Electrophysiological and Biochemical Effects of Exposure to 2,5-Hexanedione on Peripheral Nerve in Experimental Diabetic Rats

Both 2,5-hexanedione (2,5-HD) and diabetes mellitus (DM) cause peripheral neuropathy. Workers with asymptomatic DM could possibly be exposed to n-hexane converted to 2,5-HD in liver. To clarify 2,5-HD influences on peripheral nerves in DM, electrophysiological and biochemical changes in DM rats were compared in 2,5-HD treated and untreated groups. Four groups of rats were studied： the Control group consisted of non-diabetic rats treated with a placebo; the HD group, of non-diabetic rats treated with 2,5-HD; the DM group, of diabetic rats treated with a placebo; the DM+HD group, of diabetic rats treated with 2,5-HD. 2,5-HD was administered at 100 mg/kg/day, five days a week for 8 weeks. The motor nerve conduction velocity (MCV) and motor distal latency (DL) in the rats tails and glucose, fructose, sorbitol and myoinositol levels in the sciatic nerves were measured. The MCV in the DM+HD group was significantly reduced from the 4th week compared with those in the other groups. 2,5-HD had no influence on the levels of glucose, fructose, sorbitol and myo-inositol in either the diabetic or non-diabetic group. These results indicated that exposure to 2,5-HD hastened the onset of peripheral neuropathy in experimental diabetic rats. This study indicates that 2,5-HD in combination with DM enhances the neurotoxicity. But the mechanisms of the neurotoxic interactions between 2,5-HD and DM are still unknown. It can be hypothesized that workers with hyperglycemia can suffer from neuropathy due to exposure to n-hexane earlier than those without hyperglycemia.