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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