α-Lipoic acid protects against reperfusion injury following cerebral ischemia in rats

Panigrahi, Manas; Sadguna, Yarasi; Shivakumar, B. R.; Kolluri, Sastry; Roy, Sashwati; Packer, Lester; Ravindranath, Vijayalakshmi

doi:10.1016/0006-8993(96)00009-1

Cited by 172 publications

(95 citation statements)

References 18 publications

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“…Previous studies have demonstrated α-lipoic acid cytoprotective action against reperfusion injury in animal models of global 23,24 and focal 25 cerebral ischemia. C -II C-II C-II C -II C -II C -II C -II C -II C -II C -II C -II Groups C -III C -III I-II C -III C -III I -II I -II I -II I -II I -II I -II I -II C -I III -II III -II III -II I - Our demonstrations that 3.03 mM α-lipoic acid infusion promotes initial reduction and final partial EEG spectra mean absolute amplitude recuperation, allowed us to speculate that, in this condition, this substance has an initial pro-oxidant and a late antioxidant action.…”

Section: Discussionmentioning

confidence: 98%

A dual action of alpha-lipoic acid in the brain: an electrophysiological evaluation

Vale

Fonteles²,

Cabral³

et al. 2003

Arq. Neuro-Psiquiatr.

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-Oxidative stress causes metabolic and structural abnormalities during reperfusion. In an animal model of electrophysiological evaluation of cerebral ischemia-reperfusion, α-lipoic acid effect on the oxidative stress was studied by mean absolute amplitude of EEG spectra evaluation. The left carotideal infusion of 3.03 mM α-lipoic acid in Wistar rats after cerebral ischemia and reperfusion caused initial reduction and partial final recuperation of the various EEG spectral frequency mean absolute amplitudes (p<0.05). The left intracarotideal infusion of 6.06 mM α-lipoic acid significantly reverted the induced depression of mean absolute amplitude of theta and delta spectra. Nevertheless there was an increasing pattern of ischemia demonstrated by mean absolute amplitude depression of almost all EEG spectra with 60.6 mM α-lipoic acid infusion. These observations suggest that, depending on the administered concentration, α-lipoic acid may act in a dual way, protecting from ischemia at lower concentrations and worsening this process at higher doses.KEY WORDS: α-lipoic acid, anti-oxidant, pro-oxidant, cerebral ischemia, electroencephalogram (EEG), spectral mean absolute amplitude.Dupla ação do ácido Dupla ação do ácido Dupla ação do ácido Dupla ação do ácido Dupla ação do ácido α α α α α-lipoico no encéfalo: uma avaliação eletrofisiológica -lipoico no encéfalo: uma avaliação eletrofisiológica -lipoico no encéfalo: uma avaliação eletrofisiológica -lipoico no encéfalo: uma avaliação eletrofisiológica -lipoico no encéfalo: uma avaliação eletrofisiológica RESUMO -Estresse oxidativo causa anormalidades metabólicas e estruturais durante reperfusão após isquemia. Em um modelo animal de avaliação eletrofisiológica de isquemia-reperfusão, o efeito da infusão do ácido α-lipóico sobre o estresse oxidativo foi estudado por meio da avaliação da média das amplitudes absolutas dos espectros eletrencefalográficos. A infusão intracarotídea esquerda de ácido α-lipoic 3,03 mM em ratos Wistar após isquemia-reperfusão cerebral causou significante redução inicial e recuperação parcial final da média das amplitudes absolutas dos vários espectros eletro -encefalográficos (p<0,05). A infusão intracarotídea esquerda de ácido α-lipoic 6,06 mM significantemente reverteu a depressão induzida da média das amplitudes absolutas médias dos espectros teta e delta. Houve, contudo, maior depressão da média das amplitudes absolutas de quase todos os espctros com infusão de ácido α-lipóico 60,6 mM. Estas observações sugerem que, dependendo da concentração administrada, o ácido α-lipoic tem duplo efeito, protegendo da isquemia em baixas concentrações e piorando este processo em doses altas. We have previously studied the electroencephalographic effects on mean absolute amplitudes of electroencephalogram (EEG) waves in Wistar rats submitted to global cerebral ischemia due to common carotid arteries ligation, arterial hypotension and reperfusion 1 . There are only few experimental reports in the literature concerning the value of the EEG as a marker ...

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Section: Discussionmentioning

confidence: 98%

A dual action of alpha-lipoic acid in the brain: an electrophysiological evaluation

Vale

Fonteles²,

Cabral³

et al. 2003

Arq. Neuro-Psiquiatr.

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“…Lipoic acid also has an advantage over NAC in opposing GSH loss, since LA is effective in a micro molar range whereas mill molar NAC is needed for a similar effect 205) . The capability of LA to cross the blood brain barrier is an extra advantage because the brain is an important target in lead poisoning 206) . We provided experimental evidence of the beneficial effect of combined LA-succimers administration for treatment of sub-acute lead intoxication in rats.…”

Section: Melatoninmentioning

confidence: 99%

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Kalia¹,

Flora²

2005

Journal of Occupational Health

269

161

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Strategies for Safe and Effective Therapeutic Measures for Arsenic and LeadPoisoning: Kiran Kalia, et al. Department of Biosciences, Sardar Patel University, IndiaExposure to toxic metals remains a widespread occupational and environmental problem in world. There have been a number of reports in the recent past suggesting an incidence of childhood lead poisoning and chronic arsenic poisoning due to contaminated drinking water in many areas of West Bengal in India and Bangladesh has become a national calamity. Low level metal exposure in humans is caused by air, food and water intake. Lead and arsenic generally interferes with a number of body functions such as the central nervous system (CNS), the haematopoietic system, liver and kidneys. Over the past few decades there has been growing awareness and concern that the toxic biochemical and functional effects are occurring at a lower level of metal exposure than those that produce overt clinical and pathological signs and symptoms. Despite many years of research, we are still far from an effective treatment of chronic plumbism and arsenicosis. Medical treatment of acute and chronic lead and arsenic toxicity is furnished by chelating agents. Chelating agents are organic compounds capable of linking together metal ions to form complex ring-like structures called chelates. They have been used clinically as antidotes for acute and chronic poisoning. 2, 3-dimercaprol (BAL) has long been the mainstay of chelation therapy for lead or arsenic poisoning. Meso 2, 3, -dimercaptosuccinic acid (DMSA) has been tried successfully in animals as well as in a few cases of human lead and arsenic poisoning. DMSA could be a safe and effective method for treating lead or arsenic poisoning, but one of the major disadvantages of chelation with DMSA has been its Review inability to remove lead from the intracellular sites because of its lipophobic nature. Further, it does not provide protection in terms of clinical/ biochemical recovery. A new trend in chelation therapy is to use combined treatment. This includes the use of structurally different chelators or a combination of an adjuvant and a chelator to provide better clinical/ biochemical recovery in addition to lead mobilization. The present review article attempts to provide update information about the current strategies being adopted for a safe, effective and specific treatment for two major toxic metals or metalloid.

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“…Supplementing cells with antioxidants such as NAC, lipoic acid (LA) [17], tocopherol [27], and probucol [23] has shown protective effects against glutamate toxicity, mostly by replenishing GSH. However, in certain neurological diseases, such as cerebral ischemia and Parkinson's disease, enhancement of tissue GSH in brain regions may not be attained, because many antioxidant agents cross the blood -brain barrier poorly [26,14].…”

Section: Introductionmentioning

confidence: 99%

Effects of N-acetylcysteine amide (NACA), a novel thiol antioxidant against glutamate-induced cytotoxicity in neuronal cell line PC12

et al. 2005

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Oxidative stress plays an important role in neuronal cell death associated with many different neurodegenerative conditions such as cerebral ischemia and Parkinson's disease. Elevated levels of glutamate are thought to be responsible for CNS disorders through various mechanisms causing oxidative stress induced by a nonreceptor-mediated oxidative pathway which blocks cystine uptake and results in depletion of intracellular glutathione (GSH). The newly designed amide form of N-acetylcysteine (NAC), N-acetylcysteine amide (NACA), was assessed for its ability to protect PC12 cells against oxidative toxicity induced by glutamate. NACA was shown to protect PC12 cells from glutamate (Glu) toxicity, as evaluated by LDH and MTS assays. NACA prevented glutamate-induced intracellular GSH loss. In addition, NACA restored GSH synthesis in a Glu (10 mM) plus buthionine -sulfoximine (BSO) (0.2 mM)-treated group, indicating that the intracellular GSH increase is independent of g-GSC (g-glutamylcysteinyl synthetase). The increase in levels of reactive oxygen species (ROS) induced by glutamate was significantly decreased by NACA. Measurement of malondialdehyde (MDA) showed that NACA reduced glutamate-induced elevations in levels of lipid peroxidation by-products. These results demonstrate that NACA can protect PC12 cells against glutamate cytotoxicity by inhibiting lipid peroxidation, and scavenging ROS, thus preserving intracellular GSH. D

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α-Lipoic acid protects against reperfusion injury following cerebral ischemia in rats

Cited by 172 publications

References 18 publications

A dual action of alpha-lipoic acid in the brain: an electrophysiological evaluation

A dual action of alpha-lipoic acid in the brain: an electrophysiological evaluation

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Effects of N-acetylcysteine amide (NACA), a novel thiol antioxidant against glutamate-induced cytotoxicity in neuronal cell line PC12

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