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PubMed2002

Prevention of hypertension, insulin resistance, and oxidative stress by alpha-lipoic acid.

The aim of the present study was to investigate whether a dietary supplementation of alpha-lipoic acid could prevent blood pressure elevation, insulin resistance, and the increase in aorta superoxide anion production in a new experimental model of hypertension associated with insulin resistance. Sprague-Dawley rats were given 10% D-glucose in their drinking water combined either with a normal chow diet or with an alpha-lipoic acid-supplemented diet and were compared with control rats during 3 weeks. Oxidative stress was evaluated by measuring the aortic superoxide anion production using the lucigenin chemiluminescence method. Increases in blood pressure, insulin resistance, and aorta superoxide production observed in glucose-fed rats were prevented by the supplementation of the diet with lipoic acid. Positive correlations were found between aortic superoxide production and blood pressure, between insulin resistance and blood pressure, or between superoxide production and insulin resistance. Moreover, a decrease in the activity of plasma glutathione peroxidase observed in the glucose-fed rats was prevented by lipoic acid treatment. These findings demonstrate that high-glucose feeding rapidly induced hypertension and insulin resistance in association with the induction of a vascular oxidative stress. The antihypertensive action and the prevention of insulin resistance by lipoic acid appears to be associated to its antioxidative properties because it prevented the increase in oxidative stress, as reflected by the normalization of superoxide anion production in aorta and the prevention of the fall in the activity of glutathione peroxidase in the glucose-fed rats.

Animals↗
PubMed1996

Stimulation of Ca2+ release from rat liver mitochondria by the dithiol reagent alpha-lipoic acid.

Rat liver mitochondria contain a Ca(2+)-specific release pathway stimulated by Ca(2+)-dependent hydrolysis of oxidized intramitochondrial pyridine nucleotides to ADP ribose and nicotinamide. We have previously shown that NAD+ hydrolysis and subsequent Ca2+ release are inhibited by cyclosporine A and that they are only possible when some critical thiols are cross-linked or oxidized, e.g. by phenylarsine oxide, gliotoxin, or peroxynitrite. We now report that the antioxidant alpha-lipoic acid stimulates Ca2+ release from intact mitochondria, i.e. with preservation of the mitochondrial membrane potential and without large-amplitude swelling. The release stimulated by alpha-lipoic acid is inhibited by cyclosporine A and is more effective when the pyridine nucleotides are oxidized. The results strongly suggest that alpha-lipoic acid stimulates the Ca(2+)-specific release pathway from intact mitochondria by oxidizing some vicinal thiols, thereby stimulating hydrolysis of oxidized pyridine nucleotides. These observations further corroborate that intact rat liver mitochondria contain a specific Ca2+ release pathway stimulated by modification of vicinal thiols. Prolonged stimulation of Ca2+ release by lipoic acid followed by its re-uptake (Ca2+ "cycling") may contribute to the detrimental, prooxidant-like effects seen with higher concentrations of lipoic acid.

Animals↗
PubMed2002

Novel lipoic acid analogues that inhibit nitric oxide synthase.

The synthesis and biological activity of novel lipoic acid analogues are reported. Lipoic acid and structural homologues coupled to arylthiophene amidine via carboxamide linkers are metabolic antioxidants capable of protecting neuronal cells against glutamate cytotoxicity, preventing loss of intracellular glutathione, and inhibit nitric oxide synthase.

Animals↗
PubMed1989

Protective effects of DL-alpha-lipoic acid on cadmium-induced deterioration of rat hepatocytes.

The suitability of DL-alpha-lipoic acid (LA) to serve as an antidote in cadmium (Cd) toxicity in rat hepatocytes was investigated. Isolated hepatocytes were exposed to 200 and 450 microM Cd in the presence of 0.2, 1.0 and 5.0 mM LA, respectively. After 30 min of incubation various criteria of cell viability were monitored. Lipoic acid markedly diminished Cd uptake. Concomitantly, Cd-induced membrane injury, as reflected by the leakage of aspartate aminotransferase and sorbitol dehydrogenase (SDH) was decreased. Moreover, LA protected against intracellular toxic responses to Cd, such as a decrease in cellular SDH activity, a decrease in cellular acid soluble thiols, especially in total glutathione, a decrease in cellular urea and an increase in thiobarbituric acid (TBA) reactants, as a measure of lipid peroxidation. Most protective effects were seen in hepatocytes challenged with the lower Cd concentration and coincubated with 5 mM LA. In contrast, at 450 microM Cd even the highest LA concentration applied either did only reverse Cd-effects incompletely (SDH-response, TBA-reactants) or did not protect at all (Cd uptake, enzyme leakage, loss of glutathione). The data indicate that DL-alpha-lipoic acid serves as a protective tool against Cd-induced membrane damage and cell dysfunction in hepatocytes. This stands as long as Cd exposure is low enough to permit interaction with LA prior to interaction with cell structures.

Animals↗
PubMed2006

Protective effect of DL-alpha-lipoic acid on cyclophosphamide induced hyperlipidemic cardiomyopathy.

Cyclophosphamide is a potent alkylating agent used in cancer chemotherapy and immunosuppression. The present study is aimed at evaluating the role of a potent antioxidant lipoic acid in cyclophosphamide induced hyperlipidemic cardiomyopathy. Adult male Wistar rats were divided into four treatment groups. Two groups received single intraperitoneal injection of cyclophosphamide (200 mg/kg body weight) to induce cardiotoxicity, one of these groups received lipoic acid treatment (25 mg/kg body weight, orally for 10 days). A vehicle treated control group and a lipoic acid drug control were also included. Cyclophosphamide administration resulted in abnormal elevation of serum lipids. Similarly in the cardiac tissue, the levels of free cholesterol, esterified cholesterol, triglycerides were increased significantly (P<0.05) while the levels of phospholipids and free fatty acids were reduced significantly unlike serum (P<0.05). Serum Low Density Lipoprotein (LDL) and Very Low Density Lipoprotein (VLDL) cholesterol increased significantly (P<0.05) while High Density Lipoprotein (HDL) cholesterol (P<0.05) decreased significantly when compared to controls. These changes corroborated with the abnormal distortion in the activities of lipid metabolizing enzymes in cyclophosphamide treated group. Supplementation of lipoic acid reverted these abnormalities in the lipid levels and activities of lipid metabolizing enzymes to near normalcy after cyclophosphamide administration.

Animals↗
PubMed2002

Burning mouth syndrome (BMS): double blind controlled study of alpha-lipoic acid (thioctic acid) therapy.

BACKGROUND: Burning mouth syndrome (BMS) has features of a neuropathy and could be related to the production of the toxic free radicals that are released in stress situations. Alpha-lipoic acid is an antioxidant able to increase the levels of intracellular glutathione and eliminate free radicals. This study aimed to examine the effectiveness of alpha-lipoic acid in the therapy of BMS. METHOD: This was a double blind, controlled study conducted for two months on 60 patients with constant BMS. Comparing alpha-lipoic acid (test) with cellulose starch (placebo), there was no laboratory evidence of deficiencies in iron, vitamins or thyroid function and no hyperglycaemia. RESULTS AND CONCLUSION: Following treatment with alpha-lipoic acid, there was a significant symptomatic improvement, compared with placebo, with the majority showing at least some improvement after 2 months, thus supporting the hypothesis that burning mouth syndrome is a neuropathy. This improvement was maintained in over 70% of patients at the 1 year follow-up.

Adult↗
PubMed1995

Analysis of reduced and oxidized lipoic acid in biological samples by high-performance liquid chromatography.

Using HPLC with electrochemical detection at a dual Hg/Au electrode, both reduced and oxidized lipoic acid can be measured in biological samples after addition of lipoic acid. The method does not detect bound lipoic acid, which must be liberated by strong acid or base hydrolysis. The detection limit for this HPLC method is 0.01 nmol of dihydrolipoate and 0.05 nmol of lipoate. Baseline separation of lipoate and dihydrolipoate is achieved on a 10 cm octadecyl column. The analysis is rapid (8 min/sample) and uses a single HPLC pump with isocratic mobile phase. The method has been adapted to study cellular and whole animal reduction of lipoate, membrane transport of lipoate and dihydrolipoate, and subcellular enzymes that reduce lipoate.

Cell Line↗
PubMedDate not supplied

Hexosamine induction of oxidative stress, hypertrophy and laminin expression in renal mesangial cells: effect of the anti-oxidant alpha-lipoic acid.

We have previously shown that one of the potential mediators of the deleterious effects of high glucose on extracellular matrix protein (ECM) expression in renal mesangial cells is its metabolic flux through the hexosamine biosynthesis pathway (HBP). Here, we investigate further whether the hexosamines induce oxidative stress, cell-cycle arrest and ECM expression using SV-40-transformed rat mesangial (MES) cells and whether the anti-oxidant alpha-lipoic acid will reverse some of these effects. Culturing renal MES cells with high glucose (HG, 25 mM) or glucosamine (GlcN, 1.5 mM) for 48 h stimulates laminin gamma1 subunit expression significantly approximately 1.5 +/- 0.2- and 1.9 +/- 0.3-fold, respectively, when compared to low glucose (LG, 5 mM). Similarly, HG and GlcN increase the level of G0/G1 cell-cycle progression factor cyclin D1 significantly approximately 1.7 +/- 0.2- and 1.4 +/- 0.04-fold, respectively, versus LG (p < 0.01 for both). Azaserine, an inhibitor of glutamine:fruc-6-PO(4) amidotransferase (GFAT) in the HBP, blocks the HG-induced expression of laminin gamma1 and cyclin D1, but not GlcN's effect because it exerts its metabolic function distal to GFAT. HG and GlcN also elevate reactive oxygen species (ROS) generation, pro-apoptotic caspase-3 activity, and lead to mesangial cell death as revealed by TUNEL and Live/Dead assays. FACS analysis of cell-cycle progression shows that the cells are arrested at G1 phase; however, they undergo cell growth and hypertrophy as the RNA/DNA ratio is significantly (p < 0.05) increased in HG or GlcN-treated cells relative to LG. The anti-oxidant alpha-lipoic acid (150 microM) reverses ROS generation and mesangial cell death induced by HG and GlcN. Alpha-lipoic acid also reduces HG and GlcN-induced laminin gamma1 and cyclin D1 expression in MES cells. In addition, induction of diabetes in rats by streptozotocin (STZ) increases both laminin gamma1 and cyclin D1 expression in the renal cortex and treatment of the diabetic rats with alpha-lipoic acid (400 mg kg(-1) body weight) reduces the level of both proteins significantly (p < 0.05) when compared to untreated diabetic rats. These results support the hypothesis that the hexosamine pathway mediates mesangial cell oxidative stress, ECM expression and apoptosis. Anti-oxidant alpha-lipoic acid reverses the effects of high glucose, hexosamine and diabetes on oxidative stress and ECM expression in mesangial cells and rat kidney.

Animals↗
PubMed2001

Hypochlorous acid-modified low-density lipoprotein inactivates the lysosomal protease cathepsin B: protection by ascorbic and lipoic acids.

Unregulated uptake of oxidized LDL by the scavenger receptor(s) of macrophages is thought to be an early event in atherosclerotic lesion development. Accumulation of oxidized LDL within macrophages may result from resistance of the modified LDL to enzymatic hydrolysis or from direct inactivation of lysosomal enzymes by reactive LDL-associated moieties. Since HOCl-modified LDL has been detected in vivo, the effects of HOCI-modified LDL on the activities of the cysteine protease cathepsin B and the aspartyl protease cathepsin D were investigated. LDL (0.5 mg protein/ml), which had been exposed to HOCl (25-200 microM), caused rapid dose-dependent inactivation of cathepsin B, but not of cathepsin D. Exposure of LDL to HOCl results primarily in the formation of LDL-associated chloramines, and the model chloramine N(alpha)-acetyl-lysine chloramine also caused dose-dependent inactivation of cathepsin B. Incubation of HOCl-modified LDL with ascorbic and lipoic acids (25-200 microM) resulted in dose-dependent reduction of LDL-associated chloramines and concomitant protection against cathepsin B inactivation. Thus, the data indicate that HOCl-modified LDL inactivates cathepsin B by a chloramine-dependent mechanism, most likely via oxidation of the enzyme's critical cysteine residue. Furthermore, small molecule antioxidants, such as ascorbic and lipoic acids, may be able to inhibit this potentially pro-atherogenic process by scavenging LDL-associated chloramines.

Amines↗
PubMed2003

(r)-, but not (s)-alpha lipoic acid stimulates deficient brain pyruvate dehydrogenase complex in vascular dementia, but not in Alzheimer dementia.

In dementia of Alzheimer type (DAT), cerebral glucose metabolism is reduced in vivo, and enzymes involved in glucose breakdown are impaired in post-mortem brain tissue. Pyruvate dehydrogenase complex activity (PDHc) is one of the enzymes known to be reduced, while succinate dehydrogenase activity (SDH), another enzyme of oxidative glucose metabolism is unchanged. In dementia of vascular type (DVT), variable changes in glucose metabolism have been demonstrated in vivo, while changes of enzyme activities in post-mortem brain tissue are unknown. Here, PDHc and SDH activity were stimulated with each of the two stereoisomers of alpha lipoic acid in post-mortem parietal brain cortex of patients with DAT, DVT, and one case of Pick's disease and compared to stimulation effects in a control group, matched for age, sex, post-mortem delay, and storage time of brain tissue. PDHc in DAT and DVT, but not in Pick's disease was reduced. PDHc activity could be slightly stimulated by 10 micro M of the physiological stereoisomer (r)-alpha-lipoic acid, in controls and DVT (possibly also in Pick's disease), but not in DAT. In all groups investigated SDH was activated by 100 micro M and 1 mM of both isomers of alpha-lipoic acid, whereas 10 mM of both stereoisomers of alpha-lipoic acid caused an inhibition of both, PDHc and SDH activity. The loss of basal and of (r)-alpha-lipoic acid stimulated PDHc activity indicate that a functional or structural impairment of PDHc may exist in DAT and DVT which is not merely attributable to loss of mitochondria since basal and stimulated SDH activities are similar in controls, DVT and DAT, thus indicating selective vulnerability of PDHc.

Aged↗
PubMed2006

Protective efficacy of alpha-lipoic acid on acetylcholinesterase activity in aged rat brain regions.

The purpose of the present investigation was to measure the activity of acetylcholinesterase in discrete regions of young and aged rat brain before and after DL-alpha-lipoic acid supplementation. Two groups of male albino rats were used in this study (4 and 24 months of age). DL-alpha-lipoic acid was administered intraperitoneally with a regimen of 100 mg/kg body weight per day using alkaline saline as a vehicle for 7 and 14 days. The activity was measured in the cerebral cortex, cerebellum, striatum, hippocampus and hypothalamus, and found to be significantly decreased in some of the brain regions in aged rats. Administration of lipoic acid into aged rats reversed the decrease in the activity in the discrete brain regions. These results suggest that lipoic acid is effective in restoration of the activity of acetylcholinesterase in aged rats.

Acetylcholinesterase↗
PubMed2003

Creatine monohydrate supplemented in swine finishing diets and fresh pork quality: III. Evaluating the cumulative effect of creatine monohydrate and alpha-lipoic acid.

The objective of this study was to evaluate short-duration supplementation of alpha-lipoic acid (ALA) and creatine monohydrate (CMH) to improve fresh pork quality. Forty-eight commercial hybrid barrows were blocked by BW and randomly allotted to one of four treatments: 1) no CMH or ALA; 2) supplementation of 24 g of CMH(-1) x pig(-1) x d(-1); 3) supplementation of 600 mg ALA(-1) x pig(-1) x d(-1); or 4) combined CMH and ALA supplements. Twelve pigs per treatment were individually penned with ad libitum access to water and a finishing diet. Treatments were hand-fed to individual pigs daily (divided into three equal doses) for 5 d before slaughter at 113 kg BW in two separate groups of 24 pigs each. Intramuscular pH was recorded at 45 min postmortem and again at 24 h in the ham semimembranosus (SM) and the longissimus muscle (LM) between the 10th and 11th rib. A Meatcheck (SFK Technology, Peosta, IA) conductivity probe was inserted in the same anatomical locations as pH measurement, providing an index value (PY) from 0 to 100 (a higher index value indicates more intact muscle cells and higher water-holding capacity). Color (L, a, b values) measurements were obtained at 24 h postmortem on the ham gluteus medius (GM), SM, and LM. Two 2.54-cm-thick loin chops were removed from the loin for determination of Warner-Bratzler shear force and glycolytic potential. The intact SM and the posterior portion of the boneless loin were vacuum-packaged and stored for 7 d to determine purge loss. Creatine-supplemented pigs had a higher (P = 0.03) PY value in the SM (66.67) at 45 min postmortem than either ALA, singularly (63.50), or in the combined CMH/ALA (62.27) treatments. (A higher PY index indicates superior water-holding capacity.) Lipoic acid supplementation resulted in the highest pH at 45 min (P = 0.029). These results justify further evaluation of the potential positive influence of supplementing alpha-lipoic acid to improve pork quality.

Animal Feed↗
PubMed2006

alpha-Lipoic acid attenuates x-irradiation-induced oxidative stress in mice.

The development of nontoxic but effective radioprotectors is needed because of the increasing risk of human exposure to ionizing radiation. We have reported that alpha-lipoic acid confers considerable radio-protective effect in mouse tissues when given prior to x-irradiation. In the present study, alpha-lipoic acid supplementation prior to x-irradiation with 4 and 6 Gy significantly inhibited the radiation-induced decline in total antioxidant capacity (TAC) of plasma. Radiation-induced decline in non-protein sulfhydryl content (NPSH) of different tissues, namely, brain, liver, spleen, kidney, and testis, was also ameliorated significantly at both 4 and 6 Gy doses. Maximal augmentation of radiation-induced protein carbonyl content was observed in spleen followed by brain, kidney, testis, and liver. Maximal protection in terms of carbonyl content was observed in spleen (116%) at 6 Gy dose, and minimal protection was found in liver (22.94%) at 4 Gy dose. Maximal increase in MDA (malondialdehyde) content was observed in brain, followed by testis, spleen, kidney, and liver. Protection by alpha-lipoic acid pretreatment in terms of MDA content was maximal in brain (51.67%) and minimal in spleen. The findings support the idea that alpha-lipoic acid is a free-radical scavenger and a potent antioxidant.

Animals↗
PubMed1999

Alpha-lipoic acid reduces expression of vascular cell adhesion molecule-1 and endothelial adhesion of human monocytes after stimulation with advanced glycation end products.

Advanced glycation end products (AGEs) have been identified as relevant mediators of late diabetic complications such as atherosclerotic disease. The endothelial migration of monocytes is one of the first steps in atherogenesis and monocyte-endothelial interaction itself is linked to the expression of adhesion molecules like vascular cell adhesion molecule-1 (VCAM-1). Recently, stimulation of VCAM-1 by AGEs has been demonstrated. Since endothelial stimulation by AGEs is followed by generation of oxygen free radicals with subsequent activation of nuclear transcription factor kappaB, we investigated the influence of alpha-lipoic acid on the expression of VCAM-1 and monocyte adherence to endothelial cells in vitro by means of cell-associated chemiluminescence assays and quantitative reverse transcriptase polymerase chain reaction using a constructed recombinant RNA standard. We found that alpha-lipoic acid was able to decrease the number of VCAM-1 transcripts from 41. 0+/-11.2 to 9.5+/-4.7 RNA copies per cell in AGE-stimulated cell cultures. Furthermore, expression of VCAM-1 was suppressed in a time- and dose-dependent manner by alpha-lipoic acid as shown by chemiluminescence endothelial cell assay. Pretreatment of endothelial cells with 0.5 mM or 5 mM alpha-lipoic acid reduced AGE-induced endothelial binding of monocytes from 22.5+/-2.9% to 18. 3+/-1.9% and 13.8+/-1.8% respectively. Thus, we suggest that extracellularly administered alpha-lipoic acid reduces AGE-albumin-induced endothelial expression of VCAM-1 and monocyte binding to endothelium in vitro. These in vitro results may contribute to the understanding of a potential antioxidative treatment of atherosclerosis.

Antioxidants↗
PubMed2004

Alpha lipoic acid for dementia.

BACKGROUND: Oxidative processes have been implicated in the pathogenesis of neurodegenerative dementias including Alzheimer's disease. Protecting the central nervous system against these damaging mechanisms may be a useful therapeutic approach. Alpha lipoic acid (ALA) is an endogenous antioxidant that interrupts cellular oxidative processes in both its oxidized and reduced forms. These properties might qualify ALA for a modulatory role in the treatment of people with dementia. OBJECTIVES: To assess the role and clinical efficacy of alpha lipoic acid in the treatment of dementia. SEARCH STRATEGY: A search of the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (CDCIG) on 3 February 2003 using the terms 'alpha lipoic acid' and 'thioctic'. The CDCIG Specialized register is updated regularly and contains records from all major health care databases (MEDLINE, EMBASE, PsycInfo, CINAHL) as well as from many trials databases. SELECTION CRITERIA: All double-blind randomized placebo-controlled trials examining the efficacy of alpha lipoic acid in dementia DATA COLLECTION AND ANALYSIS: No trials were found that met the selection criteria MAIN RESULTS: No meta-analysis could be performed. A systematic search of the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group, as well as registers of ongoing and unpublished trials could not identify any studies investigating the use of ALA for dementia. REVIEWER'S CONCLUSIONS: In the absence of randomized double-blind placebo-controlled trials investigating ALA for dementia, no evidence exists to explore any potential effects. Until data from trials become available for analysis, ALA cannot be recommended for people with dementia.

Dementia↗
PubMed1977

Interaction between thiamine hydrochloride and lipoic acid.

An interaction between thiamine hydrochloride and DL-alpha-lipoic acid in aqueous solution was depicted. Evidence is presented through spectrophotometric as well as vapour pressure measurements to show that thiamine hydrochloride and DL-alpha-lipoic acid form a single 1:1 complex. The stability constant and the molar extinction coefficient of the complex (at 244 nm) were determined at 25 degrees C and found to be 3.1-10(4) and 970, respectively. Vapour pressure measurements at 60 degrees C reveal that more or less complete dissociation of the complete takes place at this temperature.

Solutions↗
PubMed1995

Treatment of symptomatic diabetic peripheral neuropathy with the anti-oxidant alpha-lipoic acid. A 3-week multicentre randomized controlled trial (ALADIN Study).

Anti-oxidant treatment has been shown to prevent nerve dysfunction in experimental diabetes mellitus, thus providing a rationale of potential therapeutic value for diabetic patients. The effects of the anti-oxidant alpha-lipoic acid (thioctic acid) were studied in a 3-week multicentre, randomized, double-blind placebo-controlled trial (Alpha-Lipoic Acid in Diabetic Neuropathy; ALADIN) in 328 non-insulin-dependent diabetic patients with symptomatic peripheral neuropathy who were randomly assigned to treatment with intravenous infusion of alpha-lipoic acid using three doses (1200, 600, or 100 mg ALA) or placebo (PLAC). Neuropathic symptoms (pain, burning, paraesthesiae, and numbness) were scored at baseline and at each visit (days 2-5, 8-12, and 15-19) prior to infusion. In addition, the Hamburg Pain Adjective List, a multidimensional specific pain questionnaire, and the Neuropathy Symptom and Disability Scores were assessed at baseline and day 19. According to the protocol 260 (65/63/66/66) patients completed the study. The total symptom score in the feet decreased from baseline to day 19 by -4.5 +/- 3.7 (-58.6%) points (mean +/- SD) in ALA 1200, -5.0 +/- 4.1 (-63.5%) points in ALA 600, -3.3 +/- 2.8 (-43.2%) points in ALA 100, and -2.6 +/- 3.2 (-38.4%) points in PLAC (ALA 1200 vs PLAC: p = 0.003; ALA 600 vs PLAC: p < 0.001). The response rates after 19 days, defined as an improvement in the total symptom score of at least 30%, were 70.8% in ALA 1200, 82.5% in ALA 600, 65.2% in ALA 100, and 57.6% in PLAC (ALA 600 vs PLAC; p = 0.002). The total scale of the Pain Adjective List was significantly reduced in ALA 1200 and ALA 600 as compared with PLAC after 19 days (both p < 0.01). The rates of adverse events were 32.6% in ALA 1200, 18.2% in ALA 600, 13.6% in ALA 100, and 20.7% in PLAC. These findings substantiate that intravenous treatment with alpha-lipoic acid using a dose of 600 mg/day over 3 weeks is superior to placebo in reducing symptoms of diabetic peripheral neuropathy, without causing significant adverse reactions.

Adolescent↗
PubMed1994

alpha-Lipoic acid protects against hemolysis of human erythrocytes induced by peroxyl radicals.

The azo initiator of peroxyl radicals 2,2'-azobis (2-amidinopropane) dihydrochloride (AAPH) induces oxidative hemolysis in human erythrocytes and subsequent hemoglobin oxidation. Using the degree of hemolysis versus time as an indication of the oxidative damage it was found that i) both reduced and oxidized alpha-lipoic acid protected against oxidative damage; ii) simultaneous treatment of erythrocytes with ascorbate and dihydrolipoate or alpha-lipoate has a synergistic tendency to protect cells against hemolysis; iii) glutathione in combination with dihydrolipoic acid or alpha-lipoic acid has an additive effect on hemolysis protection. The spin trapping reagent 5,5-dimethyl-1-pyrroline N-oxide (DMPO) formed an adduct with the peroxyl/alkoxyl radicals produced by thermal decomposition of AAPH in the presence of oxygen. The formation of this adduct was prevented by reduced or oxidized lipoic acid, reduced glutathione or ascorbate. It is concluded that AAPH-peroxyl radicals progressively damage the cells and the released hemoglobin is subsequently oxidized to methemoglobin which might further enhance the oxidative damage. The protective effect of antioxidants is exerted outside the cells by directly scavenging AAPH-alkoxyl radicals.

Amidines↗