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book Effects of vitamin E on T cell lipid peroxidation, membrane fluidity and T cell functions in traumatized mice
book Vitamin E ameliorates adverse effects of endothelial injury in brain arterioles
book Vitamin E, thiobarbituric acid reactive substance concentrations and superoxide dismutase activity in the blood of children with juvenile rheumatoid arthritis
book Acceleration of corneal wound healing in diabetic rats by the antioxidant trolox
book Antioxidant vitamins in hospitalized elderly patients: Analysed dietary intakes and biochemical status
book Effect of dietary Vitamin-C on compression injury of the spinal cord in a rat mutant unable to synthesize ascorbic acid and its correlation with that of vitamin E
book Antioxidant depletion, lipid peroxidation, and impairment of calcium transport induced by air-blast overpressure in rat lungs
book The use of antioxidants in healing
book Effect of vitamin e on hydrogen peroxide production by human vascular endothelial cells after hypoxia/reoxygenation
book Cerebral astrocytes transport ascorbic acid and dehydroascorbic acid through distinct mechanisms regulated by cyclic AMP .
book Osmotic swelling stimulates ascorbate efflux from cerebral astrocytes.
book Amphiphilic alpha-tocopherol analogues as inhibitors of brain lipid peroxidation.
book Update on the biological characteristics of the antioxidant micronutrients: Vitamin-C, vitamin E, and the carotenoids.
book Effect of allopurinol, sulphasalazine, and Vitamin-C on aspirin induced gastroduodenal injury in human volunteers
book Hemodynamic effects of delayed initiation of antioxidant therapy (beginning two hours after burn) in extensive third-degree burns
book Dietary intake and plasma levels of antioxidant vitamins in health and disease: A hospital-based case-control study
book Vitamin-C and pressure sores


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Effects of vitamin E on T cell lipid peroxidation, membrane fluidity and T cell functions in traumatized mice

Liang H.-P.; Wang Z.-G.
Research Institute of Surgery, Third Military Medical College, Chongqing 630042 China
Chinese Pharmacological Bulletin (China), 1996, 12/1 (47-49)

SUBFILES:Ranges of T cell malondialdehyde (MDA) contents, membrane fluidity, Tcell functions and therapeutic effects of vitamin E (V-E) were observed in traumatized mice. The results showed that T cell MDA contents were increased after trauma, membrane fluidity of T cell plasmalemma, mitochondria and microsome reduced and T lymphocytes transformation, interleukin 2 (IL-2) production, IL-2 receptor (IL-2R) expression and IL-2 mediated lymphocytes proliferation response were suppressed, which were related closely to MDA alteration. In vivo administration of V-E (50 or 100 mg/kg.d-1, im x 4 d) could reverse ahove parameters, indicating lipid peroxidation after trauma is an important cause resulting in reduced T cell membrane fluidity and were suppressed T cell functions, on which V-E shows significant therapeutic effects.



Vitamin E ameliorates adverse effects of endothelial injury in brain arterioles

Rosenblum W.I.; Nelson G.H.; Bei R.A.; Brandt R.B.; Chan W.
Dept. of Pathology (Neuropathology), Medical College of Virginia, Virginia Commonwealth Univ., Richmond, VA 23298-0017 USA
American Journal of Physiology - Heart and Circulatory Physiology (USA), 1996, 271/2 40-2 (H637-H642)

Endothelium-dependent dilation, pros unaffected after 6 mo of a diet with zero vitamin E or 8 mo of a vitamin E-enriched diet. The enriched diet did not affect constriction produced by topically applied N(G)-monomethyl-L-arginine, an inhibitor of the synthesis of endothelium-derived relaxing factor (EDRF). EDRF mediates the response to ACh and is a basally released dilator and antiplatelet paracrine substance. Endothelial injury produced by a helium- neon laser and Evans blue technique eliminates the response to ACh, but in vitamin E-enriched mice the response to ACh was unaffected by the injury. More prolonged exposure of the laser induces platelet adhesion/aggregation at the injured site. A significantly longer exposure to the laser was required to initiate adhesion/aggregation in vitamin E-enriched mice. Because effects of endothelial damage in this model are mediated at least in part by singlet oxygen produced by injured tissue, we conclude that the antioxidant, radical-scavenging actions of vitamin E explain the protective action of the vitamin E-enriched diet. However, raising vitamin E levels did not protect against putative adverse effects of normally occurring oxidants.



Vitamin E, thiobarbituric acid reactive substance concentrations and superoxide dismutase activity in the blood of children with juvenile rheumatoid arthritis

Sklodowska M.; Gromadzinska J.; Biernacka M.; Wasowicz W.; Wolkanin P.; Marszalek A.; Brozik H.; Pokuszynska K.
Dept. of Plant Physiology/Biochem., University of Lodz, Banacha St. 12/16, 90-237 Lodz Poland
Clinical and Experimental Rheumatology (Italy), 1996, 14/4 (433-439)

Objective: To study the role of amined the levels of thiobarbituric acid reactive substances (TBARS) and antioxidants of the first line antioxidative defence of the organism, i.e. vitamin E (VE) and superoxide dismutase (SOD) in the blood of 74 young patients with juvenile rheumatoid arthritis (JRA) and in 138 healthy children, all aged 3-15.

Results: A statistically significant increase of TBARS was found in the blood plasma of the children with JRA compared with the control group. In the whole group of patients and in the patients over 6 years of age, the VE concentration was significantly lower in the blood plasma and significantly higher in the erythrocytes than in the control groups. SOD activity in the red blood cells (RBC) was significantly lower in children who had suffered from JRA for more than one year and in those with the systemic form of the disease. The type of treatment also affected the values for the plasma VE and SOD in the RBC.

Conclusion: Our results seem to confirm the supposition of increased oxidative stress in children with JRA and low antioxidant levels in terms of SOD activity and vitamin E concentrations.



Acceleration of corneal wound healing in diabetic rats by the antioxidant trolox

Hallberg CK, Trocme SD, Ansari NH
Department of Human Biological Chemistry & Genetics, University of Texas Medical Branch, Galveston 77555-0647, USA.
Res Commun Mol Pathol Pharmacol 1996 Jul;93(1):3-12

Several corneal complications have been reported in patients with long standing diabetes, but their exact pathogenesis is not well understood. It has been observed that the rate of epithelial wound healing in diabetic rats is delayed compared to those in normal animals. Here we present the effect of the free radial scavenger, Trolox, a water soluble vitamin E analogue, on epithelial wound healing in diabetic rat cornea. Three groups of rats were included:

1) normal,
2) diabetic,
3) diabetic + Trolox.

After 3 months, rats were sacrificed and corneas removed. Standard 3 mm diameter corneal epithelial defects were made and residual epithelial defects were measured after 18 hours at 37degreeC in a sterile cell culture incubator. Wound healing data measured in mm2 was used for statistical analysis. There were significantly larger (p < 0.05) epithelial defects in diabetic corneas as compared to control. Treatment with Trolox antioxidant in diabetic rats produced a significantly smaller (p < 0.05) epithelial defect than that of untreated diabetic rats. These studies suggest the involvement of free radicals in the delay of corneal epithelial wound healing in diabetes.



Antioxidant vitamins in hospitalized elderly patients: Analysed dietary intakes and biochemical status

Schmuck A.; Ravel A.; Coudray C.; Alary J.; Franco A.; Roussel A.-M.
GREPO, Universite Joseph Fourier, Domaine de la Merci, 38700 La Tronche France
European Journal of Clinical Nutrition (United Kingdom), 1996, 50/7 (473-478)

Design: Descriptive study. Setting: Geriatric department of the Grenoble University Hospital.

Subjects: 24 hospitalized elderly women: 13 long-stay patients and 11 in rehabilitation after femoral neck fracture.

Main outcome measures: Retinol, carotene, tocopherol and Vitamin-C dietary intakes were evaluated by 5-day duplicate portion analysis. Circulating levels of retinol, beta-carotene, alpha-tocopherol and Vitamin-C were determined in parallel (HPLC).

Results: Mean intake of Vitamin-C (21 mg/d), and vitamin E (3.1 mg alpha-tocopherol equivalents TE/d) were low compared to recommendations, in relation with poor energy intake (5.27 MJ/d) and nutrient densities. More than 85% of the patients exhibited Vitamin-C and vitamin E intakes below two-thirds the recommendations (60 mg/d and 10 mg TE/d, respectively) and 50% did not meet recommendations for vitamin A (800 microg retinol equivalents/d). With the exception of retinol, dietary vitamin intakes were positively correlated to corresponding blood concentrations. No values below cut-off levels were found concerning plasma retinol, plasma tocopherol or ratio of alpha-tocopherol to cholesterol. In contrast, 26% and 32% of the elderly patients had low circulating levels of beta-carotene and Vitamin-C, respectively.

Conclusions: The present study highlights low antioxidant vitamin intakes, particularly concerning vitamin E and Vitamin-C, and an important proportion of low blood Vitamin-C and beta-carotene concentrations in hospitalized elderly women. Further studies are needed to determine the actual requirements of hospitalized elderly patients and to evaluate the potential benefits of providing micronutrient-enriched foods to this population.



Effect of dietary Vitamin-C on compression injury of the spinal cord in a rat mutant unable to synthesize ascorbic acid and its correlation with that of vitamin E

Katoh D, Ikata T, Katoh S, Hamada Y, Fukuzawa K
Department of Orthopedic Surgery, School of Medicine, Tokushima, Japan.
Spinal Cord (United Kingdom), 1996, 34/4 (234-238)

The roles of vitamines after spinal cord injury were investigated by evaluating the effects of dietary Vitamin-C on experimental spinal cord injury in a mutant strain of Wistar rats unable to synthesize ascorbic acid (ODS rats). Two groups of ODS rats were given Vitamin-C-deficient or Vitamin-C-supplemented diet for 1 week before injury. Motor disturbance induced by spinal cord injury was found to be greater in the Vitamin-C-deficient group. Histologically, the area of bleeding in the spinal cord was also greater in the Vitamin-C-deficient group. The levels of ascorbic acid and alpha-tocopherol in the spinal cord tissue and serum decreased during and after compression injury of the spinal cord. The decrease of alpha-tocopherol was similar in the two groups. However, the decrease of ascorbic acid was greater in the Vitamin-C-supplemented group. These results indicated that their protective effects against spinal cord injury are through scavenging water-soluble free radicals by vitamin C and lipid-soluble by vitamin E, and the effects of these vitamins were suggested to be independent.



Antioxidant depletion, lipid peroxidation, and impairment of calcium transport induced by air-blast overpressure in rat lungs

Elsayed NM, Tyurina YY, Tyurin VA, Menshikova EV, Kisin ER, Kagan VE
Department of Respiratory Research, Walter Reed Army Institute of Research, Washington, DC 20307-5100, USA.
Experimental Lung Research (USA), 1996, 22/2 (179-200)

Exposure to blast overpressure, or the sudden rise in atmospheric pressure after explosive detonation, results in damage mainly of the gas-filled organs. In addition to the physical damage, in the lung, injury may proceed via a hemorrhage-dependent mechanism initiating oxidative stress and accumulation of lipid peroxidation products. Massive rupture of capillaries and red blood cells, release of hemoglobin, its oxidation to met-hemoglobin and degradation sets the stage for heme-catalyzed oxidations. The authors hypothesized that lipid hydroperoxides interact with met-hemoglobin in the lungs of exposed animals to produce ferryl-hemoglobin, an extremely potent oxidant that induces oxidative damage by depleting antioxidants and initiating peroxidation reactions. Oxidation-induced disturbance of Ca2+ homeostasis facilitates further amplification of the damage. To test this hypothesis, groups of anesthetized rats (6 rats/group) were exposed to blast at 3 peak pressures: low (61.2 kPa), medium (95.2 kPa), high (136 kPa). One group served as an unexposed control. Immediately after exposure, the rats were euthanized and the lungs were analyzed for biochemical parameters. Blast overpressure caused:

(1) depletion of total and water-soluble pulmonary antioxidant reserves and individual antioxidants (ascorbate, vitamin E, GSH),

(2) accumulation of lipid peroxidation products (conjugated dienes, TBARS), and

(3) inhibition of ATP-dependent Ca2+ transport. The magnitude of these changes in the lungs was proportional to the peak blast overpressure. Inhibition of Ca2+ transport strongly correlated with both depletion of antioxidants and enhancement of lipid peroxidation. In model experiments, met-hemoglobin/H2O2 produced damage to Ca2+ transport in the lungs from control animals similar to that observed in the lungs from blast overpressure-exposed animals. Ascorbate, which is known to reduce ferryl- hemoglobin, protected against met-hemoglobin/H2O2-induced damage of Ca2+ transport. If ferryl-hemoglobin is the major reactive oxygen species released by hemorrhage, then its specific reductants (e.g., nitric oxide) along with other antioxidants may be beneficial protectants against pulmonary barotrauma.



The use of antioxidants in healing

Martin A
Warner-Lambert Company, Morris Plains, New Jersey 07950, USA.
Dermatologic Surgery (USA), 1996, 22/2 (156-160)

BACKGROUND. Antioxidants enhance the healing of infected and noninfected wounds by reducing the damage caused by oxygen radicals.

OBJECTIVE. Studies were conducted to determine if the CRT components (vitamin E, sodium pyruvate, and specific fatty acids) could synergistically enhance healing.

METHODS. In vitro and in vivo studies were used to assess the effect of various combination of CRT components.

RESULTS. CRT reduced oxidative damage to keratinocytes and monocytes exposed to ultraviolet light and toxic chemicals and provided protection to human subjects exposed to ultraviolet irradiation. CRT dramatically facilitated healing of infected and noninfected wounds. In herpes-infected guinea pigs, CRT reduced vaginal viral lesion development, severity, and duration, thus facilitated healing of the lesions. CRT also reversed doxorubicin cytotoxicity in monocytes and reversed doxorubicin-impaired wound healing in rats.

CONCLUSION: The CRT colly to enhancing healing of injuries.



Effect of vitamin e on hydrogen peroxide production by human vascular endothelial cells after hypoxia/reoxygenation

Martin A, Zulueta J, Hassoun P, Blumberg JB, Meydani M
Antioxidant Research Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA.
Free Radical Biology and Medicine (USA), 1996, 20/1 (99-105)

Changes in oxidative stress status play an important role in tissue injury associated with ischemia-reperfusion events such as those that occur during stroke and myocardial infarction. Endothelial cells (EC) from human saphenous vein and aorta were incubated for 22 h and found to take up vitamin E from media containing 0-60 mM vitamin E in a dose-dependent manner. EC supplemented with 23 or 28 mM vitamin E in the media for 22 h were maintained at normoxia (20% O2, 5% CO2, and balance N2) or exposed to hypoxic conditions (3% 30 min. Saphenous EC supplemented with 23 mM vitamin E produced less (p < 0.05) H2O2 than unsupplemented controls, both at normoxic condition (supplemented: 4.9 plus or minus 0.05 vs. control:10.9 plus or minus 1.3 pmol/min/106 cells) and following hypoxia/reoxygenation (supplemented: 6.4 plus or minus 0.78 vs. control:17.0 plus or minus 2.7 nmol/min/106 cells). In contrast, aortic EC, which were found to have higher superoxide dismutase and catalase activity than EC from saphenous vein, did not produce any detectable levels of H2O2. Following hypoxia/reoxygenation, the concentration of vitamin E in supplemented saphenous EC was 62% lower than cells maintained at normoxia (0.19 plus or minus 0.03 vs. 0.5 plus or minus 0.12 nmoles/106 cells. p < 0.001); in aortic EC vitamin E content was reduced by 18% following reoxygenation (0.86 plus or minus 0.16 vs, 070 plus or minus 0.09 nmoles/106 cells, p < 0.05). Therefore, enrichment of vitamin E in EC decreases H2O2 production and thus may reduce the injury associated with ischemia-reperfusion events.



Cerebral astrocytes transport ascorbic acid and dehydroascorbic acid through distinct mechanisms regulated by cyclic AMP.

Siushansian R, Tao L, Dixon SJ, Wilson JX
Department of Physiology, Faculty of Medicine, University of Western Ontario, London, Canada.
J Neurochem (United States) Jun 1997, 68 (6) p2378-85

Cerebral ischemia and trauma lead to rapid increases in cerebral concentrations of cyclic AMP and dehydroascorbic acid (DHAA; oxidized Vitamin-C), depletion of intracellular ascorbic acid (AA; reduced Vitamin-C), and formation of reactive astrocytes. We investigated astrocytic transport of AA and DHAA and the effects of cyclic AMP on these transport systems. Primary cultures of astrocytes accumulated millimolar concentrations of intracellular AA when incubated in medium containing either AA or DHAA. AA uptake was Na+-dependent and inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), whereas DHAA uptake was Na+-independent and DIDS-insensitive. DHAA uptake was inhibited by cytochalasin B, D-glucose, and glucose analogues specific for facilitative hexose transporters. Once inside the cells, DHAA was reduced to AA. DHAA reduction greatly decreased astrocytic glutathione concentration. However, experiments with astrocytes that had been previously depleted of glutathione showed that DHAA reduction does not require physiological concentrations of glutathione. Astrocyte cultures were treated with a permeant analogue of cyclic AMP or forskolin, an activator of adenylyl cyclase, to induce cellular differentiation and thus provide in vitro models of reactive astrocytes. Cyclic AMP stimulated uptake of AA, DHAA, and 2-deoxyglucose. The effects of cyclic AMP required at least 12 h and were inhibited by cycloheximide, consistent with a requirement for de novo protein synthesis. Uptake and reduction of DHAA by astrocytes may be a recycling pathway that contributes to brain AA homeostasis. These results also indicate a role for cyclic AMP in accelerating the clearance and detoxification of DHAA in the brain.



Osmotic swelling stimulates ascorbate efflux from cerebral astrocytes.

Siushansian R, Dixon SJ, Wilson JX
Department of Physiology, University of Western Ontario, London, Canada.
J Neurochem (United States) Mar 1996, 66 (3) p1227-33

Ascorbate (reduced Vitamin-C) is an important enzyme cofactor, neuromodulator, and antioxidant that is stored at millimolar concentrations in the cytosol of cerebral astrocytes. Because these cells swell during hyponatremia, cerebral ischemia,sport of ascorbate. Ascorbate efflux from primary cultures of rat astrocytes was rapidly (within 1 min) increased by incubation in hypotonic medium. Efflux also increased when astrocytes, which had been adapted to a hypertonic environment, were swollen by transfer to isotonic medium. Swelling-induced ascorbates efflux was inhibited by the anion-transport inhibitors 4,4'-diisothiocyanostilbene-2,2 '-disulfonic acid (DIDS) and 4,4'-dinitrostilbene-2,2'-disulfonic acid (DNDS). The pathway that mediates ascorbate efflux was found to be selective because a larger anion, 2',7'-bis(carboxyethyl)-5-(or -6)-carboxyfluorescein (BCECF), was retained in the swollen astrocytes. Na(+)-dependent ascorbate uptake into astrocytes was inhibited slightly during the first minute of hypotonic stress, indicating that the sodium ascorbate cotransporter does not mediate swelling-induced efflux. Cell concentration of authentic ascorbate was measured by HPLC with electrochemical detection. When astrocytes were incubated in ascorbate-free medium, hypotonicity decreased cell ascorbate concentration by 50% within 3 min. When astrocytes were incubated in ascorbate-supplemented hypotonic medium, intracellular ascorbate concentration was restored within 10 min because uptake remained effective. Many pathological conditions cause brain cell swelling and formation of reactive oxygen species. Ascorbate release during during astrocytic swelling may contribute to cellular osmoregulation in the short-term and the scavenging of reactive oxygen species.



Amphiphilic alpha-tocopherol analogues as inhibitors of brain lipid peroxidation.

Bolkenius FN, Verne-Mismer J, Wagner J, Grisar JM
Marion Merrell Dow Research Institute, Strasbourg, France
FrankBolkenius@mmd.com
Eur J Pharmacol (Netherlands) Feb 29 1996, 298 (1) p37-43

Neurological disorders, such as stroke, trauma, tardive dyskinesia, Alzheimer's and Parkinson's diseases, may be partially attributed to excessive exposition of the nervous tissue to oxygen-derived radicals. A novel water-soluble alpha-tocopherol analogue, 2,3-dihydro-2 ,2,4,6,7-pentam ethyl-3methylpiperazino) methyl-1-benzofuran-5-ol dihydrochloride (MDL), is a potent radical scavenger. Following subcutaneous administration to mice, MDL inhibited the lipid peroxidation induced in the 100-fold diluted brain homogenates, with an ID50 of 8 mg/kg. Rapid brain penetration, within 30-60 min postadministration, and even distribution into different brain areas were observed. MDL was also detected after oral administration. In brain homogenate undergoing lipid peroxidation, MDL prevented the consumption of an equal amount of alpha-tocopherol, while inhibiting the concomitant malondialdehyde formation. The radical scavenging capacity of MDL was superior to that of alpha-tocopherol, although the peak and half-peak potentials were not significantly different. However, MDL was much less lipophilic, the partition coefficient (log P) at the octanol/water interface being 1.91. Although it is yet unknown, whether the applied criteria sufficiently predict its usefulness, beneficial effects of MDL may be expected in the above mentioned disorders.



Update on the biological characteristics of the antioxidant micronutrients: Vitamin-C, vitamin E, and the carotenoids.

Rock CL, Jacob RA, Bowen PE
Program in Human Nutrition, University of Michigan, Ann Arbor 48109-2029, USA.
J Am Diet Assoc (United States) Jul 1996, 96 (7) p693-702; quiz 703-4

Under normal circumstances, free radicals that are produced through biological processes and in response to exogenous stimuli are controlled by various enzymes and antioxidants in the body. Laboratory evidence suggests that oxidative stress, which occurs when free radical formation exceeds the ability to protect against them, may form the biological basis of several acute medical problems, such as tissue injury after trauma, and chronic conditions, such as atherosclerosis and cancer. A potential role for the antioxidant micronutrients (Vitamin-C, vitamin E, and the carotenoids) in modifying the risk for conditions that may result from oxidative stress has stimulated intense research efforts, increased interest in micronutrient supplements, and heightened consumer interest in these compounds. Much remains to be learned, however, about the bioavailability, tissue uptake, metabolism, and biological activities of these micronutrients. These biological characteristics will ultimately determine their clinical usefulness in modulating oxidative stress. Also, whether the antioxidant mechanism explains their relationship with risk for acute and chronic disease in epidemiologic studies remains to be determined. Increased knowledge in this area of nutrition science will have an impact on both clinical dietetics practice and public health nutrition guidelines.



Effect of allopurinol, sulphasalazine, and Vitamin-C on aspirin induced gastroduodenal injury in human volunteers

McAlindon ME, Muller AF, Filipowicz B, Hawkey CJ
Division of Gastroenterology, University Hospital, Nattingham.
United Kingdom Gut (United Kingdom), 1996, 38/4 (518-524)

Background - The mechanisms of aspirin induced gastroduodenal injury are not fully understood. Aspirin induces the release of reactive oxygen metabolites in animal models, which may contribute to mucosal injury.

Aims - To investigate the effects of aspirin administered with placebo or antioxidants on gastric mucosal reactive oxygen metabolite release and gastroduodenal injury in human volunteers. Subjects - Fourteen healthy volunteers participated in the study (seven male; mean age 27 years, range 20-40).

Methods - In a double blind, randomised, crossover study, volunteers received aspirin 900 mg twice daily and either placebo, allopurinol 100 mg twice daily, sulphasalazine l g twice daily or Vitamin-C 1 g twice daily for three days. Injury was assessed endoscopically and by quantifying mucosal reactive oxygen metabolite release by measuring chemiluminescence before and after each treatment. The effect on prostanoids was determined by measuring ex vivo antral prostaglandin E2 (PGE2) synthesis and serum thromboxane B2 (TXB2).

Results - No drug reduced any parameter of gastric injury but Vitamin-C reduced duodenal injury assessed by Lanza score (p < 0.005). Chemiluminescence increased after aspirin both with placebo (p < 0.05) and vitamin C (p < 0.05). Post-treatment chemiluminescence was lower in subjects taking allopurinol (p < 0.05) or sulphasalazine (p < 0.005) than in those taking placebo with aspirin.

Conclusions - In this study, aspirin induced gastric injury was associated with reactive oxygen metabolite release. This was reduced by sulphasalazine and allopurinol, although macroscopic injury was not affected. Vitamin-C, however, was shown to have a previously unrecognised protective effect against aspirin induced duodenal injury.



Hemodynamic effects of delayed initiation of antioxidant therapy (beginning two hours after burn) in extensive third-degree burns

Tanaka H, Hanumadass M, Matsuda H, Shimazaki S, Walter RJ, Matsuda T
Burn Center, Cook County Hospital, Chicago, IL 60612, USA.
Journal of Burn Care and Rehabilitation (USA), 1995, 16/6 (610-615)

The hemodynamic effects of the delayed initiation of antioxidant therapy with high-dose Vitamin-C were studied in 12 guinea pigs with third-degree burns over 70% of their body surface area. All animals were resuscitated with Ringer's lactate solution (RE) according to the Parkland formula (4 ml/kg/% burn during the first 24 hours) from one-half to 2 hours after burn, and the infusion rate was reduced thereafter to 23% of that of the Parkland formula. The Vitamin-C group (n = 6) received RL with Vitamin-C (14 mg/kg/hr), and the control group (n = 6) received RE only. The 24-hour fluid intake for each group was 32.5% of the Parkland formula volume. Burn wound edema in the Vitamin-C group was significantly less than that in the control group. The Vitamin-C group maintained adequate hemodynamic stability as determined with hematocrit and cardiac output values, but the control group did not. Even though the initiation of the Vitamin-C administration is delayed until 2 hours after burn, the hourly infusion rate of the resuscitation fluid can be reduced to 25% once it is started. Thus antioxidant therapy with adjuvant Vitamin-C administration may be applicable to the clinical setting in which a patient with burns arrives at the burn care facility a few hours after the burn injury occurred.



Dietary intake and plasma levels of antioxidant vitamins in health and disease: A hospital-based case-control study

Singh R, Niaz M, Ghosh S, Beegum R
Journal of Nutritional and Environmental Medicine (United Kingdom), 1995, 5/3, p 235

Of 1667 subjects that attended the hospital, 1335 were patients with diagnosed medical conditions, together with 202 randomly selected apparently healthy controls from the same population, were studied in detail for demographic variables, dietary and biochemical data. Dietary consumption of antioxidant vitamins A, E, and C and beta-carotene and soluble fibre was lower in the majority of conditions compared to controls. Plasma concentrations of Vitamin-C and beta-carotene were significantly lower in all patient groups. Reduced vitamin E levels were noted in patients with cardiovascular diseases, stroke, Parkinson's disease, chronic renal failure, nephrotic syndrome, type A behaviour, post-partum psychosis, burns, liver diseases, cancer, rheumatoid arthritis and aluminium phosphide poisoning. Lipid peroxides (thiobarbituric acid reactive substances), which are an indicator of oxygen-derived free radical damage, were significantly higher than controls in most conditions and marginally higher in respiratory and psychiatric conditions. Lipid peroxides levels were much greater over all in acute myocardial infarction, cancer, stroke, nephrotic syndrome, chronic renal failure, liver diseases, post-partum psychosis, pregnancy, burns and aluminium phosphide poisoning. Pool dietary intake alone does not explain the decreases in plasma levels of antioxidants and increases in lipid peroxides. Decreases may also be due to increased demands for antioxidants to counter free radical damage.



Vitamin-C and pressure sores

Galley H
Journal of Dermatological Treatment (United Kingdom), 1995, 6/3, p 195

This review describes 50 years of studies on the relationship between Vitamin-C and wound healing. Several early studies in animals reported a clear link between Vitamin-C depletion and impaired wound healing, shown later to be due to an effect on collagen synthesis. Further clinical studies found that supplementary Vitamin-C improves wound healing even in apparently Vitamin-C-replete individuals. Associations between Vitamin-C and pressure sore development, and healing of pre-existing pressure sores have been described, suggesting a therapeutic role for Vitamin-C supplementation. However, this would be complementary to current nursing and skin care strategies in patients with, or at risk of developing, pressure sores, such as those elderly patients admitted with femoral neck fractures, or paraplegic subjects.


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