Alterations in neurofilaments content and calpains activity of sciatic nerve of carbon disulfide-treated rats.

Chronic exposure to carbon disulfide (CS2) can induce polyneuropathy in occupational worker and experimental animals, but underlying mechanism for CS2 neurotoxicity is currently unknown. In the present study, male Wistar rats were randomly divided into two experimental groups and one control group. The rats in two experimental groups were treated with CS2 by gavage at dosages of 300 and 500 mg/kg per day, respectively, five times per week for 12 weeks. The contents of neurofilament triplet proteins (NF-H, NF-M, NF-L) and two calpain isoforms (m-calpain and u-calpain) in sciatic nerves were determined by immunoblotting. In the meantime, the mRNA levels of NF-H, NF-M and NF-L in spinal cords were quantified by reverse transcriptase-polymerase chain reaction, and the total activity of calpains in sciatic nerves was measured by fluorescence assay. Results showed that the contents of NF-M and NF-L in CS2-treated rats sciatic nerves increased significantly except NF-M in low dose group. The contents and activity of m-calpain and u-calpain in sciatic nerve also demonstrated a significant elevation. Furthermore, the levels of mRNA expression of NFH, NFM and NFL genes were up-regulated consistently in spinal cords of treated rats. These findings suggested that CS2 intoxication was associated with the disruption of neurofilaments homeostasis and activiation of calpains in rat sciatic nerves, which might be involved in the development of CS2-induced peripheral neuropathy.