Vitamin E improves bone quality in the aged but not in young adult male mice

It is generally viewed that with advancing age, humans and other animals including mice experience a gradual decline in the rate of bone formation. This, in part, may be due to the rise in oxygen-derived free radical formation. Vitamin E, a strong antioxidant, functions as a free radical scavenger that potentially can suppress bone resorption while stimulating bone formation. Although the effects of vitamin E on immune functions are well documented, there is a paucity of information on its effect on skeletal health in vivo. The purpose of this study was to explore the influence of vitamin E supplementation on bone in young adult and old mice. Six and twenty-four month-old male C57BL/6NIA mice each were divided into two groups and fed a diet containing either adequate (30 mg/kg diet) or high (500 mg/kg diet) levels of vitamin E. Thirty days later, mice were killed and bones were removed for analyses including biomechanical testing using three-point bending and mRNA expressions of insulin-like growth factor-I (IGF-I), osteocalcin, and type 1alpha-collagen using Northern blot. In old but not the young adult mice, high-dose vitamin E enhanced bone quality as evident by improved material and structural bone properties in comparison with adequate. This improved quality was accompanied by increases in bone dry weight, protein, and mRNA transcripts for osteocalcin, type Ialpha-collagen, and IGF-I. These data demonstrate that high-dose vitamin E has pronounced effects on bone quality as well as matrix protein in old mice by augmenting bone matrix protein without reducing bone mineralization as evidenced by unaltered bone density.