Accumulation of aldehydic lipid peroxidation products during postanoxic reoxygenation of isolated rat hepatocytes

Grune, Tilman; Siems, Werner; Schneider, Wolfram

doi:10.1016/0891-5849(93)90051-u

Cited by 28 publications

(10 citation statements)

References 26 publications

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“…'5 16 Gastrointestinal mucosal xanthine oxidase activity may have a role in ischaemic injury such as NEC. The greater number of cases of NEC in the allopurinol group was not unexpectedly high compared with the usual incidence, but because of the enteral route used for dosing and the possible association of hyperosmolar feeds and NEC, the enteral route for administration could be a factor in the pathogenesis of NEC.…”

Section: Discussionmentioning

confidence: 99%

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Randomised controlled trial of allopurinol prophylaxis in very preterm infants.

Russell

Cooke

1995

Archives of Disease in Childhood - Fetal and Neonatal Edition

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Allopurinol, an inhibitor of xanthine oxidase (an enzyme capable of generating superoxide radicals following hypoxiaischaemia), was investigated in preterm infants to determine its ability to prevent the complications of neonatal intensive care which may be associated with oxidative injury. Four hundred infants of between 24 and 32 weeks' gestation were randomly allocated to receive enteral allopurinol (20 mg/ml) or an equivalent dose of placebo for seven daily doses. At admission, plasma hypoxanthine concentrations were significantly higher in infants who subsequently developed periventricular leucomalacia (PVL), bronchopulmonary dysplasia (BPD), or retinopathy of prematurity (ROP), but there was no difference in the primary endpoint (PVL) between the treated and control groups.The failure of allopurinol prophylaxis in this group of infants is probably related to the complex nature of the pathological processes and to the timing of treatment. If oxidant injury is an important mechanism of cellular injury in these preterm infants, an alternative biochemical modulator would be required, or a combination of agents might be effective.

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Section: Discussionmentioning

confidence: 99%

“…The median (interquartile range) time to maximum plasma concentration (Tmax) was 15 hours (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22), the median (interquartile range) maximum plasma concentration (Cmax) was 61-6 pumol/l (22-1-148-7), and the median t1/2 was 11 7 hours (8-2-16-5).…”

Section: Drug Formulation and Dosementioning

confidence: 99%

Randomised controlled trial of allopurinol prophylaxis in very preterm infants.

Russell

Cooke

1995

Archives of Disease in Childhood - Fetal and Neonatal Edition

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“…To remove the potassium perchlorate the samples were incubated for 1h at 4°C followed by centrifugation (1,200 × g, 5 min). The supernatant was stored at −20°C and analyzed for ATP by HPLC according to Grune T. et al, [38]. …”

Section: Methodsmentioning

confidence: 99%

Tau protein degradation is catalyzed by the ATP/ubiquitin-independent 20S proteasome under normal cell conditions

Grune

Botzen

Engels

et al. 2010

Archives of Biochemistry and Biophysics

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Tau is the major protein exhibiting intracellular accumulation in Alzheimer disease. The mechanisms leading to its accumulation are not fully understood. It has been proposed that the proteasome is responsible for degrading tau but, since proteasomal inhibitors block both the ubiquitin-dependent 26S proteasome and the ubiqutin-independent 20S proteasome pathways, it is not clear which of these pathways is involved in tau degradation. Some involvement of the ubiquitin ligase, CHIP in tau degradation has also been postulated during stress. In the current studies, we utilized HT22 cells and tau-transfected E36 cells in order to test the relative importance or possible requirement of the ubiquitin-dependent 26S proteasomal system versus the ubiquitin-independent 20S proteasome, in tau degradation. By means of ATP-depletion, ubiquitinylation-deficient E36ts20 cells, a 19S proteasomal regulator subunit MSS1-siRNA approaches, and in vitro ubiquitinylation studies, we were able to demonstrate that ubiquitinylation is not required for normal tau degradation.

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“…A major goal of biological researchers of the last 50 years is the understanding of the mechanisms of regulation of cellular metabolism. By the mid-1970s it was clear that two major mechanisms were the control of the rate of synthesis of specific proteins (gene regulation) and the control of the activity of already Grattagliano et al, 1998;Suzuki et al, 1999;Baynes and Thorpe, 1999;Miyata et al, 2003;Oh-Ishi et al, 2003;De et al, 2003 Senturker et al, 2002;England et al, 2004Exercise Witt et al, 1992Sohal et al, 1993;Saxton et al, 1994;Radak et al, 1997;Goto et al, 1999;Bejma et al, 2000;Chevion et al, 2003 Extracellular matrix oxidation Mattana et al, 1995Familial candidiasis Gangemi et al, 2003Fibrinogen oxidation Shacter et al, 1995Belisario et al, 1997Fibromyalgia Eisinger et al, 1996 Fish oil supplementation Sen et al, 1997;Sato et al, 1998;Wander andDu, 2000 Food quality Iqbal et al, 2004;Rowe et al, 2004 Fruit and Irradiation of meat Rababah et al, 2004 Ischemia-reperfusion, cerebral hemorrhage, or stroke Oliver et al, 1990;Park and Kehrer, 1991;Folbergrova et al, 1993;Grune et al, 1993;Liu et al, 1993;Ayene et al, 1992;Chang et al, 1998;He et al, 1999;Takagi et al, 1999;Robinson et al, 1999;…”

Section: Introductionmentioning

confidence: 97%