Exposure to aluminum (Al) inhibits bone formation, the principal mechanism possibly
due to oxidative stress. However, little data is available that establishes the precise
relationship. In this study, Wistar rats were exposed to 0 (GC), 0.4 (GL), 0.8 (GM)
or 1.6 (GH) mg/L aluminum trichloride (AlCl3) in drinking water for 90 days, respectively.
The concentrations of Al in serum and bone, serum markers of bone metabolism, bone
mineral density (BMD) and body weight were measured. Histological changes within femurs
were observed by H&E, ALP, and TRACP staining. Oxidative stress markers and JNK apoptotic
pathway were detected in bone. The results indicate that AlCl3 exposure decreased
BMD, numbers of ALP-positive osteoblasts and serum levels of bone formation markers
(B-ALP, PICP and BGP), and caused damaged to the trabecular structure. Serum levels
of bone resorption markers (TRACP-5b, CTX-I) and numbers of TRACP-positive osteoclasts
increased in GL, but conversely, they decreased in GM and GH. In addition, AlCl3 caused
oxidative stress, up-regulated expression of c-Jun and pro-apoptotic factors with
increased p-JNK/JNK ratio and down-regulated expression of anti-apoptotic factor Bcl-2
in bone. Taken together, these results indicate that bone impairment caused by AlCl3
is associated with activation of the oxidative stress-mediated JNK apoptotic pathway.