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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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