Fluoride (F) increases bone mass but the presence of inflammation has been observed in F treatments in rats. The lack of effectiveness of F as an anti-osteoporotic drug could be due to inflammation. Inflammation could be the consequence of an increase in reactive oxygen species (ROS), as a result of modifications of the respiratory chain activity. The aim of this work was to evaluate the effect of F on the oxygen uptake rate (VO₂) in rats treated with sodium fluoride (NaF). Eighteen Sprague-Dawley rats were divided into 3 groups (n=6 per group): NaF20, NaF40, which received orally 20 or 40 µmol NaF/100g bw.day for 30 days; and Controls that received water. VO₂ and fluoremia were measured in vivo before and after 90 min of NaF doses. After 30 days, euthanasia was performed; plasma and mitochondrial glutathione peroxidase (GPx) and catalase (CAT) activities and TBARS concentrations were measured as indexes of oxidative stress. In vitro, the effect of F 100 µM on the VO₂ of liver slices and of isolated mitochondria was also evaluated. Finally, the addition of 100 µM of F on the activity of the respiratory chain complexes was assessed. Results are expressed as mean±SEM and differences were considered significant when p<0.05(*).

In vivo, VO₂ (µmolO₂/min.100g bw) decreased after 90 min of F dose in the NaF40 group (0min: 175.8±15.67, 90min: 156.0±16.62*). Plasma and mitochondrial TBARS levels and GPx and CAT activities were higher in the NaF-treated groups. In vitro, F caused a decrease in the VO₂ by liver slices (nmolO₂/min.mg prot) (0µM: 47±4.5; 100µM: 31±3.0*) and by mitochondria (nmolO₂/min.mg prot) in state 4 (0µM: 55±5.0; 100µM: 29±3.5*) and in state 3 (0µM: 146±9.7; 100µM: 87±9.3*). The activity of complex I-III (µmol.min^-1.mg prot^-1) was also inhibited by F (without F: 1906±125; with F: 1720±71*).

Conclusions: F decreased VO₂ in vivo after an oral dose, and the same effect was observed in vitro after the addition of F at similar plasma concentrations. The effect of F on VO₂ is observed only with high values of fluoremias. F also decreased VO₂ by isolated mitochondria. The oxidative stress increased in the treatment with NaF. This results support the hypothesis that the presence of bone inflammatory foci in NaF-treated rats, could be the consequence of an increase in ROS due to a modification of the respiratory chain activity.

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