We tested the protective potential of an antioxidant amino acid derivative, N-acetyl cysteine (NAC), in controlling oxidative stress against osteoblasts. Osteoblastic cells extracted from rat bone marrow were cultured. Oxidative stress was induced by adding 100 μM H2O2 into the culture media. Then, some H2O2-treated cultures were cotreated with 2.5 or 5 mM NAC. Addition of H2O2 decreased the number of cells to 50% of untreated cultures at days 2. Addition of 5 mM NAC into H2O2 cultures resulted in a dose-dependent increase in the number of cells, with the cell number being 50% greater than that in the 100 μM H2O2 culture. The gene expression levels of type I collagen, osteopontin, and osteocalcin were downregulated threefold by H2O2 on day 7. The H2O 2-suppressed gene expression was fully recovered by NAC cotreatment. The mineralizing capability, assessed by Von Kossa staining on day 15, were approximately 1.8 times greater in the NAC + H2O2 cotreated group than in the culture with H2O2 alone. These NAC-mediated restorations were associated with an NAC dose-dependent increase of intracellular glutathione and a NAC dose-dependent decrease of intracellular reactive oxygen species. In conclusion, oxidative stress induced by H 2O2 substantially impairs the proliferation, differentiation, and mineralization of osteoblasts. More importantly, the addition of NAC into the culture was found to restore these damages to a near normal level due to the improved redox balance, warranting further in vivo studies to test its therapeutic potential as a local antioxidative stress drug.
ASJC Scopus subject areas