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R Stocker

Publications and source records attributed to R Stocker.

At least 109 records · Page 6Linked to original sources
PubMed1997

Production of cytokines following brain injury: beneficial and deleterious for the damaged tissue.

A profound inflammatory response is initiated immediately following traumatic brain injury (TBI) and is characterized by the release of several cytokines with pro- and anti-inflammatory functions. In order to elucidate which cytokines are released in the human brain in response to injury as well as in the peripheral compartment, IL-1, IL-6, IL-8, IL-10, TNF-alpha and TGF-beta were monitored in CSF and serum of severely brain-injured patients. Furthermore, we investigated the possible modulation of systemic reactions by IL-6 and the ability of IL-6 and IL-8 to promote the synthesis of nerve growth factor.

Animals↗
PubMed1997

Noninvasive monitoring of cardiac output in critically ill patients with thoracocardiography.

Thoracocardiography noninvasively estimates changes in cardiac output by recording ventricular volume curves from an inductive plethysmographic transducer placed around the chest near the xiphoid process. We evaluated performance of thoracocardiography for estimation of cardiac output in 21 critically ill patients in comparison to thermodilution. A total of 201 paired cardiac output measurements were obtained over periods of 35 to 254 min. Since thoracocardiography tracks relative changes in cardiac output but does not provide absolute values, the first cardiac output by thermodilution in each patient was used to calibrate thoracocardiography for comparisons of subsequent cardiac output estimates to thermodilution. The mean difference (bias) of cardiac output (thoracocardiography - thermodilution) was 0.0 L/min, the limits of agreement (bias +/- 2 SD) included a range from -1.5 to +1.6 L/min. For estimations of relative changes in cardiac output by thoracocardiography and thermodilution the bias was 0%, and the limits of agreement -21 and +22%. We conclude that thoracocardiography is a promising noninvasive technique for monitoring cardiac output in critically ill patients.

Adult↗
PubMed1997

Inhalation of the nitric oxide synthase cofactor tetrahydrobiopterin in healthy volunteers.

Pulmonary endothelial dysfunction is the hallmark of acute lung injury. Impaired pulmonary endothelial nitric oxide (NO) production in this event has been described. Tetrahydrobiopterin (BH4) is an essential cofactor for NO synthase and modulator of its activity. At high local concentrations, BH4 provokes local vasodilation in vivo in healthy individuals. At lower concentrations, BH4 selectively and locally restores disturbed NO-dependent vasodilation in patients with endothelial dysfunction. In this preliminary study, we therefore investigated the feasibility of BH4 inhalation in five healthy human volunteers. Inhalation of buffered, aqueous BH4-dihydrochloride solution was well tolerated; despite the buffer, BH4 stability was completely preserved. Resorption of inhaled BH4 was demonstrated by significantly increased BH4 levels in plasma and urine. Inhaled BH4 did not alter pulmonary function and had no effect on systemic hemodynamic values. Our data demonstrate that inhalation is a novel method for local BH4 administration, offering a basic therapeutic tool for investigation of restoration of impaired NO-dependent vasodilation due to pulmonary endothelial dysfunction.

Administration, Inhalation↗
PubMed1997

Prone postioning and low-volume pressure-limited ventilation improve survival in patients with severe ARDS.

STUDY OBJECTIVES: Investigating the effect of low-volume pressure-limited ventilation and repeated prone positioning on the short-term course and outcome in patients with severe ARDS. SETTING: Level 1 trauma center of a university hospital. PATIENTS: Twenty-five patients suffering from ARDS with a lung injury score (LIS) > or = 2.5 admitted consecutively to our ICU from January 1992 to December 1994. METHODS: Mechanical ventilation with peak inspiratory pressure limitation to 35 mbar, irrespective of hypercapnia and prone positioning to achieve adequate oxygenation. SCORING AND MEASUREMENTS: Patient assessment with LIS, APACHE (acute physiology and chronic health evaluation) II score, injury severity score, and multiple organ failure score. Blood gas analyses and estimation of static compliance were repeated at least every 4 h during the treatment period. PaO2/FIO2 (fraction of inspired oxygen) ratio, alveolo-arterial oxygen difference, and intrapulmonary shunt were calculated according to standard equations. The best values taken from each 4-h period during the investigation were used to evaluate the best possible performance of the lung within this interval and to investigate the entire course. RESULTS: Mean predicted mortality based on the APACHE II score was 35.4+/-15.2%. Three of the 25 patients (12%) died. However, none was related to respiratory failure. No pneumothorax occurred. Sixteen patients, lacking any contraindication for prone positioning, responded positively to this change in position, each to a different individual degree. CONCLUSION: We assume that our low mortality in patients with severe ARDS might be due mainly to low-volume pressure-limited ventilation and prone positioning. This simple strategy seems to allow successful treatment for patients with severe ARDS.

APACHE↗
PubMed1997

Separation and characterization of cholesteryl oxo- and hydroxy-linoleate isolated from human atherosclerotic plaque.

In previous work we demonstrated that up to 30% of cholesteryl linoleate in homogenates of advanced human plaque samples is present in oxidized forms. Here we show that the material from plaque hexane extracts which co-elutes with cholesteryl hydroxy-linoleate on reversed phase HPLC (Anal Biochem 1993;213:79), is composed of several isomers of cholesteryl hydroxy- and cholesteryl oxo-octadecadienoate. Enzymatic hydrolysis and measurement of liberated cholesterol and disappearance of the esters revealed that almost all of the material consisted of unoxidized cholesterol esterified to oxidized derivatives of octadecadienoate. Semi-preparative reversed-phase HPLC was used to obtain sufficient quantities of this co-eluting material to undertake normal phase HPLC separation of these components. The nature of such separated and isolated compounds was identified, by co-chromatography with authentic standards, UV spectroscopy and chemical ionization and electron impact mass spectrometry, as cholesteryl hydroxy- and cholesteryl oxo-octadecadienoate. These oxidized fatty acids have been observed previously in plaque, in agreement with our new unambiguous demonstration of their presence as cholesteryl esters. The application of the methods described for the separation of the various forms of oxidized cholesteryl octadecadienoate may aid mechanistic studies of in vitro and in vivo lipoprotein lipid oxidation.

Arteriosclerosis↗
PubMed1997

Plasma and LDL levels of major lipophilic antioxidants are similar in patients with advanced atherosclerosis and age-matched controls.

Oxidative modification of low-density lipoprotein (LDL), regarded an early event in atherogenesis, is associated with the depletion of the lipoprotein's antioxidants. We tested whether the levels of major lipophilic antioxidants in the blood of patients with advanced atherosclerosis are different to those in age-matched controls. On average, plasma ubiquinol-10, total coenzyme Q and coenzyme Q redox status were slightly lower whereas the levels of alpha-tocopherol were slightly higher in patients (63 +/- 11 years, n = 32) than controls (64 +/- 10 years, n = 24). However, these differences were not statistically significant (p > 0.05). The levels of antioxidants in LDL isolated from a subset of patients (n = 20) and controls (n = 15) were also indifferent, and hydroperoxides of cholesteryl esters were undetectable (detection limit 10 nM) in plasma of patients (n = 11) and controls (n = 10). The data suggests that plasma and LDL levels of lipophilic antioxidants are not depleted in patients suffering from severe atherosclerosis, and that neither parameter serves as a useful diagnostic indicator for this disease.

Aged↗
PubMed1996

3-Hydroxyanthranilic acid is an efficient, cell-derived co-antioxidant for alpha-tocopherol, inhibiting human low density lipoprotein and plasma lipid peroxidation.

alpha-Tocopherol (alpha-TOH) can promote lipid peroxidation in human low density lipoprotein (LDL) unless co-antioxidants are present that eliminate the chain-carrying alpha-tocopheroxyl radical (alpha-TO.) (Bowry, V. W., Mohr, D., Cleary, J., and Stocker, R. (1995) J. Biol. Chem. 270, 5756-5763). Interferon-gamma inhibits human monocyte/macrophage-facilitated LDL lipid peroxidation via induction of cellular tryptophan degradation and production and release of 3-hydroxyanthranilic acid (3HAA) (Christen, S., Thomas, S. R., Garner, B., and Stocker, R. (1994) J. Clin. Invest. 93, 2149-2158). We now report on the mechanism of antioxidant action of 3HAA. 3HAA directly reduced alpha-TO. in UV-exposed micellar dispersions of alpha-TOH or in LDL incubated with soybean 15-lipoxygenase (SLO), as assessed by electron paramagnetic resonance spectroscopy. 3HAA did not inhibit SLO enzyme activity. Anthranilic acid, which lacks the phenoxyl group, was incapable of reducing alpha-TO.. 3HAA dose-dependently inhibited the peroxidation of surface phospholipids and core cholesteryl esters in LDL exposed to SLO, peroxyl radicals (ROO.), or Cu2+; oxidants that convert alpha-TOH to alpha-TO.. In all cases, sparing of LDL's alpha-TOH, but not ubiquinol-10 (CoQ10H2), was observed until the majority of 3HAA was consumed. Addition of 3HAA or ascorbate prevented further consumption of alpha-TOH and accumulation of lipid hydroperoxides when added to aqueous or lipophilic ROO.-oxidizing LDL after complete and partial consumption of CoQ10H2 and alpha-TOH, respectively. In contrast, addition of urate, an efficient ROO. scavenger incapable of scavenging alpha-TO., did not efficiently inhibit ongoing lipid peroxidation. Oxidation of 3HAA-supplemented human plasma by aqueous ROO. resulted in the successive consumption of ascorbate, CoQ10H2, 3HAA, bilirubin, alpha-TOH, and urate. Lipid peroxidation was prevented as long as ascorbate, CoQ10H2, and 3HAA were present, but subsequently proceeded as a free-radical chain reaction concomitant with alpha-TOH, bilirubin, and urate consumption. Addition of 3HAA to aqueous ROO.-oxidizing plasma, after complete consumption of ascorbate and CoQ10H2, strongly inhibited ongoing lipid peroxidation and consumption of alpha-TOH, bilirubin, and urate immediately and as efficiently as did ascorbate. These findings demonstrate that 3HAA is a highly efficient co-antioxidant for plasma lipid peroxidation by virtue of its ability to interact with alpha-TO. in lipoproteins. Since interferon-gamma is the principal inducer of tryptophan degradation and release of 3HAA by monocytes/macrophages, this may represent a localized extracellular antioxidant defense against LDL oxidation in inflammation.

3-Hydroxyanthranilic Acid↗
PubMed1996

Inhibition of copper- and peroxyl radical-induced LDL lipid oxidation by ebselen: antioxidant actions in addition to hydroperoxide-reducing activity.

The effects of ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one) on human LDL lipid oxidation induced by different fluxes of aqueous peroxyl radicals and cupric ion (at a Cu2+:LDL ratio of 17:1) were investigated. Addition of ebselen to LDL oxidised with Cu2+ prolonged the duration of the lag-phase typical for this oxidising condition, with the increase being proportional to the square of the ebselen concentration. Ebselen also prevented the formation of lipid hydroperoxides and inhibited the consumption of endogenous antioxidants during the early period of Cu(2+)-induced oxidation, during which time the drug was converted stoichiometrically into ebselen oxide (2-phenyl-1,2-benzisoselenazol-3(2H)-one-Se-oxide). Ebselen oxide itself was antioxidant inactive. Ebselen also inhibited formation of lipid-hydroperoxides and spared alpha-tocopherol during the initial stages of LDL oxidation mediated by low-flux of aqueous peroxyl radicals, where a lag-phase was not observed. When a higher flux of aqueous peroxyl radicals was used, ebselen increased the observed inhibited phase of peroxidation in a dose-dependent manner, though less pronounced than its prolongating effect on the lag-phase of Cu(2+)-induced LDL lipid oxidation. Ebselen was also able to directly interact with Cu1+, alkyl peroxyl radicals and alpha-tocopheroxyl radicals, demonstrating that the drug has a number of potential antioxidant activities in addition to its well-known hydroperoxide-reducing activity. We conclude that the antioxidant activities of ebselen are complex and that their relative importance likely vary depending on the experimental system used.

Adult↗
PubMed1996

Rapid reduction and removal of HDL- but not LDL-associated cholesteryl ester hydroperoxides by rat liver perfused in situ.

To test whether high-density lipoproteins (HDL) could aid in the removal in vivo of potentially atherogenic oxidized lipids, we perfused rat liver in situ with buffer supplemented with isolated human HDL containing small amounts of cholesteryl linoleate hydro(pero)xides [CH18:2-O(O)H]. Perfusion resulted in the rapid removal of Ch18:2-O(O)H from HDL with a half-life (t1/2)of 11.4 min., faster than that of unoxidized cholesteryl linoleate, and dependent of the presence of the liver. In addition, the liver enhanced the reduction of Ch18:2-OOH associated with HDL remaining in the perfusate buffer. Perfusion resulted in the release of a hepatic activity that enhanced the reduction of HDL-associated CH18:2-OOH and was resistant to heat treatment. In contrast with the situation with HDL, low-density lipoprotein (LDL)-associated CH18:2-O(O)H were neither removed nor reduced by perfused rat liver within the time course studied, in support of a possible role for HDL in the detoxification of circulating lipid hydroperoxides in vivo.

Adult↗
PubMed1996

Presence of hypochlorite-modified proteins in human atherosclerotic lesions.

Oxidation of LDL may contribute to atherogenesis, though the nature of the in vivo oxidant(s) remains obscure. Myeloperoxidase, the enzyme responsible for hypochlorous acid/hypochlorite (HOCl) production in vivo, is present in active form in human atherosclerotic lesions, and HOCl aggregates and transforms LDL into a high-uptake form for macrophages in vitro. Here we demonstrate HOCl-modified proteins in human lesions using an mAb raised against HOCl-modified LDL that recognizes HOCl-oxidized proteins but does not cross-react with Cu2+-, malondialdehyde-, or 4-hydroxynonenal-modified LDL. This antibody detected significantly more material in advanced atherosclerotic lesions than normal arteries, even though azide and methionine were included during sample work-up to inhibit myeloperoxidase and to scavenge HOCl. The epitope(s) recognized was predominantly cell associated and present in monocyte/macrophages, smooth muscle, and endothelial cells. The intima and cholesterol clefts stained more heavily than the center of the thickened vessels; adventitial staining was apparent in some cases. Immunostaining was also detected in a very early lesion from an accident victim, beside healthy areas that were unreactive. LDL oxidized by HOCl in vitro, but not native LDL, effectively competed with the epitopes in lesions for antibody binding. Density centrifugation of plaque homogenates and Western blot analysis showed that, in the apo B-containing lipoprotein fraction, the mAb recognized protein(s) of molecular mass greater than apo B, similar to those produced during oxidation of LDL with HOCl in vitro. Three major proteins were recognized by the anti-HOCl-modified protein antibody but not by an anti-apo B antibody in the apo B-free fraction. Together, these results demonstrate HOCl-oxidized proteins in human atherosclerotic lesions, implicating this oxidant in LDL modification in vivo.

Arteriosclerosis↗
PubMed1996

[Added work of breathing, respiratory pattern and determination of ventilator weaning readiness in inspiratory pressure support and and automatic tube compensation].

We measured the ventilatory pattern and additional work of breathing (WOBadd) at three different levels of inspiratory pressure support [IPS 5, 10, 15 mbar above positive end-expiratory pressure (PEEP)] and in a new ventilatory mode, automatic tube compensation (ATC), in nine operative patients without lung injury nine patients ventilated for several following acute respiratory insufficiency (ARI). In ATC, endotracheal tube resistance is compensated automatically by means of closed-loop control of the calculated tracheal pressure. Pressure support in this mode, i.e. airway pressure above PEEP, is equal to the actual flow-dependent pressure drop across the endotracheal tube (ETT). Airway pressure rises at the beginning of inspiration and falls towards the end. As the tube resistance of ETT seriously hinders expiration and can cause desynchronization between ventilator and patient, airway pressure is reduced below PEEP during expiration in the same way as it is increased during inspiration. The result is a near-constant tracheal pressure at PEEP both during inspiration and during expiration. This mode could be best termed as "electronic extubation". The most striking difference between the postoperative patients and the ARI patients was their minute ventilation (17.8 +/- 1.85 l/min in ARI patients vs 7.3 +/- 3.1 l/min in the postoperative patients). In the postoperative patients augmentation of IPS from 5 to 15 mbar induced a steady increase in tidal volume (VT) and a consecutive decrease in respiratory rate (rr) compared with ATC (VTATC,postop = 463 +/- 78 ml; rrATC,postop = 16 +/- 4 min-1; VTIPS5.postop = 505 +/- 79 ml; rrIPS5,postop = 15 +/- 4 min-1; VTIPS10,postop = 562 +/- 86 ml; rrIPS15,postop = 14 +/- 4 min-1; VTIPS15.postop = 660 +/- 151 ml; rrTPS15,postop = 12 +/- 4 min-1), whereas the augmentation of IPS of 5 and 10 mbar in the ARI patients could not compensate for the increase in rr and the decrease in VT, after switching from ATC to IPS (VTATC,ARI 724 +/- 308 ml, rrATC,ARI = 24 +/- 6 min-1; VTIPS5,ARI = 649 +/- 315 ml; rrIPS5,ARI = 27 +/- 8 min-1; VTIPS10,ARI = 653 +/- 353 ml; rrIPS10,ARI = 25 +/- 8 min-1: Even IPS 15 was not able to reestablish VT at the values observed during ATC (VTIPS15,ARI = 680 +/- 312 ml). During ATC WOBadd was small in both postoperative and ARI patients (WOBadd,ATC,postop = 93 +/- 36 mJ/l, WOBadd,ATC,ARI = 116 +/- 72 mJ/l). In the postoperative patients, an inspiratory pressure support of 5 mbar was not sufficient to compensate WOBadd compared with ATC. However, IPS 10 and 15 mbar were able to compensate for WOBadd (WOBadd,ATC5.postop WOBadd,IPS5,postop = 189 +/- 77 mJ/l; WOBadd,IPS10,postop = 55 +/- 30 mJ/l; WOBadd,IPS15,postop = 21 +/- 11 mJ/l). In the ARI patients an IPS 5, 10 or 15 mbar was not sufficient to compensate for WOBadd (WOBadd,IPS 5,ARI = 1126 +/- 262 mJ/l; WOBadd,IPS 10,ARI 863 +/- 253 mJ/l; WOBadd,IPS15,ARI 763 +/- 298 mJ/l). Under ATC, WOBadd was only 15% of WOBadd under IPS of 15 mbar. All but two patients were successfully extubated after the investigation. These two patients were not extubated because they were dependent on an FIO2 > 0.5. Our results strongly indicate that ventilatory dependence in ARI patients may be caused by the ETT rather than by mechanical dysfunction of the lung. ATC is a very helpful mode to use in distinguishing between ventilatory failure caused by ETT and real ventilatory dependence.

Adult↗
PubMed1996

Radical-initiated lipid peroxidation in low density lipoproteins: insights obtained from kinetic modeling.

We present kinetic models of various complexity for radical-initiated lipid peroxidation in low density lipoproteins (LDL). The models, comprised of simultaneous differential equations programmed in Mathematica, were used to evaluate the concentration profiles of the reactants of interest. Single-phase reaction schemes describing lipid peroxidation and antioxidation according to the "conventional" and tocopherol-mediated peroxidation (TMP) model were simulated for conditions of low and high radical fluxes produced by thermolabile azo initiators. The results show that the particular dependencies of the rates of lipid peroxidation (Rp) on the rates of initiation (Ri) for the two reaction schemes were accurately predicted by the simulations. Both models qualitatively predicted inhibition of lipid peroxidation in the presence of alpha-tocopherol (alpha-TOH) under high radical flux conditions, suggesting that both can describe inhibited lipid peroxidation in solution under these conditions. TMP, but not the conventional model, could also predict the experimentally observed complex behavior of LDL lipid peroxidation induced with different concentrations of azo initiators. Specifically, TMP faithfully reproduced the observed kinetic chain length of lipid peroxidation of > > 1 at low and < < 1 at high concentration of the initiator (i.e., 0.2 and 10 mM, respectively for LDL at 1 mumol apoB-100/L) during the alpha-TOH-containing period of oxidation. It also demonstrated the experimentally observed nondependence of RpTMP on Ri. Kinetic analysis of radical generation and initiation of lipid peroxidation in an extended, two-compartment model of TMP showed that phase separation of bimolecular reactions in a suspension of LDL particles can lead to a approximately 400-fold increase in the rate of lipid hydroperoxide formation. The experimentally observed co-antioxidant action of water-soluble ascorbate and lipid-soluble ubiquinol-10 were verified using this model. A simple biophysical model constituting the reactions of TMP and incorporating the compartmental nature of an LDL suspension is proposed. Together, the results demonstrate that TMP is the only model that fits the experimental data describing the early stages of LDL lipid peroxidation under various oxidizing conditions. The implications of our findings are discussed in relation to atherogenesis and a recently proposed alternative model of LDL lipid peroxidation (Abuja and Esterbauer (1995) Chem. Res. Toxicol. 8, 753).

Antioxidants↗
PubMed1996

Different pattern of local and systemic release of proinflammatory and anti-inflammatory mediators in severely injured patients with chest trauma.

BACKGROUND: Excessive release of proinflammatory cytokines has been involved in pathogenesis of acute respiratory distress syndrome. DESIGN: Since injured patients with chest trauma reveal a high risk for posttraumatic acute respiratory distress syndrome, local and systemic release of proinflammatory cytokines and their naturally occurring inhibitors were determined in the early posttraumatic period. MATERIALS AND METHODS: Proinflammatory and anti-inflammatory mediators were measured in plasma and bronchoalveolar lavage fluid (BALF) from 16 patients with multiple injuries including severe chest injury (Injury Severity Score of 34.4 +/- 2.3 points) and compared with healthy volunteers (n = 17). RESULTS: Tumor necrosis factor-alpha was detectable neither in plasma nor in BALF. Interleukin-1beta and interleukin-8 were significantly increased in BALF from injured patients, while plasma levels were similar in both groups. Soluble tumor necrosis factor receptors p55 and p75 and interleukin-1ra were markedly elevated in plasma (p < or = 0.01) and BALF (p < or = 0.001) from injured patients compared with controls. CONCLUSION: Highly increased concentrations of proinflammatory cytokines in BALF, but not in circulation, indicate a strong local inflammatory response early after multiple injuries combined with chest injury rather than severe systemic inflammation. In contrast, anti-inflammatory mechanisms seem to be activated locally and systemically.

Adult↗
PubMed1996

Cosupplementation with coenzyme Q prevents the prooxidant effect of alpha-tocopherol and increases the resistance of LDL to transition metal-dependent oxidation initiation.

There is considerable interest in the ability of antioxidant supplementation, in particular with vitamin E, to attenuate LDL oxidation, a process implicated in atherogenesis. Since vitamin E can also promote LDL lipid peroxidation, we investigated the effects of supplementation with vitamin E alone or in combination with coenzyme Q on the early stages of the oxidation of isolated LDL. Isolated LDL was obtained from healthy subjects before and after in vitro enrichment with vitamin E (D-alpha-tocopherol, alpha-TOH) or dietary supplementation with D-alpha-TOH (1 g/d) and/or coenzyme Q (100 mg/d). LDL oxidation initiation was assessed by measurement of the consumption of alpha-TOH and cholesteryl esters containing polyunsaturated fatty acids and the accumulation of cholesteryl ester hydroperoxides during incubation of LDL in the transition metal-containing Ham's F-10 medium in the absence and presence of human monocyte-derived macrophages (MDMs). Native LDL contained 8.5 +/- 2 molecules of alpha-TOH and 0.5 to 0.8 molecules of ubiquinol-10 (CoQ10H2, the reduced form of coenzyme Q) per lipoprotein particle. Incubation of this LDL in Ham's F-10 medium resulted in a time-dependent loss of alpha-TOH with concomitant stoichiometric conversion of the major cholesteryl esters to their respective hydroperoxides. MDMs enhanced this process. LDL lipid peroxidation occurred via a radical chain reaction in the presence of alpha-TOH, and the rate of this oxidation decreased on alpha-TOH depletion. In vitro enrichment of LDL with alpha-TOH resulted in an LDL particle containing sixfold to sevenfold more alpha-TOH, and such enriched LDL was more readily oxidized in the absence and presence of MDMs compared with native LDL. In vivo alpha-TOH-deficient LDL, isolated from a patient with familial isolated vitamin E deficiency, was highly resistant to Ham's F-10-initiated oxidation, whereas dietary supplementation with vitamin E restored the oxidizability of the patient's LDL. Oral supplementation of healthy individuals for 5 days with either alpha-TOH or coenzyme Q increased the LDL levels of alpha-TOH and CoQ10H2 by two to three or three to four times, respectively. alpha-TOH-supplemented LDL was significantly more prone to oxidation, whereas CoQ10H2-enriched LDL was more resistant to oxidation initiation by Ham's F-10 medium than native LDL. Cosupplementation with both alpha-TOH and coenzyme Q resulted in LDL with increased levels of alpha-TOH and CoQ10H2, and such LDL was markedly more resistant to initiation of oxidation than native or alpha-TOH-enriched LDL. These results demonstrate that oral supplementation with alpha-TOH alone results in LDL that is more prone to oxidation initiation, whereas cosupplementation with coenzyme Q not only prevents this prooxidant activity of vitamin E but also provides the lipoprotein with increased resistance to oxidation.

Cell Line↗