A duality in the roles of reactive oxygen species with respect to bone metabolism.

摘要

BACKGROUND: Rampant production in skeletal abnormalities can lead to hyperoxidant stress though the production of "reactive oxygen species" (ROS) by osteoclasts, which assist in bone remodeling under physiological conditions. METHODS: Thirty cases each of post-menopausal osteoporosis, renal osteodystrophy and bone fractures constituted the test groups. Thirty healthy subjects made up the control group. Serum total alkaline phosphatase served as an index of osteoblastic activity. Serum calcium and phosphorous indicated bone remodeling status. Serum superoxide dismutase, glutathione peroxidase and glutathione reductase represented the enzymatic antioxidants. RESULTS: Mean values for malondialdehyde were significantly elevated (P<0.001) in test groups, indicating enhanced osteoclastic activity. Significantly depressed (P<0.001) activities of superoxide dismutase and glutathione peroxidase reinforced hyperoxidant stress. Mean values of glutathione reductase remained unaltered. Diminished osteoblastic activity in post-menopausal osteoporosis was indicated by depressed alkaline phosphatase (P<0.001). Increased serum calcium (P<0.001) and decreased serum phosphorous (P<0.001) in renal osteodystrophy indicated compensatory hyperparathyroidism. CONCLUSIONS: The findings indicate that ROS have a major role to play in bone metabolism.