Effects of α-tocopherol on nerve conduction velocity and regeneration following a freeze lesion in immature diabetic rats
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We investigated whether anti-oxidant treatment with α-tocopherol (1 g kg–1 day–1) could prevent the blunting of the normal maturational increase in motor and sensory nerve conduction velocity when diabetes is induced by streptozotocin in young rats. A further study in the same rats examined effects on myelinated fibre regeneration distance 14 days after a punctate sciatic nerve lesion by a liquid nitrogen cooled probe.
In non-diabetic rats between 8 and 14 weeks of age, sciatic motor and saphenous sensory conduction velocity increased by approximately 28% (P < 0.001) and 21% (P < 0.001) respectively. Diabetes induced at 8 weeks blunted this maturational change by 65% for sciatic motor and almost completely for saphenous sensory fibres (P < 0.001). Treatment with α-tocopherol from diabetes induction totally prevented motor conduction velocity deficits (P < 0.001). For sensory saphenous nerve, conduction abnormalities were markedly attenuated (72%, P < 0.001) although a significant deficit remained compared to age-matched non-diabetic rats (P < 0.01). Sciatic nerve myelinated fibre regeneration distance, 14 days post lesion, was 15% reduced (P < 0.001) by untreated diabetes. However, in diabetic rats treated with α-tocopherol, regeneration distance was significantly improved (P < 0.001), being within the non-diabetic range. Thus, the data highlight the importance of reactive oxygen species in the aetiology of impaired nerve maturation and regeneration in experimental diabetes and indirectly support the view that anti-oxidant treatment could have a therapeutic role in patients.
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