Comparison of the effects of aminoguanidine and L-carnitine treatments on somatosensorial evoked potentials in alloxan-diabetic rats

• Published in: Naunyn-Schmiedeberg's archives of pharmacology Vol. 354; no. 4; pp. 526 - 531
• Main Authors: Yildiz, O, Ozata, M, Ozkardeş, A, Deniz, G, Yildirimkaya, M, Corakçi, A, Yardim, M, Gündoğan, M A
• Format: Journal Article
• Language: English
• Published: Germany 01-10-1996
• Subjects: Alloxan; Animals; Blood Glucose - drug effects; Body Weight - drug effects; Carnitine - administration & dosage; Carnitine - pharmacology; Diabetes Mellitus, Experimental - complications; Diabetes Mellitus, Experimental - physiopathology; Diabetic Neuropathies - etiology; Diabetic Neuropathies - physiopathology; Electrophysiology; Evoked Potentials, Somatosensory - drug effects; Guanidines - administration & dosage; Guanidines - pharmacology; Lipid Peroxidation - drug effects; Male; Nerve Tissue - drug effects; Nerve Tissue - metabolism; Rats; Rats, Wistar; Reaction Time; Thiobarbituric Acid Reactive Substances - metabolism
• ISSN: 0028-1298; 1432-1912
• DOI: 10.1007/BF00168446

The effects of aminoguanidine (AG) and L-carnitine (LC) on somatosensorial evoked potential (SEP) latency and neural levels of thiobarbituric acid reactive substances (TBARS), products of lipid peroxidation, were compared in alloxan-diabetic rats. AG and LC were given to diabetic rats starting from the 3rd week after the induction of diabetes and lasting for 4 weeks. SEP latency was measured by stimulating via caudal nerve and recording via cortex, once weekly during the treatments. Diabetes caused deficits in SEP (P < 0.05 vs non-diabetic control rats, respectively). AG and LC restored SEP latencies slightly but not significantly, with the exception of the prominent effect of AG at the first week and both treatments at the 4th week of the treatments (P < 0.05 vs untreated diabetic rats, respectively). Diabetes caused elevation in neural TBARS levels (P < 0.05 vs non-diabetic group), which was prevented by both AG and LC (P < 0.05 vs untreated diabetic rats, respectively). Weight and the glucose levels were not influenced by the treatments. Our results suggest that AG improves SEP latencies better than LC. Our results also suggest that the beneficial effects of both AG and LC on diabetic neuropathy are not associated with the regulation of glycemia, but these effects may be related in part with prevention of lipid peroxidation.