| 1. |
- Basu, Samar, et al.
(author)
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Association between oxidative stress and bone mineral density
- 2001
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In: Biochemical and Biophysical Research Communications - BBRC. - : Elsevier BV. - 0006-291X .- 1090-2104. ; 288:1, s. 275-9
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Journal article (peer-reviewed)abstract
- Free radicals have been shown to be involved in bone resorption in vitro and in rodents. We studied the effect of oxidative stress on bone mineral density (BMD) in 48 women and 53 men from a population-based study. The levels of 8-iso-PGF(2alpha) (a major F(2)-isoprostane and a biomarker of oxidative stress) and a control, 15-keto-dihydro-PGF(2alpha) (a biomarker of inflammatory response), were measured in urinary samples and their association with BMD and quantitative ultrasound (QUS) measurements were examined. In multivariate linear regression analyses, 8-iso-PGF(2alpha) levels were negatively associated with both BMD and QUS. In contrast, no association was found for 15-keto-dihydro-PGF(2alpha). Our findings establish a biochemical link between increased oxidative stress and reduced bone density and provide a rational for further studies investigating the role of pro- and antioxidants in osteoporosis. Copyright 2001 Academic Press.
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| 2. |
- Basu, Samar, et al.
(author)
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Biomarkers of free radical injury during spinal cord ischemia
- 2001
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In: FEBS Letters. - 0014-5793 .- 1873-3468. ; 508:1, s. 36-38
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Journal article (peer-reviewed)abstract
- Plasma and urinary levels of 8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha) were analysed at baseline and during the ischemia-reperfusion period in experimental spinal cord ischemia. A significant and immediate increase of 8-iso-PGF(2alpha) in plasma at the start and up to 60 min, and in the urine at 90-150 min following ischemia indicate an association of oxidative injury. The inflammatory response indicator 15-keto-dihydro-PGF(2alpha) in plasma increased significantly at the start and up to 60 min after ischemia. No such increase was seen in animals with no spinal cord ischemia. Thus, free radical mediated and cyclooxygenase catalysed products of arachidonic acid are increased during spinal cord ischemia as a consequence of oxidative injury and inflammation.
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| 3. |
- Basu, Samar, et al.
(author)
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Propofol (Diprivan-EDTA) counteracts oxidative injury and deterioration of the arterial oxygen tension during experimental septic shock
- 2001
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In: Resuscitation. - 0300-9572 .- 1873-1570. ; 50:3, s. 341-348
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Journal article (peer-reviewed)abstract
- PURPOSE: Human septic shock can be replicated in the endotoxaemic pig. Endotoxaemia causes a multitude of events, including reduced PaO(2) and increased lipid peroxidation. This study was designed to evaluate the possible effects of a commonly used anaesthetic drug with known antioxidant properties (propofol) during porcine endotoxaemia.METHODS: Ten pigs were anaesthetised and given a 6 h E. coli endotoxin infusion. The animals received, randomly, a supplementary continuous infusion of propofol emulsion (containing 0.005% EDTA) or the corresponding volume of vehicle (controls). Pathophysiologic responses were determined. Non-enzymatic (by measuring plasma 8-iso-PGF(2 alpha) and enzymatic (by measuring plasma 15-keto-dihydro-PGF(2 alpha)) lipid peroxidations were evaluated. Plasma levels of the endogenous antioxidants alpha- and gamma-tocopherols, were also analysed.RESULTS: Endotoxaemia increased plasma levels of 8-iso-PGF(2 alpha) (1st-4th h) and 15-keto-dihydro-PGF(2 alpha) (1st-4th h) significantly more in controls than in the propofol+endotoxin group. PaO(2) was significantly less affected by endotoxin in the propofol treated animals (2nd-4th h). Mean arterial pressure (4th-6th h) and systemic vascular resistance (6th h) were reduced significantly more by endotoxin among the propofol-treated animals. Vitamin E (alpha-tocopherol) increased in all animals, significantly more in the propofol+endotoxin group (1/2-6th h) than in the control group.CONCLUSIONS: Propofol reduced endotoxin-induced free radical mediated and cyclooxygenase catalysed lipid peroxidation significantly. The implication is that propofol counteracts endotoxin-induced deterioration of PaO(2).
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| 4. |
- Basu, Samar, et al.
(author)
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Retinol palmitate counteracts oxidative injury during experimental septic shock
- 2001
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In: Annals of the Academy of Medicine, Singapore. - 0304-4602. ; 30:3, s. 265-269
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Journal article (peer-reviewed)abstract
- INTRODUCTION: Retinols seem to be of clinical importance in ameliorating the clinical consequences of septic shock. These beneficial effects of retinols are suggested to be due to an antioxidant property. The present study was undertaken in order to confirm or rule out such an effect of retinol palmitate (RP) in experimental septic shock by measuring F2-isoprostanes and a major prostaglandin F2 alpha metabolite as indicators of oxidative injury and inflammatory response, respectively. MATERIALS AND METHODS: Fourteen anaesthetised pigs were randomly given an injection of RP (2.300 IU x kg-1) or the corresponding volume of vehicle. All pigs received a continuous infusion of E. coli endotoxin (10 micrograms x kg-1 x h-1). Blood samples were analysed for lipid peroxidation products (8-iso-PGF2 alpha), indicating free radical induced oxidative injury and 15-keto-dihydro-PGF2 alpha indicating cyclooxygenase-mediated inflammatory response). RESULTS: Significantly elevated levels of 8-iso-PGF2 alpha were seen at 3, 5 and 6 hours of endotoxaemia in the vehicle + endotoxin group as compared to RP + endotoxin group. Endotoxin induced cyclooxygenase-mediated inflammatory response was not affected by RP. CONCLUSIONS: This study is the first one to show that RP counteracts oxidative injury rather than inflammatory response in experimental septic shock. These results may be of importance for the understanding of some beneficial effects of RP during endotoxaemia (i.e. improved systemic haemodynamics and reduced serum levels of endotoxin). Our results may explain the therapeutic effects of nutrients rich in caroten/retinols used in some clinical studies.
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| 5. |
- Cederberg, Jonas, et al.
(author)
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Increased rate of lipid peroxidation and protein carbonylation inexperimental diabetic pregnancy.
- 2001
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In: Diabetologia. ; 44, s. 766-774
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Journal article (peer-reviewed)abstract
- BACKGROUND: Diabetic pregnancy displays increased incidence of congenital malformations and elevated levels of lipid peroxides in the offspring. The aim of the present work was to study if exogenous administration of one lipid peroxide, the isoprostane 8-iso-PGF(2alpha), is teratogenic per se in rat embryos in vitro, and if such teratological effects may be diminished by supplementation of an antioxidative agent, i.e., N-acetylcysteine or superoxide dismutase, to the culture medium. METHODS: Day-9 embryos were cultured in vitro for 48 hr and subjected to 8-iso-PGF(2alpha) with and without N-acetylcysteine or superoxide dismutase. RESULTS: Addition of 2 micromol/l of the isoprostane 8-iso-PGF(2alpha) to the culture medium caused high malformation rate, decreased protein and DNA contents, decreased somite number and crown-rump-length as well as marked accumulation of the isoprostane in the embryonic tissues. Adding N-acetylcysteine or superoxide dismutase to the culture medium with isoprostane normalized almost all morphological and biochemical parameters, including the elevated tissue concentration of 8-iso-PGF(2alpha). CONCLUSIONS: Results indicate that the isoprostane (8-iso-PGF(2alpha)) serves both as an oxidative stress indicator and a teratogenic agent. The findings support earlier studies of enhanced oxidative stress and increased malformation rate in embryos exposed to a diabetes-like environment, and suggest prevention of dysmorphogenesis by administration of antioxidative agents.
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| 6. |
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| 7. |
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| 8. |
- Mutschler, Diana K., et al.
(author)
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Riksstämman 2001
- 2001
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Other publication (other academic/artistic)
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