National Academy of Sciences
References
141. Biomed Biochim Acta
1991;50(3):265-72
Effect of ascorbic acid on hydroxyl radical generation by
chemical, enzymatic and cellular systems. Importance for
antioxidant prevention of pulmonary emphysema.
Nowak D, Piasecka G, Antczak A, Pietras T
Department of Pneumonology and Allergology, Medical Academy,
Lodz, Poland.
The ability of ascorbic acid (AA) (25 to 500 microM) to
increase OH production
by a chemical (Fe(2+)-EDTA-H2O2), an enzymatic
(xanthine-xanthine
oxidase-Fe(2+)-EDTA) and a cellular system (3.10(6) human
polymorphonuclear
leukocytes (PMNL) or murine peritoneal macrophages (PM)
activated with 7.2 ng
PMA/ml) was studied. At all concentrations used AA strongly
enhanced OH
generation by the chemical and the enzymatic systems.
However, the maximal
increase of about 14-fold was found for incomplete chemical
system (10 microM
Fe(2+)-20 microM EDTA) and 500 microM AA. In the case
of
phorbol-myristate-acetate-activated-PMNL and macrophages,
the moderate increase
in OH formation was only caused by low AA concentrations. At
50 microM AA, the
OH formation was 112 +/- 3 and 117 +/- 4% of control,
respectively. Higher AA
concentrations had no influence or even decreased OH
formation by phagocytes. It
is suggested that administration of AA will not
significantly enhance OH
generation from pulmonary phagocytes and could be useful for
prevention of the
oxidant-mediated lung injury related to inflammation.
142. J Pharm Sci 1990
Oct;79(10):913-5
Oxidation kinetics of an antiasthmatic,
2-[(4-hydroxyphenyl)amino]-5-methoxybenzenemethanol, and
stabilization with ascorbic acid.
Yu AB, Portmann GA
Pharmaceutical Sciences, Sterling Drug, Inc., Rensselaer, NY
12144.
A novel antiasthmatic,
2-[(4-hydroxyphenyl)amino]-5-methoxybenzenemethanol
(1),
oxidizes to the corresponding iminoquinone in aqueous
solutions. The reaction
was monitored by a paired-ion reversed-phase HPLC method.
The oxidation rate was
highly dependent on the solution pH, with a large rate
increase occurring above
pH 6.1. In nonaqueous solution, the oxidation reaction was
significantly slower.
Ascorbic acid protects 1 from oxidation. The aqueous
solution of the decomposed
product is reduced to 1 in the presence of ascorbic
acid.
143. S Afr Med J 1983 Apr
23;63(17):649-52
Ascorbic acid in bronchial asthma.
Anderson R, Hay I, van Wyk HA, Theron A
Sixteen White children with bronchial asthma were divided
into two groups; one
received standard anti-asthma chemoprophylaxis (SAC) and the
other SAC
supplemented with 1 g ascorbic acid (Redoxon) given as a
single daily dose for a
6-month period. In 10 patients the effects of ascorbic acid
on exercise-induced
bronchoconstriction (EIB) were assessed by comparing the
pre-ascorbic acid
results with those obtained 2 1/2 hours after the
intravenous injection of 1 g
ascorbic acid. Immunological investigations performed on the
two groups were
assessment of polymorphonuclear leucocyte (PMNL) motility,
phagocytosis and
nitroblue tetrazolium reduction and measurement of secretory
IgA, serum
immunoglobulin and total haemolytic complement levels and
levels of the
components C3 and C4, alpha 1-antitrypsin, antistreptolysin
O (ASO), C-reactive
protein and antibodies to certain respiratory viruses. These
investigations were
performed before and 1, 3 and 6 months after the
commencement of therapy. Radio-allergosorbent testing for
sensitivity to four common allergens was
carried out at the outset and after 6 months of therapy.
Injection of ascorbic
acid had no detectable effects on the degree of EIB. Slight
but not significant
immunological changes were observed in the SAC group over
the 6-month study
period. However, in the SAC plus ascorbic acid group
significantly improved PMNL
motility and decreased ASO levels and reduced (although not
to a significant
extent) IgE levels and titres of antibodies to the
respiratory viruses were
observed.
144. Am Rev Respir Dis 1983
Feb;127(2):143-7
Effect of ascorbic acid on response to methacholine
challenge in asthmatic subjects.
Mohsenin V, Dubois AB, Douglas JS
We studied the effect of ascorbic acid in 14 mild
asthmatic subjects. The effect
of ascorbic acid (1.0 g orally) was assessed by the changes
in concentration of
methacholine required to decrease the specific airway
conductance by 40% (pD40).
Ascorbic acid increased pD40 from control values of 9.38
1.97 mg/ml mean SEM) to 12.59 mg/ml 2.52 (p less than 0.05).
Administration of 50 mg of
indomethacin, orally, reversed the effect of ascorbic acid.
Indomethacin alone
had no effect on the mean pD40. The results suggest that
ascorbic acid exerts
its effect via alteration of arachidonic acid
metabolism.
145. Plucne Bolesti 1991
Jan-Jun;43(1-2):94-7
[Effect of vitamin C on exercise-induced
bronchoconstriction].
[Article in Serbo-Croatian (Roman)]
Miric M, Haxhiu MA
Institut za klinicku fiziologiju, Medicinski fakultet,
Pristina.
The effect of vitamin C on exercise-induced airway
constriction was studied.
Pretreatment with ascorbic acid prevented the significant
alteration in airway
geometry induced by exercise asthmatic patients. These
results suggest that
vitamin C deficiency might augment airway responses to
exercise and other
bronchospasmogenic factors, and treatment with vitamin C may
decrease airway
hyperresponsiveness.
146. S Afr Med J 1980 Dec
13;58(24):974-7
The effect of ascorbate on cellular humoral immunity in
asthmatic children.
Anderson R, Hay I, van Wyk H, Oosthuizen R, Theron A
Ten White children with bronchial asthma and
exercise-induced
bronchoconstriction were assessed immunologically before and
1, 3 and 6 months
after the commencement of standard therapy supplemented with
ascorbate 1 g/d.
The tests of cellular immune function were neutrophil
chemotaxis, phagocytosis
and resting and stimulated nitroblue tetrazolium reduction,
and lymphocyte
mitogen-induced transformation. Humoral functions measured
were secretory IgA,
serum immunoglobulins, alpha 1-antitrypsin, C3, C4 and total
haemolytic
complement, antistreptolysin O (ASO) and C-reactive
protein.
Radio-allergosorbent testing to the common allergens Cynodon
dactylon (grass),
Dermatophagoides pteronyssinus (mite), house dust and cat
epithelium was
performed on each child before and 3 and 6 months after
treatment. Two children
had depressed neutrophil motility, 4 had depressed
lymphocyte transformation,
and 7 had elevated levels of ASO. These functions normalized
after 6 months of
ascorbate-supplemented therapy. Serum total IgE levels but
not specific IgE
levels were likewise reduced after 6 months of therapy.
Reduced levels of serum
alpha 1-antitrypsin were observed in 2 children, and
remained unchanged
throughout the study.
147. Trop Geogr Med 1980
Jun;32(2):132-7
High dose ascorbic acid in Nigerian asthmatics.
Anah CO, Jarike LN, Baig HA
Forty-one asthmatic patients in remission were randomly
allocated to two
treatment groups in a double-blind trial. One group took 1
g, of ascorbic acid
as one effervescent tablet once daily and the second group
took a matching
placebo. The asthmatics were selected from those attending
the Asthma Clinic.
One criterion for selection was the increase in exacerbation
during the rainy
season. These exacerbations were precipitated by respiratory
infection. After 14
weeks, an assessment of the severity and rate of attacks
showed that those on
ascorbic acid suffered less severe and less frequent attacks
of asthma during
the study period. Plasma ascorbic acid astimations showed a
significant rise in
the level in those taking ascorbic acid over those on
placebo. (P < 0.01).
Cessation of ascorbic acid in the group taking it increased
attack rates. It is
concluded that high dose ascorbic acid is probably a good
prophylaxis in some
bronchial asthmatics.
148. Am J Epidemiol 1998 Jul
1;148(1):45-50
Cohort study of vitamin C intake and cognitive
impairment.
Paleologos M, Cumming RG, Lazarus R
Department of Public Health and Community Medicine, Faculty
of Medicine,
University of Sydney, New South Wales, Australia.
To test the hypothesis that vitamin C protects against
cognitive impairment, the
authors conducted a cohort study (n=117) in a retirement
community in Sydney,
Australia. Vitamin C intake was assessed at baseline (1991)
with a
semiquantitative food frequency questionnaire, and cognitive
function was
assessed 4 years later (1995). After adjustment for age,
sex, smoking,
education, total energy intake, and use of psychotropic
medications, consumption
of vitamin C supplements was associated with a lower
prevalence of more severe
cognitive impairment (based on scores on the Mini-Mental
State Examination;
adjusted odds ratio=0.39, 95% confidence interval
0.18-0.84). There were no
associations between vitamin C intake and scores on tests of
verbal and category
fluency. This study suggests that vitamin C might protect
against cognitive
impairment.
149. Am J Clin Nutr 2000
May;71(5):1194-200
Direct correlation of glutathione and ascorbate and their
dependence on age and season in human lymphocytes.
Lenton KJ, Therriault H, Cantin AM, Fulop T, Payette H,
Wagner JR
Centre de Recherche, Institut Universitaire de Geriatrie de
Sherbrooke,
Sherbrooke, Canada, and Unite de Recherche Pulmonaire,
Centre de Sante de l'Estrie, Fleurimont, Canada.
BACKGROUND: Endogenous reactive oxygen species appear to
contribute to aging and
cancer and dietary antioxidants, present in fruit and
vegetables, counteract
these effects. OBJECTIVE: The objective was to examine the
association between
intracellular glutathione, ascorbate (vitamin C), and
alpha-tocopherol (vitamin
E) in human lymphocytes. DESIGN: The study group consisted
of 240 healthy
nonsmoking volunteers with an approximately equal number of
male and female
subjects subdivided into 3 age groups: 18-39, 40-59, and
>/=60 y). Glutathione,
glutathione disulfide, ascorbate, and alpha-tocopherol were
measured in
lymphocytes by HPLC. RESULTS: The average concentration of
antioxidants in
lymphocytes was 27 8 nmol/mg protein for glutathione, 21 8
nmol/mg
protein for ascorbate, and 0.4 0.2 nmol/mg protein for
alpha-tocopherol.
There was a strong positive correlation between glutathione
and ascorbate (r =
0.62, P < 0.001). No correlation was observed for
glutathione and ascorbate with
alpha-tocopherol. The concentration of glutathione in
lymphocytes was inversely
correlated with age (r = -0.19, P < 0.01), as was that of
ascorbate (r = -0.22,
P < 0.01), with 10-20% lower values in elderly than in
young and elderly
subjects. The concentrations of glutathione in lymphocytes
were as much as 25%
higher and those of ascorbate were as much as 38% higher
during the summer than
during the winter. The seasonal variation of ascorbate in
lymphocytes was
described by a linear function for age and a periodic sine
function for season.
CONCLUSION: Glutathione and ascorbate are directly
correlated in human
lymphocytes.
150. J Pediatr 1994
Feb;124(2):229-33
Effect of ascorbate or N-acetylcysteine treatment in a
patient with hereditary glutathione synthetase
deficiency.
Jain A, Buist NR, Kennaway NG, Powell BR, Auld PA,
Martensson J
Department of Internal Medicine, Greenwich Hospital/Yale
University School of Medicine, CT 06830-4697.
A 45-month-old girl with 5-oxoprolinuria (pyroglutamic
aciduria), hemolysis, and
marked glutathione depletion caused by deficiency of
glutathione synthetase was
followed before and during treatment with ascorbate or
N-acetylcysteine. High
doses of ascorbate (0.7 mmol/kg per day) or N-acetylcysteine
(6 mmol/kg per day)
were given for 1 to 2 weeks without any obvious deleterious
side effects.
Ascorbate markedly increased lymphocyte (4-fold) and plasma
(8-fold) levels of
glutathione. N-Acetylcysteine also increased lymphocyte
(3.5-fold) and plasma
(6-fold) levels of glutathione. After these treatments were
discontinued,
lymphocyte and plasma glutathione levels decreased rapidly
to pretreatment
levels. Ascorbate treatment was extended for 1 year, and
lymphocyte (4-fold) and
plasma (2- to 5-fold) glutathione levels remained elevated
above baseline. In
parallel, the hematocrit increased from 25.4% to 32.6%, and
the reticulocyte
count decreased from 11% to 4%. The results demonstrate that
ascorbate and
N-acetylcysteine can decrease erythrocyte turnover in
patients with hereditary
glutathione deficiency by increasing glutathione levels.