The effects of acetyl salicyclic acid (ASA) on somatosensory evoked potenti
als (SEP) and neural levels of thiobarbituric acid reactive substances (TBA
RS), products of lipid peroxidation, were studied in streptozotocin-diabeti
c rats. ASA (100 mg/kg, in rat chow) was given to diabetic rats (n = 8) aft
er 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) we
re 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 contr
ol group (60.1 +/- 2.2 nmol/g) was significantly, higher than that in norma
l 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 resu
lts suggest that ASA has beneficial effect on diabetic neuropathy and this
effect may be related in part with prevention of lipid peroxidation. (C) 19
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