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H Esterbauer

Publications and source records attributed to H Esterbauer.

At least 37 records · Page 2Linked to original sources
PubMed1997

Risk factors for microangiopathy-related cerebral damage in the Austrian stroke prevention study.

Microangiopathy-related cerebral damage (MARCD) represents a common incidental MRI observation in the elderly. The risk factors of such findings are widely unknown. We therefore performed MRI in 349 randomly selected volunteers (ages 50 to 70 years) without neuropsychiatric disease, and evaluated the association of MARCD with conventional and recently suggested cerebrovascular risk factors such as apolipoprotein E genotypes, plasma concentrations of essential antioxidants and anticardiolipin antibody titres. MARCD was defined as evidence of early confluent and confluent deep white matter hyperintensities and lacunes. It was present in 71 (20.3%) subjects. Individuals with MARCD were older than those without such findings (62.7 years vs 59.6 years; P=0.0001). They had a higher rate of arterial hypertension (45.1% vs 28.1%; P=0.006) and cardiac disease (50.7% vs 37.1%; P=0.04), higher systolic blood pressure readings at exam (144.4 mmHg vs 136.7 mmHg; P=0.004), and higher serum fibrinogen concentrations (327.1 mg/dl vs 292.5 mg/dl; P=0.001). Their levels of total cholesterol (217.6 mg/dl vs 231.2; P=0.009), apolipoprotein A-I (167.3 mg/dl vs 177.4 mg/dl, P=0.02), lycopene (0.17 micromol/l vs 0.24 micromol/l; P=0.003), retinol (1.91 micromol/l vs 2.10 micromol/l; P=0.02) and alpha-tocopherol (27.55 micromol/l vs 31.14 micromol/l; P=0.001) were significantly lower. Forward stepwise regression analysis created a model of independent predictors of MARCD with age entering first (odds ratio 2.01/10 years), fibrinogen second (odds ratio 2.45/100 mg/dl), alpha-tocopherol third (odds ratio 0.55/10 micromol/l), and arterial hypertension fourth (odds ratio 1.96). The association of MARCD with various treatable clinical conditions may have preventive implications.

Aged↗
PubMed1997

Low and very low density lipoprotein composition and resistance to copper-induced oxidation are not notably modified in smokers.

To study whether tobacco use was associated with oxidative phenomena affecting lipoproteins, we estimated susceptibility of LDL and VLDL to an in vitro copper-mediated oxidation, and measured serum autoantibody titers against oxidized LDL in 45 middle-age healthy nonsmokers, 35 smokers and 37 ex-smokers of both sexes, taking into account the detailed lipid composition of the lipoproteins. VLDL from female smokers had higher triglyceride, phospholipid, apolipoprotein E and alpha-tocopherol content and showed a higher rate of copper-induced oxidation in comparison with those from nonsmokers (P < or = 0.05) whereas the relative composition of these particles in saturated, mono- or poly-unsaturated fatty acids was not modified by tobacco consumption. After adjustment for triglyceride content, no statistically significant difference in oxidation rate was observed. Lipid, alpha-tocopherol and protein composition of LDL did not appear to be influenced by smoking; in accordance with these observations, no difference in indices of in vitro oxidizability of LDL was noticed between the different groups. Autoantibody titers against oxLDL were similar in smokers and nonsmokers. We conclude that, in supposed healthy individuals, smoking does not seem to be associated with notable variations in composition of VLDL and LDL or with an increase of oxidizability of these atherogenic lipoproteins.

Adolescent↗
PubMed1997

Antioxidant role of melatonin in lipid peroxidation of human LDL.

The antioxidant effect of melatonin on LDL oxidation was studied in vitro using either a thermolabile initiator or copper ions to induce lipid peroxidation. Loading of LDL with melatonin showed only weak protection against oxidative damage as compared to alpha-tocopherol. In the presence of high concentrations of melatonin (1000 mol/mol LDL) in the medium a clear protective effect was found during lag- and propagation phase, albeit weaker than after loading with alpha-tocopherol. It is concluded that melatonin is not incorporated into LDL in sufficient concentrations to prevent lipid peroxidation effectively. When melatonin is present in the incubation medium during oxidation, a partitioning equilibrium between aqueous and lipid phase is established. Only under these conditions can melatonin act as a chain breaking antioxidant. The concentrations required, however, are far beyond those found in human plasma. Therefore, the data in this study do not support a direct physiological relevance of melatonin as an antioxidant in lipid peroxidation processes.

Amidines↗
PubMed1997

The interaction of lower alcohols with apoB in spin labeled human plasma low density lipoproteins (LDL).

In this study the interaction of alcohol with the macromolecular lipid-protein assembly represented by human plasma low density lipoproteins (LDL) was investigated. The spin label which covalently binds to the side chain amino group of lysines as well as terminal amino groups was attached to the spin labeled apoprotein (apoB) of native LDL in order to observe the protein component in the electron spin resonance (ESR) spectrum. The interaction of different lower alcohols (methanol, ethanol, propanol and butanol) with the spin labeled LDL was studied for two alcohol concentrations (0.3 and 3.0 M). The ESR spectra indicate a decrease of the hyperfine splitting and narrowing of the linewidth upon the action of alcohol that leads to the conclusion that alcohol provokes a change in the apoB conformation. These findings are explained by following the arguments of the phospholipid mediated mechanism of alcohol action, through the modulation of the lipid packing free volume which results in the protein conformational change.

Alcohols↗
PubMed1997

Increased stress parameter synthesis in the yeast Saccharomyces cerevisiae after treatment with 4-hydroxy-2-nonenal.

The metabolism of glutathione (GSH), a marker of oxidative stress and trehalose, a rather general physiological stress marker, was examined in exponentially growing Saccharomyces cerevisiae cells after treatment with 4-hydroxynonenal (HNE). GSH was entirely depleted within a 2 h incubation with 250 microM HNE. After removal of the aldehyde it was replenished by de novo synthesis leading to an overshooting GSH level, which later decreased to the basal level. In addition, trehalose was elevated 4-fold in HNE-treated yeast cells compared to control cells. We conclude that increased GSH levels upon HNE treatment are a general phenomenon of eukaryotic cells to ensure protection and survival during further harsh conditions. Furthermore, we have discovered a new indication for the stress marker trehalose in S. cerevisiae.

Aldehydes↗
PubMed1997

Chondroitin 4-sulphate exhibits inhibitory effect during Cu2+-mediated LDL oxidation.

Chondroitin 4-sulphate (C4S), a basic component of the extracellular matrix of the artery wall, inhibited copper-induced low density lipoprotein (LDL) oxidation by prolonging the lag time and reducing the rate of propagation. LDL oxidation was assessed by monitoring conjugated dienes and low level chemiluminescence. A possible initial key reaction in LDL oxidation, the reduction of copper(II) to copper(I) by LDL, was decreased in the presence of C4S. Moreover, C4S protected tryptophan residues of Apo-B-100 in the early stage of LDL oxidation and during the subsequent propagation phase. The presence of the sulphate group in position 4 of N-acetylgalactosaminyl residues of C4S is crucial for protective activity. In fact, the structurally related chondroitin 6-sulphate, also present in tissues, had no effect on LDL oxidation. These data suggest that C4S may contribute to protect LDL against oxidation in arterial intima.

Adult↗
PubMed1997

Nitroxide reduction with ascorbic acid in spin labeled human plasma LDL and VLDL.

The LDL and VLDL were spin labeled with Tempo which partitions both in the aqueous and lipid phase. The ESR spectra were measured in the equilibrium state as well as during the reduction of the spin label with ascorbic acid. The kinetics of the concentration decay curves was parametrized with two exponentials. The theoretical simulation of the experimental spectra revealed a drastic linewidth narrowing in the VLDL samples exposed to the ascorbic acid. Since the transport properties of the specific monolayer are reflected in the observed reaction rates, the analysis of the fatty acid composition of phospholipids, triglycerides and cholesterol esters in LDL and VLDL was performed. It is concluded that different lipid packing at the surface of LDL and VLDL might be the consequence of different intermolecular forces between phospholipids and cholesterol. This finding was connected to the experimentally detected different reaction kinetics in LDL and VLDL as well as their different susceptibility to the ESR linebroadening effects during the nonequilibrium conditions of the spin label reduction with ascorbic acid.

Ascorbic Acid↗
PubMed1997

Quantitative determination of oLAb titers in various animal species.

It is generally accepted, that lipid peroxidation plays a pathogenic role in atherosclerosis. Furthermore, recent studies indicate that antibodies directed against oxidative modifications of Low Density Lipoprotein (oLAb) contribute to atherosclerotic processes and may have some function in other disorders. These antibodies have been determined predominantly in humans, because assays for oLAb measurement use species specific anti IgG conjugates. From such assay designs it is not possible to get directly comparable data from various animal species. Main advantages of comparable data between animal species are that results of animal experiments can be interpreted using human calibrators and that results of immunisations and production of monoclonal antibodies are directly comparable not only within, but also between animal species. The aim of this study was to find a modification for ELISAs for oLAb determination, which allows to measure sera of various animal species simultaneously. Microtitration plates were coated with oxidised LDL and blocked with bovine serum albumine. Human and animal sera were then pipetted into the plate in logarithmic serial dilutions and incubated for 2 h at 37 degrees C. After washing, a protein A horse-radish peroxidase conjugate (Biomakor, Israel) was added to each well in a dilution of 1:20,000. The incubation conditions had to be optimized to achieve reliable results. After another washing step, the assay was developed with TMB. Absorptions were read at 450 nm in a microplate photometer. Following the manufacturers incubation instructions, which recommended a duration of 1 h at room temperature, the system did not work optimally. No binding of protein A to IgG molecules bound to oxidised LDL could be observed, if the system was incubated at 37 degrees C. In our hands, best results were achieved for several animal species, if the conjugate was incubated for two hours at 2-4 degrees C in a refrigerator. Under these conditions, assay sensitivity was the same as in the standard method, which uses anti-species IgG conjugates. The protein A modification of oLAb allows direct reading of animal oLAb titres from human calibrators. With this method, results of animal experiments can be interpreted on the basis of the situation in humans. Preliminary results obtained show that immunisation experiments with oxidised LDL give serum titres in animals, which are in the same order of magnitude as human sera with high oLAb concentrations. The results of this study, in accordance with findings of other authors, give further indications that atherosclerotic processes are influenced by the specific immune system.

Animals↗
PubMed1997

Antioxidant vitamins in prevention.

The authors are aware that there is still a need for much research to elucidate the possible preventive effects of antioxidant vitamins with regard to degenerative and neoplastic diseases. There must also be vigorous examination of the evidence that antioxidant vitamins can play a crucial part in a large number of other disorders (Alzheimer's disease, Parkinson's disease, diabetes, chronic and acute inflammations, airway disorders, reperfusion syndrome). The aim of prevention-oriented medical research must be to develop suitable measures able to make a considerable contribution to the overall prevention policy. Although there is still uncertainty about the mode of action and the optimal dosage of antioxidant nutrients and dietary constituents, particularly because of the safety when the dosage is correct, more information must be provided about early prevention of an inappropriate, low antioxidant intake; intake in the diet should definitely be preferred to supplementation because of the other beneficial effects of the recommended foodstuffs.

Journal Article↗
PubMed1997

Increased neopterin in patients with chronic and acute coronary syndromes.

OBJECTIVES: The aim of our study was to determine neopterin levels in patients with chronic and acute coronary syndromes. BACKGROUND: In chronic and acute coronary syndromes the release of different cytokines activates cellular defense. Infiltration of neutrophils and monocytes/macrophages is detected in the vessel wall as well as in the myocardium. Neopterin, which is a by-product of the guanosine triphosphate-biopterin pathway, is a marker for those activated macrophages. METHODS: We studied 123 subjects: 1) 21 consecutive patients (17 men, 4 women; mean age +/- SD 66 +/- 15 years, range 31 to 87) with acute myocardial infarction (AMI); 2) 62 consecutive patients (50 men, 12 women; mean age 61 +/- 8 years, range 43 to 81) with signs and symptoms of clinically stable coronary artery disease (CAD); and 3) 40 healthy blood donors (28 men, 12 women; mean age 35 +/- 13 years). Neopterin levels were determined with a commercially available enzyme-linked immunosorbent assay method. RESULTS: In patients with AMI before thrombolytic therapy, neopterin levels were significantly higher than levels in patients with CAD and control subjects (13.7 vs. 8.6 and vs. 6.8 nmol/liter, p < 0.0001). Values also differed significantly between patients with CAD and control subjects (p < 0.0001). Neopterin levels in patients with AMI were measured seven times during a 72-h period. Within-group comparison showed significant differences over this period (p < 0.00001). The lowest value (11.4 nmol/liter) was observed after 4 h and differed significantly from the initial value and values after 24 and 72 h (p < 0.05). After 72 h, neopterin increased to 14.9 nmol/liter, a value significantly different from all values other than the initial one. There was no correlation between neopterin and creatine kinase (CK); CK, MB isoenzyme; or lactate dehydrogenase as markers for the extent of the myocardial infarction during the observation period. CONCLUSIONS: Our data support the hypothesis of an activation of monocytes and macrophages in patients with an acute or chronic coronary syndrome. Neopterin as a marker for macrophage activation is significantly increased in patients with chronic CAD and more pronounced in patients with AMI shortly after the onset of symptoms.

Adult↗
PubMed1997

Increased levels of 4-hydroxynonenal modified proteins in plasma of children with autoimmune diseases.

Analysis of serum samples of healthy children (n = 11) and children with Systemic Lupus Erythematosus (SLE), (n = 21) was performed by SDS-PAGE and immunoblot with an antibody directed against proteins modified by lipid peroxidation (LPO) product 4-hydroxynonenal (HNE). A single major stained protein band was detected. By comparison of the molecular weights in nonreducing and reducing SDS-PAGE was found that the main protein modified by HNE is immunoglobulin G. Significantly higher concentrations of the aldehyde modified protein were found in children with high disease activity of SLE measured by SLE disease activity index (SLEDAI). Lipid peroxidation measured by malondialdehyde and 4-hydroxynonenal concentrations show an enhanced level of both compounds also in patients with the active autoimmune disease. Therefore, it can be assumed that free radical mediated processes play a pathophysiological role in the active phase of SLE and HNE-modified serum proteins are a further parameter for the detection of in vivo LPO.

Adolescent↗
PubMed1997

Simulation of the induction of oxidation of low-density lipoprotein by high copper concentrations: evidence for a nonconstant rate of initiation.

Kinetic simulation can help obtain deeper insight into the molecular mechanisms of complex processes, such as lipid peroxidation (LPO) in low-density lipoprotein (LDL). We have previously set up a single-compartment model of this process, initiating with radicals generated externally at a constant rate to show the interplay of radical scavenging and chain propagation. Here we focus on the initiating events, substituting constant rate of initiation (Ri) by redox cycling of Cu2+ and Cu+. Our simulation reveals that early events in copper-mediated LDL oxidation include (1) the reduction of Cu2+ by tocopherol (TocOH) which generates tocopheroxyl radical (TocO.), (2) the fate of TocO. which either is recycled or recombines with lipid peroxyl radical (LOO.), and (3) the reoxidation of Cu+ by lipid hydroperoxide which results in alkoxyl radical (LO.) formation. So TocO., LOO., and LO. can be regarded as primordial radicals, and the sum of their formation rates is the total rate of initiation, Ri. As experimental information of these initiating events cannot be obtained experimentally, the whole model was validated experimentally by comparison of LDL oxidation in the presence and absence of bathocuproine as predicted by simulation. Simulation predicts that Ri decreases by 2 orders of magnitude during lag time. This has important consequences for the estimation of oxidation resistance in copper-mediated LDL oxidation: after consumption of tocopherol, even small amounts of antioxidants may prolong the lag phase for a considerable time.

Computer Simulation↗
PubMed1997

Enhanced plasma level of lipid peroxidation in Iranians could be improved by antioxidants supplementation.

OBJECTIVE: To study the influence of supplementation with antioxidants on factors, which might increase the risk of coronary heart disease (CHD) in Iranians. DESIGN: Twenty-one male volunteers enter the prospective, single-blind, randomized study. SETTING: The supplementation was conducted at the Cardiovascular Center, University of Tehran, the biochemical analysis were carried out in the University of Graz. SUBJECTS: Twenty-one male medical students were recruited by advertisement. Five subjects were dropped out due to lack of the compliance. METHODS: One group of Iranians received 30 mg/d beta-carotene and placebo for alpha-tocopherol; the other received beta-carotene plus 400 IU alpha-tocopherol for ten weeks. Concentrations of antioxidants in plasma and low density lipoproteins (LDL), plasma lipid profile, autoantibody against oxidized LDL (oLAb) and malondialdehyde (MDA) concentrations in plasma were measured. Oxidative resistance of LDL was estimated using conjugated diene assay. RESULTS: Iranians had a significantly lower plasma levels of total cholesterol (P < 0.002), LDL-cholesterol (P < 0.01) and high density lipoprotein-cholesterol (P < 0.002), compared to healthy Austrian subjects (n = 13). Although the baseline concentrations of alpha-tocopherol and beta-carotene were comparable with Austrians, lycopene, canthaxanthin and lutein were significantly higher in Iranians (P < 0.03-0.001). In vitro oxidative resistance of LDL, measured as lag-time, was slightly higher (P < 0.01) in Iranians comparing with Austrians. Plasma MDA and oLAb concentrations were significantly higher in Iranians (P < 0.001). Both dietary supplementations reduced plasma MDA concentrations (P < 0.001-0.001). A key finding was that a supplement combined with alpha-tocopherol caused also a significant increase of oLAb concentration (P > 0.01) as well as the significant increase of lag-time (P > 0.005). CONCLUSIONS: This study shows that high plasma MDA level of Iranians can be decreased by beta-carotene supplementation with or without alpha-tocopherol. However, alpha-tocopherol is a more powerful antioxidant, which can increase the resistance of LDL to oxidation, reduce the MDA concentrations in plasma and increase autoantibodies to oLDL.

Adult↗
PubMed1997

Immunological evidence for hypochlorite-modified proteins in human kidney.

Oxygen radicals and oxidatively modified proteins seem to participate in degenerative vascular and inflammatory diseases. Factors that contribute to the development of atherosclerosis, eg, oxidation of low-density lipoproteins (LDLs), may also contribute to glomerulosclerosis. Although the nature of the in vivo oxidants remains unknown, recent findings indicated that the myeloperoxidase (MPO)-H2O2-halide system could play an important role in modification of (lipo)proteins in human tissues. MPO, the enzyme responsible for hypochlorite (HOCl/OCl-) formation, is present in human atherosclerotic lesions and in inflammatory conditions. In the present study, MPO was identified by Western blot analysis and immunohistochemical technique in diseased human kidney either with primarily sclerotic or inflammatory lesions. Furthermore, the presence of HOCl-modified proteins was demonstrated in diseased renal tissues using a specific monoclonal antibody (clone 2D10G9), raised against HOCl-modified LDL, that does not cross-react with native LDL or Cu(2+)-, 4-hydroxynonenal-, or malondialdehyde-modified LDL. The antibody recognized HOCl-modified proteins in glomerular and tubulointerstitial inflammatory and fibrotic lesions and pronounced immunostaining was demonstrated in mononuclear cells. LDL or human serum albumin oxidized by HOCl in vitro, but not native LDL or human serum albumin, effectively competed with epitopes in diseased kidney for antibody binding. Western blot analysis in diseased kidney protein samples revealed at least two major proteins recognized by the anti-HOCl-modified protein monoclonal antibody. Densitometric evaluation of immunoreactive bands obtained under these conditions demonstrated that expression of HOCl-modified proteins is tightly coupled to expression of immunoreactive MPO in the same tissue samples. From our studies it is proposed that oxidation of proteins by HOCl might be a leading event in glomerular and tubulointerstitial injury. By this mechanism, mononuclear cells, a permanent source for MPO, may play a key role in the development of nephrosclerosis, glomerulo-clerosis, and tubulointerstitial fibrosis, respectively.

Adult↗
PubMed1997

Metabolic fate of 4-hydroxynonenal in hepatocytes: 1,4-dihydroxynonene is not the main product.

4-Hydroxynonenal (HNE) is a major aldehydic product of lipid peroxidation known to exert several biological and cytotoxic effects. The metabolic fate of this aldehyde was investigated in hepatocytes as a cell type with a rapid HNE degradation. The experiments were carried out in rat hepatocytes at 37 degrees C at initial HNE concentrations of 1 microM-that means in the range of physiological and pathophysiologically relevant HNE levels-, 5 microM or 100 microM, respectively. About 95% of 100 microM HNE was degraded within 3 min of incubation. At 1 microM HNE the physiological level of about 0.1 to 0.2 microM was restored already after 30 sec. As primary products of HNE in hepatocytes the glutathione-HNE- 1:1-adduct, the hydroxynonenoic acid and the corresponding alcohol of HNE, the 1,4-dihydroxynon-2-ene, were identified. In contrast to previous reports, the corresponding alcohol of the HNE, 1,4-dihydroxynon-2-ene, was not the main HNE metabolite by far. The sum of these three primary HNE products accounts for about two-thirds of the total HNE degradation after 3 min of incubation. Furthermore, the beta-oxidation of hydroxynonenoic acid including the formation of water was demonstrated. The quantitative share of HNE binding to proteins, contrary to its great functional importance, is low with about 3% of total HNE consumption after 3 min incubation. The glycine-cysteine-HNE, cysteine-HNE adducts, and the mercapturic acid from glutathione-HNE adduct are not formed. In total, almost 90% of HNE degradation could be balanced by the formation of different HNE metabolites. The fast metabolism underlines the role of HNE degrading pathways in hepatocytes as one important part of the antioxidative defense system in order to protect proteins from modification by aldehydic lipid peroxidation products.

Aldehydes↗
PubMed1997

[Prevalence and risk factors in the population of Graz (Austrian Stroke Prevention Study)].

The Austrian Stroke Prevention Study recruited 1960 randomly selected subjects aged 50 to 75 years during a 3-year period of enrollment. The response rate of the study was 32.4%. A telephone interview with 200 randomly selected non-responders yielded no differences to responders regarding the frequency of major vascular risk factors known to the subjects. Besides demographics, the study assessed arterial hypertension, diabetes mellitus, cardiac disease, smoking, a complete lipid status including the apolipoprotein-E genotype, serum fibrinogen and anticardiolipin antibodies as well as various natural antioxidants such as vitamins A, C, E and beta-carotene. Arterial hypertension, diabetes mellitus, cardiac disease and hypercholesterolemia > 200 mg/dl were strikingly common and occurred in 38%, 7.6%, 32% and 76%, respectively. Suboptimal plasma concentrations of vitamin A, E, and beta-carotene were noted in 77.2%, 56.1% and in 53.2% of study participants. The rate of treatment of major risk factors known to the subjects prior to study entry were 60.3% and 70% for arterial hypertension and diabetes mellitus, but only 37.1% and 6.3% for cardiac disease and hypercholesterolemia > 250 mg/dl. Diet was commonly used to treat diabetes but was almost neglected in the treatment of other vascular risk factors. These data provide an orientation on the prevalence of risk factors and the use of primary preventive measures for stroke treatment in our community.

Adult↗
PubMed1997

RRR-alpha-tocopherol can be substituted for by Trolox in determination of kinetic parameters of LDL oxidizability by copper.

LDL resistance to oxidation is characterized by the lag time that precedes the rapid generation of conjugated dienes in copper-induced oxidation. Lag time (y) is described by the equation y = kx + a, where k is the efficacy constant of alpha-tocopherol (alpha-TOH), x the alpha-TOH content of LDL, and a the alpha-TOH-independent variable, all of which show considerable between-subject variability. To answer the question of whether loading of LDL with Trolox can substitute for the more timeconsuming loading with RRR-alpha-TOH in large scale studies focusing on determination of k and a values, LDL from 15 healthy subjects was loaded in vitro with 0-50 mol Trolox/mol LDL or 0-250 mM RRR-alpha-TOH. In addition, five of these subjects were supplemented in vivo with 800-1200 IU/d RRR-alpha-TOH for 17 days and k and a were determined. The ratios k(Trolox):k(alpha-TOH) and alpha(Trolox):a(alpha-TOH) were calculated. The k(Trolox) was only slightly higher than k(alpha-TOH), in contrast to alpha(Trolox), which was almost twice as high as a(alpha-TOH), indicating that, in the case of Trolox, a includes the contribution of alpha-TOH to the lag time. In the case of alpha-TOH, a includes only the additional antioxidants that occur naturally in LDL. The ratios k(Trolox):k(alpha-TOH) and alpha(Trolox):a(alpha-TOH) showed little variability, both between subjects and between in vitro and in vivo experiments. A close correlation was found between k(alpha-TOH) and a(alpha0TOH), calculated using this ratio, and k(alpha-TOH) and a(alpha-TOH), obtained in our experiments. We conclude that from this ratio, k(alpha-TOH) and a(alpha-TOH) can be reliably calculated when k(Trolox) and a(Trolox) are determined experimentally, thus allowing us to obtain k and a values in a more convenient way.

Adult↗