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Dive into the research topics where Herbert de Groot is active.

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Featured researches published by Herbert de Groot.


Steroids | 1994

Antioxidant effects of estradiol and 2-hydroxyestradiol on iron-induced lipid peroxidation of rat liver microsomes.

Ma Begoña Ruiz-Larrea; Ana M. Leal; Mariana Liza; Mercedes Lacort; Herbert de Groot

In the present study, the antioxidant effects of estradiol (E2) and 2-hydroxyestradiol (2-OHE2) on microsomal lipid peroxidation induced by Fe3+/ADP/NADPH and Fe2+/ascorbate are described. The extent of lipid peroxidation was measured by thiobarbituric acid reactive substances (TBARS) detection, low-level chemiluminescence, and oxygen consumption. 2-OHE2 had a potent antioxidant activity, which in all cases was higher than that of E2. In the Fe2+/ascorbate model, 2-OHE2 showed a similar pattern of inhibition, irrespective of the presence of NADPH or the functionality of microsomes. However, E2 produced only a slight inhibition when either denatured microsomes or native microsomes without NADPH were used, whereas its protective effect increased considerably when microsomal E2 metabolism was favored. During enzymic Fe3+/ADP/NADPH-induced lipid peroxidation, both E2 and 2-OHE2 were found to provide good protection. Results underline the importance of the chemical structure of these compounds and the role of estradiol metabolism in its antioxidant effects.


Journal of Hepatology | 1994

Low vitamin E content in plasma of patients with alcoholic liver disease, hemochromatosis and wilson's disease

Alexandra von Herbay; Herbert de Groot; Udo Hegi; Wolfgang Stremmel; Georg Strohmeyer; Helmut Sies

The RRR-alpha-tocopherol (vitamin E) content in plasma from 46 patients with liver diseases and 23 healthy controls was determined by high performance liquid chromatography and electrochemical detection. Patients were divided into three groups: alcoholic liver diseases (n = 17; group A), hemochromatosis (n = 17; group B) and Wilsons disease (n = 12; group C). Lipid-standardized alpha-tocopherol levels were determined to neutralize differences due to hyperlipemia. The ratio of serum vitamin E to serum lipids (cholesterol, triglycerides, phospholipids) was highest in healthy controls and in patients in group A with cirrhosis and normal transaminases and bilirubin. Patients in group A with acute or chronic ethanol intoxication and high bilirubin levels had a 37% lower lipid-standardized vitamin E level than controls. Patients in group B with hemochromatosis, showing high serum iron (> 180 micrograms/dl), a low free iron binding capacity (< 8 mumol/l) and high ferritin-levels (< 450 micrograms/l), had a 34% lower vitamin E/lipid ratio than healthy controls. No significant lowering of the vitamin E/lipid ratio was observed in the other patients in group B. A significant decrease (37%) in the vitamin E/lipid ratio was only detectable in patients with Wilsons disease (group C) showing high free serum copper (> 10 micrograms/dl). The data support a role for free radicals in the pathogenesis of active liver diseases.


Free Radical Biology and Medicine | 1992

Production of reactive oxygen by mitochondria from normoxic and hypoxic rat heart tissue

Thomas Paraidathathu; Herbert de Groot; James P. Kehrer

Reactive oxygen species (ROS), which may be involved in ischemic or reperfusion heart injury, can be produced by mitochondria. Previous work indicated that coupled mitochondria from ischemic heart tissue incubated in calcium-free medium produced less ROS than normal. The effects of calcium, which may be elevated in hypoxic or ischemic tissue, were not examined. The relative production of ROS by mitochondria from normoxic or hypoxic rat heart tissue was estimated by measuring the oxidation of dichlorofluorescin to the fluorescent compound, dichlorofluorescein. ROS were detectable during succinate-stimulated State 4 respiration. In the absence of calcium, mitochondria from hypoxic (60 min) heart tissue produced less ROS than mitochondria from normoxic heart tissue. In the presence of 0.1, 1 or 10 microM calcium, ROS produced by hypoxic mitochondria were increased to normoxic levels. While function was depressed in mitochondria from hypoxic tissue, the presence of 0.1 and 1 microM calcium had no further effect. Respiration was uncoupled in the presence of 10 microM calcium in mitochondria from both normoxic and hypoxic heart tissue. ROS production was increased in mitochondria from hypoxic tissue with both increasing concentrations of calcium and increasing duration of exposure. ROS production in mitochondria from normoxic heart tissue was only stimulated after 200 or more seconds of exposure to 1 or 10 microM calcium. Production of ROS in mitochondria from hypoxic tissue in the presence of 1 microM calcium was inhibited by rotenone (80%), ruthenium red (69%), and a combination of these agents (96%). In contrast, ruthenium red had no effect on ROS production by mitochondria from normoxic heart tissue.(ABSTRACT TRUNCATED AT 250 WORDS)


FEBS Letters | 1993

Loss of α‐tocopherol upon exposure to nitric oxide or the sydnonimine SIN‐1

Herbert de Groot; Udo Hegi; Helmut Sies

SIN‐1 which spontaneously decomposes to yield nitric oxide (NO. and Superoxide anion (O2 .− radicals caused a loss of microsomal α‐tocopherol paralleled by the formation of α‐tocopheryl quinone. The loss was partially prevented by Superoxide dismutase but not by catalase. The SIN‐1‐induced loss of α‐tocopherol also occurred when tocopherol was dissolved in ethanol/potassium phosphate buffer (20/80, v/v). Likewise, addition of authentic NO. to α‐tocopherol dissolved in ethanol resulted in loss of the vitamin and quinone formation. These results suggest that NO. or its products such as peroxynitrite or nitrogen dioxide react with α‐tocopherol, the quinone derivative being a major oxidation product. Depletion of vitamin E by NO. may contribute to tissue injury, e.g. in neuronal tissues.


Biochemical Pharmacology | 1981

Self-catalysed, O2-independent inactivation of nadph- or dithionite-reduced microsomal cytochrome P-450 by carbon tetrachloride

Herbert de Groot; Wolfgang Haas

Abstract Rat liver microsomes were incubated under anaerobic conditions in the presence of NADPH, dithionite and CCl 4 . It was found: (1) that in the presence of NADPH/CC1 4 or dithionite/CC1 4 the microsomal cytochrome P-450 (P-450) content rapidly declined and low amounts of CO were produced; (2) that the decrease of P-450 was always accompanied by an almost equimolar loss of microsomal heme; (3) that both the loss of P-450 and the formation of CO were inhibited by metyrapone and O 2 ; the decrease of P-450 was also inhibited by high concentrations of CO; and (4) that the pretreatment of rats with phenobarbital enhanced markedly both the loss of P-450 and the formation of CO, whereas the pretreatment with 3-methylcholanthrene significantly stimulated only the formation of CO. These results suggest: (1) that mainly the phenobarbital-induced species of P-450 are damaged by a direct, O 2 -independent attack of CCl 4 metabolites on its heme moiety; (2) that these reactive CCl 4 metabolites, probably CCl 3 or ¦CCl 2 , are intermediates of the metabolism of CC1 4 to CO; and (3) that this metabolism is catalysed in a suicidai manner by the reduced form of P-450 itself.


FEBS Letters | 1980

O2‐independent damage of cytochrome P450 by CCl4‐metabolites in hepatic microsomes

Herbert de Groot; Wolfgang Haas

The metabolism of CC& by the hepatic endoplasmic monooxygenase system results in the peroxidation of microsomal lipids and the covalent binding of CCL,-metabolites to microsomal proteins and lipids (reviewed [ 1,2]). The inactivation of cytochrome P4S0, the terminus of the endoplasmic monooxygenase system, is one of the earliest signs of damage following the administration of CCL, a hepatotoxic compound, in vivo [3-61. Similarly, the addition of Ccl4 in vitro to liver microsomes in the presence of NADPH also results in an early inactivation of cytochrome P450 [7-91. It is unclear [lo] whether cytochrome P450 is inactivated by the attack of reactive CCL,-metabolites directly [ 111 or whether these metabolites act indirectly by initiating 02-dependent lipid pero~dation [8]. We present here evidence that cytochrome P450 can be damaged by CCL,-metabolites under conditions which prevent the production of detectable quantities of lipid peroxides.


Transplant International | 1993

Injury to cultured liver endothelial cells during cold preservation: energy-dependent versus energy-deficiency injury

Ursula Rauen; Karin Hintz; Maren Hanßen; W. Lauchart; Horst D. Becker; Herbert de Groot

Previously, we demonstrated an energy-dependent injury to cultured liver endothelial cells during cold incubation in University of Wisconsin (UW) solution. Here, the effects of Histidine-Tryptophan-Ketoglutarate (HTK) and Euro-Collins (EC) solutions on these cells were studied. In HTK solution, 83%±4% of the cells had lost viability after 9 h of incubation at 4°C. The addition of cyanide (1 mM) to simulate hypoxic conditions protected the cells to the extent that only 9%±1% of the cells lost viability over the same period; the addition of glucose (10 mM) led to increased cell injury. ATP levels were highest in the incubations with the most rapid loss of viability. In Krebs-Henseleit buffer and EC solution, in contrast, cell injury increased upon addition of cyanide; the addition of glucose to Krebs-Henseleit buffer decreased injury. We conclude that the injury to cultured liver endothelial cells during cold incubation in HTK solution is energy-dependent, as it is in UW solution, whereas cells behave differently in EC solution and Krebs-Henseleit buffer.


Transplant International | 1994

MHC antigen presentation on the surface of hepatocytes: modulation during and after hypoxic stress.

C. F. Eisenberger; R. Viebahn; W. Lauchart; Herbert de Groot; Horst D. Becker

Abstract Presentation and recognition of MHC antigen on the surface of cells is the basic process of initiating rejection and distinguishing “self and not self‘. This is considered to begin when a transplanted organ is reperfused with the blood of the recipient. In this study, the modulation of MHC I antigen presentation during preservation was investigated in a cell culture model using primary hepatocyte cultures of male Wistar rats. By incubation with different preservation solutions used in clinical transplantation, expression of the MHC antigen was observed during cold hypoxia. Primary hepatocyte cultures were isolated from male Wistar rats by a modified Seglen technique and seeded to glass slides, thus obtaining monolayer cultures. After 1 day of resting the cultures were incubated under different conditions using Krebs Henseleit solution (KH), Euro‐Collins solution (EC), HTK solution of Bretschneider (HTK) and University of Wisconsin solution (UW) as incubation media. The conditions of incubation were warm normoxia (37°C, pO2 100 mmHg) and cold hypoxia (4°C, pO2 < 0.1 mmHg), which is the main condition of organ preservation. Incubation time was 6 h. Before starting the incubation reference cultures were fixed and every 60 min several cultures were withdrawn from the experiment and fixed also. MHC expression was studied by staining the cultures with monoclonal antibodies against rat MHC class I and class II. As expected, MHC class II was not present on the surface of hepatocytes, while MHC class I was demonstrated on the controls as well as on the cultures that were incubated using KH and EC independent of temperature and hypoxia or normoxia. At the end of the incubation they were still positive but not as strong as in the beginning. During incubation using HTK and UW, MHC I was not detectable at all phases of the experiment. In conclusion, hypoxic stress did not completely eradicate MHC I expression in rat hepatocytes, while the composition of the preservation medium may result in a hepatocyte surface negative for MHC I. Hydroxyethylstarch may be the substance in UW that covers the MHC antigen, while in HTK, mannitol or the histidine complex may play the same role. MHC negativity of the cells of a preserved transplant is another reason for the benefit of UW or HTK.


Archive | 1994

Reaktiver Sauerstoff als Mediator der Gewebezerstörung

Herbert de Groot

Zu den aktivierten Formen des Sauerstoffs zahlen unter anderem Wasserstoffperoxid (H2O2), organisches Hydroperoxid (ROOH), Singulettsauerstoff (1O2), Triplettcarbonyl (3R=O), Hypochlorit (CIO-) und die Radikale Hydroxyl (OH▪), Alkoxyl (RO▪), Peroxyl (ROO▪), Superoxidion (O2 - ▪) und Stickstoffmonoxid (NO▪). Die aktivierten Sauerstoffspezies unterscheiden sich deutlich voneinander in ihrer Reaktivitat mit biologischen Molekulen (Sies 1986; Halliwell u. Gutteridge 1989; Elstner 1990). Wahrend einige Spezies, wie z.B. O2 - ▪ und H2O2, nur mit wenigen biologischen Molekulen reagieren, reagieren andere, wie z.B. das OH-Radikal, nahezu sofort mit einer Vielzahl von verschiedenen Substanzen. Aus den weniger reaktiven aktivierten Sauerstoffspezies konnen allerdings die reaktiveren entstehen. So kann in der durch Eisen oder Kupfer katalysierten Haber-WeissReaktion aus O2 - ▪ und H2O2 das OH-Radikal gebildet werden. Ionen der Ubergangsmetalle Eisen und Kupfer spielen als Chelat-Komplexe nicht nur bei dieser Reaktion, sondern insgesamt eine herausragende Rolle bei der Entstehung des reaktiven Sauerstoffs, z.B. auch bei der Lipidperoxidation, auf die spater noch eingegangen wird. Nicht immer ist jedoch Metallionenkatalyse notwendig, um zur Bildung der besonders reaktiven Formen der aktivierten Sauerstoffspezies zu gelangen. Ein Beispiel hierfur ist die Reaktion von NO▪ mit O2 - ▪ (Beckman et al. 1990). Beide Radikale lagern sich zunachst zum Peroxinitrition (ONOO-) zusammen. Dies kann nach Protonierung zum OH- und Stickstoffdioxid-Radikal (NO2 ▪) zerfallen.


Free Radical Biology and Medicine | 1993

Reactive oxygen species associated with cell differentiation in Neurospora crassa

Wilhelm Hansberg; Herbert de Groot; Helmut Sies

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Ursula Rauen

University of Düsseldorf

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Helmut Sies

University of Düsseldorf

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F. Petrat

Medical University of Vienna

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Udo Hegi

University of Düsseldorf

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W. Lauchart

University of Tübingen

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Wilhelm Hansberg

National Autonomous University of Mexico

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