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Biomedical subjects

R Stocker

Publications and source records attributed to R Stocker.

At least 19 recordsLinked to original sources
PubMed2002

Extubation after breathing trials with automatic tube compensation, T-tube, or pressure support ventilation.

BACKGROUND: Automatic tube compensation (ATC) is a new option to compensate for the pressure drop across the endotracheal or tracheostomy tube (ETT), especially during ventilator-assisted spontaneous breathing. While several benefits of this mode have so far been documented, ATC has not yet been used to predict whether the ETT could be safely removed at the end of weaning, from mechanical ventilation. METHODS: We undertook a systematic trial using a randomized block design. During a 2-year period, all eligible patients of a medical intensive care unit were treated with ATC, conventional pressure support ventilation (PSV, 5 cmH2O), or T-tube for 2-h. Tolerance of the breathing trial served as a basis for the decision to remove the endotracheal tube. Extubation failure was considered if reintubation was necessary or if the patient required non-invasive ventilatory assistance (both within 48 h). RESULTS AND CONCLUSIONS: After the inclusion of 90 patients (30 per group) we did not observe significant differences between the modes. Twelve patients failed the initial weaning trial. However, half of the patients who appeared to fail the spontaneous breathing trial on the T-tube, PSV, or both, were successfully extubated after a succeeding trial with ATC. Extubation was thus withheld from four and three of these patients while breathing with PSV or the T-tube, respectively, but to any patient breathing with ATC. It seems that ATC can be used as an alternative mode during the final phase of weaning from mechanical ventilation. Furthermore, this study may promote a larger multicenter trial on weaning with ATC compared with standard modes.

Device Removal↗
PubMed2002

First clinical experience with Molecular Adsorbent Recirculating System (MARS) in six patients with severe acute on chronic liver failure.

UNLABELLED: Despite recent advances in general supportive care, the mortality rate of patients with severe liver insufficiency remains high. Recently a new artificial liver support system MARS has been used for selective removal of albumin-bound toxins. AIM: To assess the safety and efficacy of MARS treatment in patients with acute on chronic liver disease (n = 5) or liver failure after extended hepatic resection (n = 1). DESIGN/PATIENTS: Six patients, aged 34-58 years, with severe liver insufficiency (mean MELD-score 31 (range 24-35)) were treated one to 16 times with the MARS system. At baseline three patients were intubated, three were encephalopathic (HE) and three had multifactorial kidney failure requiring kidney replacement therapy. RESULTS AND CONCLUSION: In all the patients MARS treatment significantly reduced the serum bilirubin levels. In three patients encephalopathy improved. In two patients the extracorporeal treatment precipitated a disseminated intravascular coagulation with clinically significant bleeding. Bridging to liver transplantation was possible in one patient, the other five patients died 30 days (2-74 days) after starting MARS therapy. Our case series shows that MARS treatment in general can be safely performed in patients with severe liver disease. However, in patients with an activated clotting system severe bleeding complication can be triggered and MARS treatment should be used very cautiously in these situations. MARS seems to be a promising new treatment option for patients with acute on chronic liver failure. However, carefully conducted randomized controlled trials are necessary to define its potential place in the treatment of patients with severe liver disease.

Acute Disease↗
PubMed2002

Late oesophageal perforation after intraoperative transoesophageal echocardiography.

Serious haemodynamic instability occurred during emergency surgery for a perforated duodenal ulcer in a 72-year-old man with acute myocardial infarction. Intraoperative transoesophageal echocardiography was crucial for diagnosis of the location of myocardial infarction in the right ventricle and the subsequent haemodynamic management. Postoperatively, a thrombus in the right coronary artery was removed by coronary angiography. The patient's trachea was extubated on the fourth postoperative day. Another 4 days later a leak in the lower oesophagus was suspected because of pleural empyema, and verified. The patient's trachea had to be re-intubated and an oesophageal stent was inserted. The patient was discharged, fully recovered, 2 months after the operation.

Aged↗
PubMed2001

Correlation between intima-to-media ratio, apolipoprotein B-100, myeloperoxidase, and hypochlorite-oxidized proteins in human atherosclerosis.

The oxidative modification of low-density lipoprotein (LDL) is thought to contribute to atherogenesis, and there is evidence that oxidants derived from myeloperoxidase (MPO) contribute to such oxidative damage. Using human iliac arteries we investigated the relationship between lesion stage indicated by the intima-to-media (I/M) ratio and the presence of apolipoprotein B-100 (apoB, a marker for LDL), MPO, and hypochlorite (HOCl)-oxidized proteins identified by immunohistochemistry in the intima, media, and adventitia. More staining for apoB, MPO, and HOCl-oxidized proteins was observed in diseased than healthy vessels. Diseased segments also stained more for the three parameters than healthy segments in the same diseased vessel, highlighting the variability that can occur within a single cross-section of a vessel. However, significant positive correlation between I/M ratio and positive staining for apoB, MPO, and HOCl-oxidized proteins in different segments of individual arteries were apparent in segments with an I/M ratio of > 1.8. Also, the overall extent of intimal staining for apoB, MPO, and HOCl-oxidized proteins increased with increasing I/M ratio. In addition, the extent of apoB staining was greater and appeared at comparatively lower I/M ratios than that of MPO and HOCl-oxidized proteins. Our results support a contribution to atherogenesis of all three parameters assessed, although MPO and HOCl-oxidized proteins appear to participate in the disease process at a later stage than apoB.

Adult↗
PubMed2001

Effect of vitamin E on aortic lipid oxidation and intimal proliferation after arterial injury in cholesterol-fed rabbits.

Oxidized low-density lipoproteins (LDL) are implicated in atherosclerosis. However, large-scale intervention studies designed to test whether antioxidants, such as vitamin E, can ameliorate cardiovascular disease have generated ambivalent results. This may relate to the fact that the mechanism whereby lipid oxidation is initiated in vivo is unknown and the lack of direct evidence for a deficiency of antioxidants in atherosclerotic lesions. Further, there is little evidence to suggest that vitamin E acts as an antioxidant for lipid peroxidation in vivo. Here we tested the antioxidant effect of dietary vitamin E (alpha-tocopherol) supplementation on intimal proliferation and lipid oxidation in balloon-injured, hypercholesterolemic rabbits. alpha-Tocopherol supplementation increased vascular content of alpha-tocopherol over 30-fold compared to nonsupplemented and alpha-tocopherol-deficient chows. Balloon injury resulted in oxidized lipid deposition in the aorta. Maximum levels of primary lipid oxidation products, measured as hydroperoxides of esterified lipid (LOOH) and oxidized linoleate (HODE), were 0.22 and 1.10 nmol/mg, representing 0.21 and 0.39% of the precursor molecule, respectively. Secondary lipid oxidation products, measured as oxysterols, were maximal at 5.60 nmol/mg or 1.48% of the precursor compound. Vascular HODE and oxysterols were significantly reduced by vitamin E supplementation. However, the intima/media ratio of aortic vessels increased with vitamin E supplementation, suggesting that the antioxidant promoted intimal proliferation. Thus, the study demonstrates a dissociation of aortic lipid oxidation and lesion development, and suggests that vitamin E does not prevent lesion development in this animal model.

Angioplasty, Balloon↗
PubMed2001

ATP-binding cassette transporter A1 mediates cellular secretion of alpha-tocopherol.

Alpha-tocopherol (alpha-TOH) is associated with plasma lipoproteins and accumulates in cell membranes throughout the body, suggesting that lipoproteins play a role in transporting alpha-TOH between tissues. Here we show that secretion of alpha-TOH from cultured cells is mediated in part by ABCA1, an ATP-binding cassette protein that transports cellular cholesterol and phospholipids to lipid-poor high density lipoprotein (HDL) apolipoproteins such as apoA-I. Treatment of human fibroblasts and murine RAW264 macrophages with cholesterol and/or 8-bromo-cyclic AMP, which induces ABCA1 expression, enhanced apoA-I-mediated alpha-TOH efflux. ApoA-I lacked the ability to remove alpha-TOH from Tangier disease fibroblasts that have a nonfunctional ABCA1. BHK cells that lack an active ABCA1 pathway markedly increased secretion of alpha-TOH to apoA-I when forced to express ABCA1. ABCA1 also mediated a fraction of the alpha-TOH efflux promoted by lipid-containing HDL particles, indicating that HDL promotes alpha-TOH efflux by both ABCA1-dependent and -independent processes. Exposing apoA-I to ABCA1-expressing cells did not enhance its ability to remove alpha-TOH from cells lacking ABCA1, consistent with this transporter participating directly in the translocation of alpha-TOH to apolipoproteins. These studies provide evidence that ABCA1 mediates secretion of cellular alpha-TOH into the HDL metabolic pathway, a process that may facilitate vitamin transport between tissues and influence lipid oxidation.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2001

Reaction of human myoglobin and peroxynitrite: characterizing biomarkers for myoglobin-derived oxidative stress.

Mixtures of human myoglobin (Mb) (or the Y103F variant of human Mb), authentic peroxynitrite (ONOO(-), ONOO(-):protein 2 mol/mol), and 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) gave radicals adducts at cysteine-110 (DMPO-C110) that are detected directly by electron paramagnetic magnetic spectroscopy (EPR). DMPO-C110 was detected exclusively over a range of DMPO concentrations (DMPO:protein ratios 25-100 mol/mol). Treatment of human Mb (or Y103F Mb) with the ONOO(-) generator 5-amino-3-(4-morpholinyl)-1,2,3-oxadiazolium (SIN-1) chloride (ONOO(-):protein 5 mol/mol) yielded a cross-linked Mb dimer as judged by SDS-PAGE analyses. Addition of DMPO or carbonate effectively eliminated the cross-linked product. Mass analyses of samples containing human Mb (or Y103F Mb), carbonate, and ONOO(-) indicated that nitration occurs exclusively at Y103. Thus, reaction of human Mb and ONOO(-) yields specific products that depend on the presence or absence of physiological concentrations of carbonate. These products may serve as biomarkers for the participation of Mb-derived radicals in the oxidative damage associated with myocardial reperfusion injury.

Biomarkers↗
PubMed2001

Antioxidants inhibit indoleamine 2,3-dioxygenase in IFN-gamma-activated human macrophages: posttranslational regulation by pyrrolidine dithiocarbamate.

Induction of the heme-containing indoleamine 2,3-dioxygenase (IDO) by IFN-gamma is implicated in anti-microbial and pro-inflammatory activities of human macrophages. Antioxidants can modulate the expression of immune and inflammatory genes, and pyrrolidine dithiocarbamate (PDTC) is a frequently used antioxidant to inhibit the transcription factor NF-kappaB. Here we show that IFN-gamma treatment of human monocyte-derived macrophages (hMDMs) increased the proportion of oxidized glutathione. PDTC attenuated this increase and inhibited IDO activity, although it increased IDO protein expression and did not affect IDO mRNA expression and enzyme activity directly. Other antioxidants, 2-ME, ebselen, and t-butyl hydroquinone, inhibited IDO protein expression. Similar to PDTC, the heme biosynthesis inhibitor succinylacetone (SA) and the iron-chelator pyridoxal isonicotinoyl hydrazone inhibited cellular IDO activity without affecting protein expression, whereas addition of hemin or the heme precursor delta-aminolevulinic acid increased IDO activity. Also, incubation of IFN-gamma-activated hMDM with delta-[(14)C]-aminolevulinic acid resulted in the incorporation of label into immunoprecipitated IDO, a process inhibited by PDTC and SA. Furthermore, supplementation of lysates from PDTC- or SA-treated hMDM with hemin fully restored IDO activity to control levels, and hemin also reversed the inhibitory action of SA but not PDTC in intact cells. Together these results establish a requirement for de novo heme synthesis for IDO activity in IFN-gamma-activated hMDM. They show that, similar to other pro-inflammatory proteins, the activity of IDO is modulated by antioxidants though in the case of PDTC this takes place posttranslationally, in part by limiting the availability of heme for the formation of holo-IDO.

Antioxidants↗
PubMed2001

Improved results after lung transplantation--analysis of factors.

Better recipient selection, sophisticated postoperative surveillance and new immunosuppressive and anti-infective regimens can improve the results of lung transplantation. We compared the results of lung transplants performed between 1992 and 1996 (early period; 47) and between 1997 and 2000 (recent period; 46) in a cohort study to assess which factors influenced survival. Estimates of relative hazards were adjusted for possible confounding effects with the use of Cox regression analysis. Overall 2-year survival was 70%. Survival by this time was significantly better in the recent period (82% vs. 60%; p = 0.0093). Acute rejection episodes and death due to BOS were less frequent in the recent period. There were no technical failures, and the cumulative incidence of BOS was low (34% at 5 years). The beneficial effect of the transplantation date 1997 or later at a hazard ratio of 0.33 (95% CI, 0.13-0.84) was materially changed only by the adjustment for ganciclovir prophylaxis (0.50; 95% CI, 0.09-2.91) and immunosuppression with mycophenolate mofetil (0.80; 95% CI, 0.27-2.36). After adjustment for both ganciclovir and mycophenolate mofetil, the beneficial time period effect was completely removed (1.24; 95% CI, 0.14-11.39). Immunosuppressive therapy with mycophenolate mofetil and use of ganciclovir prophylaxis in addition to careful postoperative surveillance and surgical expertise can lead to improved results after lung transplantation.

Adolescent↗
PubMed2001

Relative reactivities of N-chloramines and hypochlorous acid with human plasma constituents.

Hypochlorous acid (HOCl), the major strong oxidant produced by the phagocyte enzyme myeloperoxidase, reacts readily with free amino groups to form N-chloramines. Since different N-chloramines have different stabilities and reactivities depending on their structures, we investigated the relative reactivities of three model N-chloramines and HOCl with human plasma constituents. TheN-chloramines studied were N(alpha)-acetyl-lysine chloramine (LysCA, a model of protein-associated N-chloramines), taurine chloramine (TaurCA, the primary N-chloramine produced by activated neutrophils), and monochloramine (MonoCA, a lipophilic N-chloramine). Addition of these chlorine species (100--1000 microM each) to plasma resulted in rapid loss of thiols, with the extent of thiol oxidation decreasing in the order TaurCA = LysCA > MonoCA = HOCl. The single reduced thiol of albumin was the major target. Loss of plasma ascorbate also occurred, with the extent decreasing in the order HOCl > LysCA > TaurCA > MonoCA. Experiments comparing equimolar albumin thiols and ascorbate showed that while HOCl caused equivalent loss of thiols and ascorbate, theN-chloramines reacted preferentially with thiols. The chlorine species also inactivated alpha(1)-antiproteinase, implicating oxidation of methionine residues, and ascorbate provided variable protection depending on the chlorine species involved. Together, our data indicate that in biological fluids N-chloramines react more readily with protein thiols than with methionine residues or ascorbate, and thus may cause biologically relevant, selective loss of thiol groups.

Ascorbic Acid↗
PubMed2001

[Automatic tube compensation (ATC)].

The endotracheal tube (ETT) is a considerably flow-dependent and, therefore, variable mechanical load. Conventional modes of respiratory support cannot adequately compensate for the tube resistance in inspiratorion and not at all in expiration. Automatic tube compensation (ATC) compensates for the flow-dependent pressure drop across the tracheal tube by a positive pressure support in inspiration and by a negative pressure support in expiration. The pressure support closely follows the nonlinear pressure-flow curve of the ETT. Automatic tube compensation has an indirect closed-loop working principle since the target tracheal pressure is not directly measured but rather calculated from continuously measured airway pressure and flow rate. It is not an own ventilatory mode but rather a component of flow-proportional pressure support which can be combined with all conventional ventilatory modes, and provides a rational basis for subdividing the pressure support to overcome the mechanical load of the tubing and to overcome that of the respiratory system. Partial tube obstructions, which could decrease the effectivity of ATC, could be detected automatically by analysing the expiratory flow signal using a software, which could be easily implemented into the ventilator. The effectivity of ATC during long-term application can be maintained by intermittent short-term measurement of the tracheal pressure. Up to now there is no commercially available ventilator which allows complete expiratory ATC. Studies in volunteers and in mechanically ventilated patients have convincingly shown that ATC reduces work of breathing and increases respiratory comfort. In addition, successful extubation could be better predicted with this mode in difficult-to-wean patients compared to other modes. There are no special rules in the clinical application of ATC. However, to prevent overassist the support level of the ventilatory mode which is combined with ATC should be reduced.

Algorithms↗
PubMed2001

[Experiences with using a potentially temporary vena cava filter in multiple trauma patients].

INTRODUCTION: In Europe, there is little experience in the application of temporary cava filters in patients with multiple injuries. Especially patients with pelvic injuries, fractures of the spine, and the lower extremities are at high risk for thromboembolic events like thrombosis or pulmonary emboli. Moreover, in patients with severe head injuries, anticoagulation is contraindicated. METHOD: We present in this paper our experience with 24 consecutive patients with multiple injuries who were treated with a temporary cava filter. The insertion site was either the femoral (n = 20) or the jugular (n = 4) vein. The 24 patients revealed a mean ISS of 35.1 +/- 2.01 points. Nineteen patients had pelvic injuries and 17 patients suffered from severe head injury. In 17 patients the insertion of the filter was prophylactic, in 4 patients a thrombosis was present and in 3 patients a non-fatal pulmonary emboli was diagnosed before the application of a cava filter. RESULTS: No complication occurred due to insertion of the filter. In one patient a thrombosis of the cava was observed as the only overall complication (1 of 24 = 4.2%). CONCLUSION: The insertion of a cava filter in patients with multiple injuries with contraindication for anticoagulation is a safe and effective procedure to prevent fatal pulmonary emboli.

Adult↗
PubMed2001

Is ischemia involved in the pathogenesis of murine cerebral malaria?

Sequestration of parasitized erythrocytes in the central nervous system microcirculation and increased cerebrospinal fluid lactate are prominent features of cerebral malaria (CM), suggesting that sequestration causes mechanical obstruction and ischemia. To examine the potential role of ischemia in the pathogenesis of CM, Plasmodium berghei ANKA (PbA) infection in CBA mice was compared to infection with P. berghei K173 (PbK) which does not cause CM (the non-CM model, NCM). Cerebral metabolite pools were measured by (1)H nuclear magnetic resonance spectroscopy during PbA and PbK infections. Lactate and alanine concentrations increased significantly at the terminal stage of CM, but not in NCM mice at any stage. These changes did not correlate with parasitemia. Brain NAD/NADH ratio was unchanged in CM and NCM mice at any time studied, but the total NAD pool size decreased significantly in the CM mice on day 7 after inoculation. Brain levels of glutamine and several essential amino acids were increased significantly in CM mice. There was a significant linear correlation between the time elapsed after infection and small, progressive decreases in the cell density/cell viability markers glycerophosphocholine and N-acetylaspartate in CM, indicative of gradual loss of cell viability. The metabolite changes followed a different pattern, with a sudden significant alteration in the levels of lactate, alanine, and glutamine at the time of terminal CM. In NCM, there were significant decreases with time of glutamate, the osmolyte myo-inositol, and glycerophosphocholine. These results are consistent with an ischemic change in the metabolic pattern of the brain in CM mice, whereas in NCM mice the changes were more consistent with hypoxia without vascular obstruction. Mild obstructive ischemia is a likely cause of the metabolic changes during CM, but a role for immune cell effector molecules cannot be ruled out.

Adenosine Triphosphate↗
PubMed2001

Oxidants and antioxidants in atherosclerosis.

The oxidative theory suggests that LDL oxidation contributes to atherogenesis, implying that attenuation of this process by antioxidants should decrease atherosclerosis. However, a causative link between LDL oxidation and atherogenesis is not firmly established. It requires the identification of the oxidants that are responsible for the initiation of LDL oxidation, and an understanding of the modified moieties that are responsible for the proatherogenic activities of oxidized LDL. The present review summarizes recent data on potential biological oxidants for LDL in the vessel wall, and discusses the antiatherogenic role(s) of selected antioxidants.

Antioxidants↗
PubMed2001

Limiting light-induced lipid peroxidation and vitamin loss in infant parenteral nutrition by adding multivitamin preparations to Intralipid.

UNLABELLED: Parenteral lipids are susceptible to light-induced peroxidation, particularly under phototherapy. Ascorbic acid is protective. The aim of this study was to investigate whether dark delivery tubing and/or coadministration of multivitamin preparations could prevent peroxidation of Intralipid without undue vitamin loss. In experiments carried out on the benchtop, lipid peroxidation occurred in ambient light and was more extensive under phototherapy. Dark tubing decreased peroxide formation, but only by about 65%. In simulated clinical conditions in which solutions were pumped through standard clear or dark minibore plastic tubing. Intralipid accumulated lipid peroxides as measured by the FOX assay (280 microM) or as triglyceride hydroperoxides (52 microM). Multivitamin preparations (MVIP or Soluvit/Vitlipid) inhibited peroxide formation almost completely, and were fully protective when used with dark tubing. There was loss of riboflavin (65% from Soluvit and 35% from MVIP) in clear tubing but this was decreased to 18% and 11%, respectively, in dark tubing. Ascorbate loss was 20% (MVIP) and 50% (Soluvit) and only slightly less in dark tubing. Ascorbate loss was also seen in the absence of Intralipid and is due to riboflavin-induced photo-oxidation. CONCLUSION: Multivitamin preparations protect Intralipid against light-induced formation of lipid hydroperoxides, and administering multivitamins with Intralipid via dark delivery tubing provides a practical way of preventing peroxidation of the lipid while limiting vitamin loss. This procedure should be considered for routine use as well as with phototherapy.

Ascorbic Acid↗
PubMed2001

Dietary cosupplementation with vitamin E and coenzyme Q(10) inhibits atherosclerosis in apolipoprotein E gene knockout mice.

Intimal oxidation of LDL is considered an important early event in atherogenesis, and certain antioxidants are antiatherogenic. Dietary coenrichment with vitamin E (VitE) plus ubiquinone-10 (CoQ(10), which is reduced during intestinal uptake to the antioxidant ubiquinol-10, CoQ(10)H(2)) protects, whereas enrichment with VitE alone can increase oxidizability of LDL lipid against ex vivo oxidation. In the present study, we tested whether VitE plus CoQ(10) cosupplementation is more antiatherogenic than either antioxidant alone, by use of apolipoprotein E-deficient (apoE-/-) mice fed a high-fat diet without (control) or with 0.2% (wt/wt) VitE, 0.5% CoQ(10), or 0.2% VitE plus 0.5% CoQ(10) (VitE+CoQ(10)) for 24 weeks. None of the supplements affected plasma cholesterol concentrations, whereas in the VitE and CoQ(10) groups, plasma level of the respective supplement increased. Compared with control, plasma from CoQ(10) or VitE+CoQ(10) but not VitE-supplemented animals was more resistant to ex vivo lipid peroxidation induced by peroxyl radicals. VitE supplementation increased VitE levels in aorta, heart, brain, and skeletal muscle, whereas CoQ(10) supplementation increased CoQ(10) only in plasma and aorta and lowered tissue VITE: All treatments significantly lowered aortic cholesterol compared with control, but only VitE+CoQ(10) supplementation significantly decreased tissue lipid hydroperoxides when expressed per parent lipid. In contrast, none of the treatments affected aortic ratios of 7-ketocholesterol to cholesterol. Compared with controls, VitE+CoQ(10) supplementation decreased atherosclerosis at the aortic root and arch and descending thoracic aorta to an extent that increased with increasing distance from the aortic root. CoQ(10) significantly inhibited atherosclerosis at aortic root and arch, whereas VitE decreased disease at aortic root only. Thus, in apoE-/- mice, VitE+CoQ(10) supplements are more antiatherogenic than CoQ(10) or VitE supplements alone and disease inhibition is associated with a decrease in aortic lipid hydroperoxides but not 7-ketocholesterol.

Animals↗
PubMed2001

Oxidation of LDL by rabbit and human 15-lipoxygenase: prevalence of nonenzymatic reactions.

15-Lipoxygenase (15-LO)-induced oxidation of lipids in human LDL may be pro-atherogenic. However, the extent to which 15-LO promotes enzymatic oxidation of esterified (i.e., major) lipids in LDL may depend on various factors. Here, we show that overall, LDL lipid oxidation was favored with high activity of human 15-LO, that phospholipids were the preferred esterified substrate, and that low temperature maintained a higher proportion of enzymatic product. However, under all conditions, 15-LO induced alpha-tocopherol consumption and the accumulation of nonenzymatic products that predominated with increasing time of incubation and inactivation of the enzyme. Lysates prepared from cells overexpressing human 15-LO oxidized linoleic acid readily and in an almost exclusive enzymatic manner. In sharp contrast, such lysates failed to oxidize LDL lipids unless linoleic acid was added, in which case nonenzymatic oxidation of LDL lipids occurred. We conclude that although purified 15-LO can oxidize isolated LDL lipids in vitro, such oxygenation always includes nonenzymatic reactions that likely play a major role in the more extensive oxidation of LDL by cell-derived 15-LO.

Animals↗