Vitamin C prophylaxis promotes oxidative lipid damage during surgical ischemia–reperfusion

Bailey, Damian Miles; Raman, Swathi; McEneny, Jane; Young, Ian S.; Parham, Kelly L.; Hullin, David A.; Davies, Bruce; McKeeman, G; McCord, Joe M.; Lewis, M. H.

doi:10.1016/j.freeradbiomed.2005.09.024

Cited by 59 publications

(46 citation statements)

References 46 publications

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“…The patients were randomized to ascorbate prophylaxis or placebo in a double-blinded, randomized manner. During lower limb ischemia, the patients receiving ascorbate exhibited a release of lipid hydroperoxide across the ischemic vascular bed, and the systemic levels of lipid-derived alkoxyl and alkyl radicals increased during reperfusion (Bailey et al, 2006). Analogous mechanisms may contribute to oxidative-nitrosative stress upon ischemia-reperfusion of the cerebrovascular bed, as indicated by findings from patients undergoing carotid endarterectomy (Bailey et al, 2007).…”

Section: Ascorbate and A-tocopherolmentioning

confidence: 99%

Neuro-oxidative-nitrosative stress in sepsis

Berg

Møller

Bailey

2011

J Cereb Blood Flow Metab

140

109

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Neuro-oxidative-nitrosative stress may prove the molecular basis underlying brain dysfunction in sepsis. In the current review, we describe how sepsis-induced reactive oxygen and nitrogen species (ROS/RNS) trigger lipid peroxidation chain reactions throughout the cerebrovasculature and surrounding brain parenchyma, due to failure of the local antioxidant systems. ROS/RNS cause structural membrane damage, induce inflammation, and scavenge nitric oxide (NO) to yield peroxynitrite (ONOO À ). This activates the inducible NO synthase, which further compounds ONOO À formation. ROS/RNS cause mitochondrial dysfunction by inhibiting the mitochondrial electron transport chain and uncoupling oxidative phosphorylation, which ultimately leads to neuronal bioenergetic failure. Furthermore, in certain 'at risk' areas of the brain, free radicals may induce neuronal apoptosis. In the present review, we define a role for ROS/RNS-mediated neuronal bioenergetic failure and apoptosis as a primary mechanism underlying sepsis-associated encephalopathy and, in sepsis survivors, permanent cognitive deficits.

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Section: Ascorbate and A-tocopherolmentioning

confidence: 99%

Neuro-oxidative-nitrosative stress in sepsis

Berg

Møller

Bailey

2011

J Cereb Blood Flow Metab

140

109

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“…Concerns have been raised about the administration of ascorbic acid in the presence of redoxactive transition metal ions, since ascorbate can reduce transition metal ions and catalyse the Fenton-driven generation of hydroxyl and alkoxyl radicals in vitro [13]. Although the thermodynamics of this reaction in vivo remain controversial [14], an acute bout of physical exercise has been shown to liberate extracellular 'catalytic' iron [15] that, in the presence of supplementary ascorbic acid, may potentially compound the generation of ROS [16].…”

Section: Introductionmentioning

confidence: 99%

Molecular detection of exercise-induced free radicals following ascorbate prophylaxis in type 1 diabetes mellitus: a randomised controlled trial

et al. 2008

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Aims/hypothesis Patients with type 1 diabetes mellitus are more susceptible than healthy individuals to exercise-induced oxidative stress and vascular endothelial dysfunction, which has important implications for the progression of disease. Thus, in the present study, we designed a randomised doubleblind, placebo-controlled trial to test the original hypothesis that oral prophylaxis with vitamin C attenuates rest and exercise-induced free radical-mediated lipid peroxidation in type 1 diabetes mellitus. Methods All data were collected from hospitalised diabetic patients. The electron paramagnetic resonance spectroscopic detection of spin-trapped α-phenyl-tert-butylnitrone (PBN) adducts was combined with the use of supporting markers of lipid peroxidation and non-enzymatic antioxidants to assess exercise-induced oxidative stress in male patients with type 1 diabetes (HbA 1c 7.9±1%, n=12) and healthy controls (HbA 1c 4.6±0.5%, n=14). Following participant randomisation using numbers in a sealed envelope, venous blood samples were obtained at rest, after a maximal exercise challenge and before and 2 h after oral ingestion of 1 g ascorbate or placebo. Participants and lead investigators were blinded to the administration of either placebo or ascorbate treatments. Primary outcome was the difference in changes in free radicals following ascorbate ingestion. Results Six diabetic patients and seven healthy control participants were randomised to each of the placebo and ascorbate groups. Diabetic patients (n=12) exhibited an elevated concentration of PBN adducts (p<0.05 vs healthy, n=14), which were confirmed as secondary, lipid-derived oxygen-centred alkoxyl (RO·) radicals (a nitrogen =1.37 mT and aβ hydrogen =0.18 mT). Lipid hydroperoxides were also selectively elevated and associated with a depression of retinol and lycopene (p<0.05 vs healthy). Vitamin C supplementation increased plasma vitamin C concentration to a similar degree in both groups (p<0.05 vs presupplementation) and attenuated the exercise-induced oxidative stress response (p<0.05 vs healthy).There were no selective treatment differences between groups in the primary outcome variable. Conclusions/interpretation These findings are the first to suggest that oral vitamin C supplementation provides an Diabetologia

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“…This was reflected in an increase of LH, vascular endothelial growth factor and creatine phosphokinase during reperfusion. The findings of these authors suggest that sodium ascorbate can promote lipid oxidative damage induced by iron during the ischemic phase of the operation 15 . Perhaps the ascorbic acid may, at therapeutic doses, have a negative effect on ischemia-reperfusion injury by increasing inflammatory activity, being then indicated in smaller quantities.…”

Section: Discussion Discussion Discussion Discussionmentioning

confidence: 92%

Antioxidantes enterais em lesões de isquemia e reperfusão em ratos

Köhler

Delucca

Neto

2011

Rev. Col. Bras. Cir.

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Enteral antioxidants in ischemia/reperfusion injuries in rats Enteral antioxidants in ischemia/reperfusion injuries in rats Enteral antioxidants in ischemia/reperfusion injuries in rats Enteral antioxidants in ischemia/reperfusion injuries in rats Enteral antioxidants in ischemia/reperfusion injuries in rats Antioxidantes enterais em lesões de isquemia e reperfusão em ratos Antioxidantes enterais em lesões de isquemia e reperfusão em ratos Antioxidantes enterais em lesões de isquemia e reperfusão em ratos Antioxidantes enterais em lesões de isquemia e reperfusão em ratos Antioxidantes enterais em lesões de isquemia e reperfusão em ratos HUGO Methods Methods Methods Methods: Ninety adult male Wistar rats were used. An intestinal segment was isolated based on its vascular pedicle. A control biopsy was performed and the pedicle was sectioned and sutured again, ensuring a time of 60 minutes of ischemia followed by reperfusion. Sequential biopsies were performed at the end of the ischemic period and every 15 minutes during reperfusion. The treatment consisted of saline, vitamin C, vitamin E or a combination of the latter two. Quantitative and qualitative assessments of the biopsies were performed. Results Results ResultsResults Results: The groups treated with vitamin E alone or vitamin E combined with vitamin C showed a statistically significant attenuation of ischemia-reperfusion, with reduced loss of height of the villi and lower neutrophilic infiltration at the end of the study when compared to the control and vitamin C- INTRODUCTION INTRODUCTION INTRODUCTION INTRODUCTION INTRODUCTIONT he restoration of blood flow to an ischemic tissue can lead to greater harm than that originally caused by ischemia. This event is called ischemia and reperfusion (I/R) injury. The small intestine is particularly susceptible to injury from I/R 1 and its occurrence is associated with high morbidity and mortality 2 . Although the mechanisms involved are not fully elucidated, it is believed that oxidative stress mediators, such as reactive oxygen species (ROS), polymorphonuclear neutrophils (PMN) and nitric oxide (NO) play an important role 3 . Due to the involvement of ROS in I/R injury, various antioxidants have been tested, among them vitamin C (ascorbic acid) and vitamin E. Ascorbic acid is an water-soluble antioxidant with chelating and reducing properties and it is used to prevent I/R injury 4 . Vitamin E (á-tocopherol) is a nonenzymatic, lipid soluble antioxidant that acts against oxidative stress by stabilizing membrane unsaturated fatty acids. Thus, tissues treated with vitamin E have an increased capacity to reduce ROS and be protected against membrane lipid peroxidation 5 . Vitamins C and E can act synergistically because ascorbic acid is unable to reduce the peroxyl radical, but it can regenerate á-tocopherol from the tocoferoxil radical, recycling the á-tocopherol 6 . I/R can occur in a variety of clinical situations, one being the microsurgical transfer of jejunal segments. The jejunal flap was first described in 1957...

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Vitamin C prophylaxis promotes oxidative lipid damage during surgical ischemia–reperfusion

Cited by 59 publications

References 46 publications

Neuro-oxidative-nitrosative stress in sepsis

Neuro-oxidative-nitrosative stress in sepsis

Molecular detection of exercise-induced free radicals following ascorbate prophylaxis in type 1 diabetes mellitus: a randomised controlled trial

Antioxidantes enterais em lesões de isquemia e reperfusão em ratos

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