Sodium fluoride (NaF) has been found to interfere with the reproductive system of animals. However, the cellular mechanisms underlying the reproductive toxicity of fluoride are unclear. The present study aims to define a possible mechanism of NaF-induced reproductive toxicity with respect to mineral, oxidative stress and c-Fos expression and the role of aluminum (Al) in intervening the toxic effect of NaF on rat testes. Fifty-six male Wistar rats were treated with normal saline, 1.0, 2.0, and 3.0 mg NaF/kg body weight (bw)/day, and each NaF concentration plus Al ion (0.1 mg Al3+/kg bw/day). After 90 days, no significant changes in the contents of Fe and Cu were observed in any of the NaF-treated groups compared with those of the control group. There were, however, significant decreases in the contents of Ca in the 1.0 mg NaF group, Zn in all NaF-treated groups and Mg in the 3.0 mg NaF group. The levels of malondialdehyde (MDA) in the 1.0 mg NaF group and hydrogen peroxide (H2O2) in the 2.0 mg NaF group significantly increased, whereas the activity of nitric oxide synthase (NOS) significantly decreased in the 1.0 mg NaF group. Meanwhile, the protein expression of c-Fos increased significantly in the 1.0 and 2.0 mg NaF groups compared with the control group. Conversely, these changes were partially attenuated in rats simultaneously administered Al. The present study suggested that NaF could decrease the contents of Ca, Fe and Mg and enhance oxidative stress leading to c-Fos overexpression, and some deleterious effects were more prominent at lower NaF intake. Furthermore, Al within the research concentration could minimize reproductive toxicity caused by fluoride.