The effects of acetyl salicyclic acid (ASA) on somatosensory evoked potentials (SEP) and neural levels of thiobarbituric acid reactive substances (TBARS), products of lipid peroxidation, were studied in streptozotocin-diabetic rats. ASA (100 mg/kg, in rat chow) was given to diabetic rats (n = 8) after the induction of diabetes for 16 weeks. ASA-treated normal control rats (n = 8), untreated diabetic rats (n = 8) and normal control rats (n = 8) were used for comparison. At the 8 weeks, SEP latency in diabetic group (15.4 +/- 0.5 ms) was significantly longer than that in normal control group (10.0 +/- 0.8 ms, P < 0.05). When compared to levels in diabetic control group, ASA shortened SEP latency significantly (12.7 +/- 0.1 ms; P < 0.05). This effect of ASA was significant in all three measurements from week 8 to 16 (P < 0.05 vs. diabetic control group). Neural TBARS level in diabetic control group (60.1 +/- 2.2 nmol/g) was significantly, higher than that in normal control group (28.5 +/- 3.6 nmol/g, P < 0.05). When compared to levels in diabetic control group, ASA depressed TBARS level significantly (41.5 +/- 12 nmol/g; P < 0.05). TBARS level in ASA-treated diabetic group (27.2 +/- 5.7 nmol/g) was comparable with that in normal control group (NS). These results suggest that ASA has beneficial effect on diabetic neuropathy and this effect may be related in part with prevention of lipid peroxidation.
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