RNS may be involved in physiological cell functions in young and in aged odontoblasts. The low formation of RNS in aged odontoblasts cannot be considered as a reason for aging in odontoblasts. Higher expressions of SOD1 and SOD2 in aged odontoblasts suggested that odontoblasts have ability to develop a compensation against RNS in aging.
Methods: The decalcified frozen free-floating sections of the young and aged molars were incubated with antibodies against inducible nitric oxide synthase (iNOS), 3-nitrotyrosine (3-NT) (a marker for ONOO-), SOD1 and SOD2 using quantitative immunohistochemistry. The subcellular localizations of iNOS, 3-NT, SOD1 and SOD2 in young and aged odontoblasts were examined by double immunofluorescence incubations.
Results: In comparison to the young odontoblasts, aged odontoblasts revealed higher staining intensities for SOD1 and SOD2 but low staining intensities for iNOS and 3-NT. SOD1, SOD2, iNOS and 3-NT were detected in cytoplasm of young and aged odontoblasts, while iNOS and 3-NT were detected in nucleus of a small number of young odontoblasts.
Conclusions: RNS may be involved in physiological cell functions in young and in aged odontoblasts. The low formation of RNS in aged odontoblasts cannot be considered as a reason for aging in odontoblasts. Higher expressions of SOD1 and SOD2 in aged odontoblasts suggested that odontoblasts have ability to develop a compensation against RNS in aging.