Cigarette consumption increases oxidative stress in many organs. Increased oxidative stress harms bone cells, which negatively affects bone-matter and -stability. This leads to an increased fracture risk and delayed f...Cigarette consumption increases oxidative stress in many organs. Increased oxidative stress harms bone cells, which negatively affects bone-matter and -stability. This leads to an increased fracture risk and delayed fracture healing in smokers. A supporting therapy with antioxidants could be of great benefit for surgeons dealing with delayed fracture healing due to increased oxidative stress. In this article we complement and compare our published data with hitherto unpublished data and show the protective effect of 15 different antioxidants on cigarette smoke induced damage in primary human osteoblasts. Exposure to cigarette smoke medium (CSM) rapidly induces formation of ROS in osteoblasts in a concentration- and time-dependent manner. Massive cell damage is seen already after 4 h (EC50 ≈ 0.75 OD320). Pre-, co- and post-incubation with the different antioxidants reduces the formation of ROS and consequently improves the viability of the CSM exposed osteoblasts. Small compounds, e.g. N-acetylcysteine, proved highly effective if pre- or co-incubated before exposure to the CSM. Thus, they are good candidates for acute therapy support as they can be administered in high doses. However, our data suggest that a balanced daily diet could lead to an accumulation of various natural antioxidants (flavonoids) that effectively protect osteoblasts from oxidative stress-induced damage in all three settings investigated. Together with their partly phytoestrogenic properties this may even abate alterations in bone and thus reduce fracture risk on the long run.展开更多
文摘Cigarette consumption increases oxidative stress in many organs. Increased oxidative stress harms bone cells, which negatively affects bone-matter and -stability. This leads to an increased fracture risk and delayed fracture healing in smokers. A supporting therapy with antioxidants could be of great benefit for surgeons dealing with delayed fracture healing due to increased oxidative stress. In this article we complement and compare our published data with hitherto unpublished data and show the protective effect of 15 different antioxidants on cigarette smoke induced damage in primary human osteoblasts. Exposure to cigarette smoke medium (CSM) rapidly induces formation of ROS in osteoblasts in a concentration- and time-dependent manner. Massive cell damage is seen already after 4 h (EC50 ≈ 0.75 OD320). Pre-, co- and post-incubation with the different antioxidants reduces the formation of ROS and consequently improves the viability of the CSM exposed osteoblasts. Small compounds, e.g. N-acetylcysteine, proved highly effective if pre- or co-incubated before exposure to the CSM. Thus, they are good candidates for acute therapy support as they can be administered in high doses. However, our data suggest that a balanced daily diet could lead to an accumulation of various natural antioxidants (flavonoids) that effectively protect osteoblasts from oxidative stress-induced damage in all three settings investigated. Together with their partly phytoestrogenic properties this may even abate alterations in bone and thus reduce fracture risk on the long run.
