Aluminum exposure for 60 days at an equivalent human dietary level promotes peripheral dysfunction in rats

Abstract

Aluminum (Al) is a neurotoxic associated with a number of chronic human diseases. We investigated the effects of Al exposure at doses similar to human dietary levels on the peripheral nervous system over a 60 day period. Wistar male rats were divided into two major groups and received orally: 1) Low aluminum level - rats were subdivided and treated for 60 days as follows: a) Untreated - ultrapure water; b) AlCl3 at a dose of 8.3 mg/kg bw for 60 days, representing human Al exposure by diet; and 2) High aluminum level - rats were subdivided and treated for 42 days as follows: C) Untreated – ultrapure water; d) AlCl3 at 100 mg/kg bw for 42 days, representing a high level of human exposure to Al. Von Frey hair and plantar tests were used to verify the tactile and thermal sensitivities, respectively. The presence of catalepsy behavior and the spontaneous motor activity were investigated by “ring test” and using individual photocell activity chambers. Reactive oxygen species, lipid peroxidation and total antioxidant capacity in plasma, were measured. Immunohistochemistry to investigate the nerve inflammation and, the specific presence of Al in the sciatic nerve fibers were investigated. Al exposure at a representative human dietary level promotes the development of mechanical allodynia, catalepsy behavior, increased the number of activated macrophages in the sciatic nerve, systemic oxidative stress and, is able to be retained among the sciatic nerve fibers. The effects of Al in the peripheral nervous system were similar to those found in rats exposed to Al at a dose much higher (100 mg/kg). Therefore, our findings suggest that Al may be considered toxic for the peripheral nervous system, thus inducing peripheral dysfunction.