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Titolo:
Taurine counteracts oxidative stress and nerve growth factor deficit in early experimental diabetic neuropathy
Autore:
Obrosova, IG; Fathallah, L; Stevens, MJ;
Indirizzi:
Univ Michigan, Med Ctr, Dept Internal Med, Div Endocrinol & Metab, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 nol & Metab, Ann Arbor, MI 48109 USA Vet Affairs Med Ctr, Ann Arbor, MI 48105 USA Vet Affairs Med Ctr Ann Arbor MI USA 48105 d Ctr, Ann Arbor, MI 48105 USA
Titolo Testata:
EXPERIMENTAL NEUROLOGY
fascicolo: 1, volume: 172, anno: 2001,
pagine: 211 - 219
SICI:
0014-4886(200111)172:1<211:TCOSAN>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALPHA-LIPOIC ACID; ALDOSE REDUCTASE INHIBITION; SORBITOL DEHYDROGENASE INHIBITOR; GLYCATION END-PRODUCTS; ESSENTIAL FATTY-ACIDS; PERIPHERAL-NERVE; FREE-RADICALS; BLOOD-FLOW; SCIATIC-NERVE; NEUROVASCULAR FUNCTION;
Keywords:
ascorbate; glutathione; 4-hydroxy-alkenals; malondialdehyde; nerve growth factor; oxidative stress; rat; sciatic nerve; streptozotocin-induced diabetes; taurine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
94
Recensione:
Indirizzi per estratti:
Indirizzo: Obrosova, IG Univ Michigan, Med Ctr, Dept Internal Med, Div Endocrinol & Metab, 1150 W Med Ctr Dr,MSRB 2,Room 5570, Ann Arbor, MI 48109 USA Univ Michigan 1150 W Med Ctr Dr,MSRB 2,Room 5570 Ann Arbor MI USA 48109
Citazione:
I.G. Obrosova et al., "Taurine counteracts oxidative stress and nerve growth factor deficit in early experimental diabetic neuropathy", EXP NEUROL, 172(1), 2001, pp. 211-219

Abstract

Oxidative stress has a key role in the pathogenesis of diabetic complications. We have previously reported that taurine (T), which is known to counteract oxidative stress in tissues (lens, kidney, retina) of diabetic rats, attenuates nerve blood flow and conduction deficits in early experimental diabetic neuropathy (EDN). The purpose of this study was to evaluate whether dietary T supplementation counteracts oxidative stress and the nerve growthfactor (NGF) deficit in the diabetic peripheral nerve. The experiments were performed in control rats and streptozotocin-diabetic rats fed standard or 1% T-supplemented diets for 6 weeks. All measurements were performed in the sciatic nerve. Malondialdehyde (MDA) plus 4-hydroxyalkenals (4-HA) were quantified with N-methyl-2-phenylindole. GSH, GSSG, dehydroascorbate (DHAA), and ascorbate (AA) were assayed spectrofluorometrically, T by reverse-phase HPLC, and NGF by ELISA. MDA plus 4-HA concentration (mean +/- SEM) was increased in diabetic rats (0.127 +/-0.006 vs 0.053 +/-0.003 mu mol/g in controls, P<0.01), and this increase was partially prevented by T (0.096<plus/minus>0.004, P<0.01 vs untreated diabetic group). GSH levels were similarlydecreased in diabetic rats treated with or without taurine vs controls. GSSG levels were similar in control and diabetic rats but were lower in diabetic rats treated with T (P<0.05 vs controls). AA levels were decreased in diabetic rats (0.133+0.015 vs 0.219 +/-0.023 mu mol/g in controls, P<0.05), and this deficit was prevented by T. DHAA/AA ratio was increased in diabetic rats vs controls (P<0.05), and this increase was prevented by T. T levelswere decreased in diabetic rats (2.7 +/-0.16 vs 3.8 +/-0.1 mu mol/g in controls, P<0.05) and were repleted by T supplementation (4.2<plus/minus>0.3). NGF levels were decreased in diabetic rats (2.35 +/-0.20 vs 3.57 +/-0.20 ng/g in controls, P<0.01), and this decrease was attenuated by T treatment (3.16<plus/minus>0.28, P<0.05 vs diabetic group). In conclusion, T counteracts oxidative stress and the NGF deficit in early EDN. Antioxidant effects of T in peripheral nerve are, at least in part, mediated through the ascorbate system of antioxidative defense. The findings are consistent with the important role for oxidative stress in impaired neurotrophic support in EDN. (C) 2001 Academic Press.

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Documento generato il 04/12/20 alle ore 13:28:15