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Antioxidants are thought to be important in protecting against damage from
active oxygen species. The effects of the antioxidant nutrients vitamins C and E
have been investigated after bleomycin treatment in the Salmonella typhimurium
bacterial mutation assay, in the human peripheral lymphocyte chromosome
aberration assay, and in the mouse micronucleus assay in peripheral blood and
bone marrow cells. There were no protective effects from vitamins C and E in the
bacterial mutation assay, but vitamin C and not vitamin E abolished chromosome
damaging responses in human peripheral lymphocytes, and both vitamins reduced
responses in micronuclei from peripheral blood cells in mice. This would suggest
that in human cells in vitro and mouse cells in vivo these vitamins could have a
protective role.

The study focuses on the assessment of chromosomal damage associated with folate
and vitamin B12 deficiency, and with cigarette smoking in a tissue directly
exposed to cigarette smoke (buccal mucosa) while controlling for potential
confounding factors. A cross-sectional study was carried out among 39 current
smokers (CSs) and 60 noncurrent smokers (NCSs). Buccal mucosal cells, saliva,
and blood samples were collected from each subject. The Health Habits and
History Questionnaire (Block et al., 1986) was modified to obtain dietary and
other relevant information. Methods used to measure folate, vitamin B12 levels,
and the frequency of micronucleated cells in buccal mucosal cells gave
reproducible results. The study results suggest that CSs have buccal mucosal
folate and vitamin B12 levels that are lower than those among NCSs. CSs were
three times more likely to have micronucleated buccal mucosal cells compared to
NCSs. There appeared to be no association between low buccal folate and vitamin
B12 levels chromosomal damage. The salivary vitamin B12 concentrations and
plasma vitamin C and E concentrations, however, seem to be marginally protective
against the occurrence of buccal mucosal micronuclei, whereas plasma
beta-carotene seems to increase the occurrence of micronuclei. Overall, the
results do not support the concept that localized folate and vitamin B12
deficiencies in the buccal mucosal cells of smokers are associated with
chromosomal damage in those cells. The presence of vitamin B12 deficiencies in
the buccal mucosal cells of smokers are associated with chromosomal damage in
those cells. The presence of vitamin B12 in the immediate environment (saliva)
and vitamin C and E in the plasma, however, appear to be marginally protective
against chromosomal damage in buccal mucosal cells.

A regular dose of 10 mg/kg body wt/day of vitamin C as a part of the daily diet
markedly reduced T-2 toxin-induced abnormalities in the chromosomal cells in
mice (Mus musculus). The preventive effect on individual types of change in
chromosomes such as breakages, chromatid gaps, ring formations and widespread
fragmentation, was increased.

Some chemotherapeutic approaches have proposed the use of antioxidants such as
vitamin C (VC) to minimize the cytotoxicity and damage induced in normal tissue
by antitumor agents that produce free radicals. Nevertheless, VC can also be
cytotoxic, genotoxic, and harmful when combined with antitumor agents in human
cells in vitro. The present study was undertaken to investigate the effects of
VC (100, 200, 500, and 1,000 microg/ml) on human peripheral blood lymphocytes in
vitro and its anticlastogenic effect on chromosomal aberrations induced by
doxorubicin (DXR). VC did not show a clastogenic effect by itself, except at
1,000 microg/ml. At the concentration of 100 or 200 microg/ml of VC,
administered in pre-, post-, or simultaneous treatment, there was a significant
reduction in both chromosome aberrations and number of abnormal metaphases
induced by DXR. At the doses of 500 or 1,000 microg/ml, VC did not present the
same protective effect and was cytotoxic. Under the present experimental
conditions, the efficiency of VC in protecting against chromosome damage was
dependent on the doses used.

Helicobacter pylori (HP), undoubtedly, the most common world-wide infection
plays an important role in pathogenesis of peptic ulcer. Proof for a causal role
for HP in peptic ulcer rests in two major points; 1) the majority of ulcer
patients are HP infected and the prevalence of this infection for both gastric
ulcer (GU) and duodenal ulcer (DU) is much higher than for gender- and
age-adjusted controls and 2) the cure of HP infection dramatically reduces ulcer
recurrence. Conclusions regarding the mechanisms by which HP induces peptic
ulcer are restricted mainly to studies observing the consequences of its
eradication by antibiotics combined with gastric inhibitors or bismuth agents.
Several specific virulence factors such as cytotoxin-associated gene A (CagA)
and vacuolating cytotoxin A (VacA) as well as other noxious substances including
ammonia, lipopolysaccharide (endotoxin), platelet activating factor (PAF),
nitric oxide (NO) and others have been implicated in gastritis and were found to
be significantly more frequent in gastric cancer than in gender- and age-matched
controls, especially in younger generation. Chronic inflammation, atrophic
gastritis, intestinal metaplasia, impaired defense mechanisms combined with
hypergastrinemia, deficiency of vitamin C in the stomach , excessive oxygen
metabolites and epithelial cell proliferation have been associated with gastric
cancer. This multi-step pathway originally proposed by Correa and his
colleagues, long before the HP was discovered in the stomach, leads to cancer
but may be reversed by eradication of HP. This is, however, a controversial
issue because gastric atrophy and intestinal metaplasia may be also caused by
other factors such as bile reflux, dietary irritants, and autoimmunity. The
implication of HP in MALT-lymphoma is based on the observations that eradication
of HP in early stage of low-grade of this tumor leads to complete remission. The
significance of HP in non-ulcer dyspepsia remains questionable and requires
further studies.

Helicobacter pylori is a gram-negative bacterium affecting about half of the
world population, causing chronic gastritis type B dominated by activated
phagocytes. In some patients the disease evolves into gastric ulcer, duodenal
ulcer, gastric cancer or MALT lymphoma. The pathogenesis is in part caused by
the immunological response. In mouse models and in human disease, the mucosal
immune response is characterized by activated phagocytes. Mucosal T-lymphocytes
are producing IFN-gamma thus increasing mucosal inflammation and mucosal damage.
A low dietary intake of antioxidants such as carotenoids and vitamin C may be an
important factor for acquisition of H. pylori by humans. Dietary antioxidants
may also affect both acquisition of the infection and the bacterial load of H.
pylori infected mice. Antioxidants, including carotenoids, have
anti-inflammatory effects. The aim of the present study was to investigate
whether dietary antoxidant induced modulation of H. pylori in mice affected the
cytokines produced by H. pylori specific T-cells. We found that treatment of H.
pylori infected mice with an algal cell extract containing the antioxidant
astaxanthin reduces bacterial load and gastric inflammation. These changes are
associated with a shift of the T-lymphocyte response from a predominant
Th1-response dominated by IFN-gamma to a Th1/Th2-response with IFN-gamma and
IL-4. To our knowledge, a switch from a Th1-response to a mixed Th1/Th2-response
during an ongoing infection has not been reported previously.

BACKGROUND: Maori and Pacific Island ethnic groups in New Zealand have a high
risk for gastric cancer. Low levels of gastric juice ascorbic acid (vitamin C)
have been suggested to be a risk factor for gastric cancer. Previous studies
have shown that gastric juice ascorbic acid may be independently associated with
both ethnicity and Helicobacter pylori infection. This study aimed to examine
the interrelationship between H. pylori and ethnicity in New Zealand. METHODS:
Gastric juice was collected into 70% perchloric acid preservative and stored at
-80 degrees C. Ascorbic acid was analysed by high-performance liquid
chromatography using ion-pair chromatography and electrochemical detection.
Inflammation and atrophy was graded from biopsies from multiple sites in the
antrum and body. Gastric juice was collected from 89 patients during routine
endoscopy. RESULTS: There was a wide range of measured gastric juice ascorbic
acid from 0.001 to 410 microg/mL. The median concentration of ascorbic acid for
H. pylori-negative patients was 1.78 microg/mL (n = 57) and 0.12 microg/mL (n =
32) for H. pylori-positive patients (P = 0.001). Gastric juice ascorbic acid
concentration was not associated with age, endoscopic diagnosis or intestinal
metaplasia, but was significantly associated with the degree of acute
inflammation (P = 0.01) and the presence of atrophy (P = 0.04).The median
ascorbic acid concentration for European patients was 0.92 microg/mL (n = 44)
and 0.09 microg/mL (n = 38) for Maori and Pacific Island ethnic groups combined
(P = 0.1). Multiple step-wise regression analysis showed that only H. pylori
infection was a significant factor for predicting ascorbic acid concentrations
(r2 = 0.12). CONCLUSIONS: This study has confirmed that gastric juice ascorbic
acid concentration is lower in the presence of H. pylori infection.

BACKGROUND: To date it is not known whether gastric juice vitamin C levels are
influenced by Helicobacter pylori CagA(+) strains. The aim of the present study,
therefore, was to study the impact of H. pylori CagA status on gastric juice
vitamin C levels. MATERIALS AND METHODS: We studied 30 H. pylori(+) patients,
and the results were compared with 10 endoscopically and histologically normal
H. pylori(-) subjects (control group) who were similar to the H. pylori(+) group
in terms of age and sex. In all patients, gastric juice vitamin C levels were
determined and the severity of gastritis was graded on a scale of 0 (absent) to
3 (severe). CagA was determined by immunoblotting the sera from patients against
H. pylori antigens. RESULTS: Among 30 H. pylori(+) patients, 20 were CagA(+) and
10 CagA(-). In the entire group of H. pylori(+) patients, the median gastric
juice vitamin C levels (mg L-1) were 16.35 (range 3.5-33.6) and were
significantly lower (P < 0.001) than in the control group of H. pylori(-)
patients [35.5 (23.1-50.2)]. In addition, in the entire group of H. pylori(+)
patients there was a highly significant (P < 0.0001) inverse correlation between
the gastritis activity score and the gastric juice vitamin C levels. In the
group of H. pylori CagA(+) patients, the median levels of gastric juice vitamin
C were 13.8 (3.5-31.2) and were significantly lower than the corresponding
levels in both the H. pylori CagA(-) group [24.8 (22-33.6), P < 0.01] and the H.
pylori(-) control group [35.5 (23.1-50.2), P < 0.001], the last groups being
similar. Furthermore, the gastritis activity median score in the H. pylori
CagA(+) group [2 (1-3)] was significantly higher (P < 0.05) than in the H.
pylori CagA(-) group [1 (1-2)]. CONCLUSION: These data indicate that infection
with CagA(+) H. pylori strains significantly lowers the gastric juice vitamin C
levels in comparison with CagA(-) H. pylori strains, which might have a
significant impact on gastric carcinogenesis.

Low gastric juice total vitamin C concentration in the presence of Helicobacter
pylori (H. pylori) infection probably plays a role in gastric carcinogenesis. In
vitro vitamin C has been shown to inhibit the growth of H. pylori. The aims of
this study were to determine the effect of high dose vitamin C administration on
H. pylori infection and on gastric juice total vitamin C concentration in
patients with H. pylori related chronic gastritis. Sixty patients with dyspeptic
symptoms and proven chronic gastritis and H. pylori infection, who were
undergoing routine endoscopy, entered the study after giving informed consent.
They were randomly coded into two treatment groups. Group 1 (controls, n = 28)
were treated with antacids for 4 weeks and Group 2 (n = 32) received vitamin C
5g daily also for 4 weeks. Nine patients did not complete the study and were
excluded. Plasma and gastric juice total vitamin C levels were measured at
baseline, at the end of 4 weeks treatment and again 4 weeks after treatment
cessation. In the control group H. pylori infection remained unchanged in all 24
patients throughout as did the mean gastric juice total vitamin C concentration.
However, in the vitamin C treated group eight of 27 patients (30%) who completed
the treatment course the H. pylori infection was eradicated (P = 0.01). In these
patients the mean gastric juice total vitamin C concentration rose significantly
from 7.2 1.6 micrograms/ml after 4 weeks treatment (P < M 0.001) and 19.8
micrograms/ml 4 weeks after treatment was discontinued (P < 0.001). In the
remaining 19 patients with persistent H. pylori infection, the mean gastric
juice total vitamin C concentration rose less than in those with successful H.
pylori eradication; 6.3 1.7 micrograms/ml before treatment, 10.8 1.5
micrograms/ml after 4 weeks treatment (P < 0.05) and a return to pre-treatment
levels (7.1 2.7 micrograms/ml) 4 weeks after vitamin C intake stopped. There
were no side effects of vitamin C treatment. This study has shown that 4 weeks
daily high dose vitamin C treatment in H. pylori infected patients with chronic
gastritis resulted in apparent H. pylori eradication in 30% of those treated. In
those patients there was also a highly significant rise in gastric juice total
vitamin C concentration which persisted for at least 4 weeks after the treatment
ceased. A significant, though less marked, gastric juice total vitamin C
concentration increase was observed during vitamin C treatment even in subjects
with persistent H. pylori infection, though this was not maintained after
treatment ended. The mechanism whereby vitamin C treatment appeared to result in
H. pylori eradication is unclear. Further confirmatory studies are indicated.

BACKGROUND: Vitamin C may be protective against gastric cancer though infection
with Helicobacter pylori is associated with a reduction in intragastric
concentrations of vitamin C. AIMS: To examine the effects of H pylori infection,
gastric juice pH, the severity and extent of gastric inflammation, and CagA
antibody status of the individual on gastric juice and mucosal vitamin C
concentrations. PATIENTS: One hundred and fifteen patients undergoing routine
gastroscopy for investigation of dyspepsia. METHODS: High performance liquid
chromatography was used to determine vitamin C concentrations. CagA antibody was
detected by western blot analysis. RESULTS: Gastric juice ascorbic acid
concentration was significantly lower in patients infected with H pylori
compared with those uninfected (19.3 mumol/l (interquartile range (IQR)
10.7-44.5) versus 66.9 mumol/l (IQR 24.4-94.2), p = 0.003). The reduction in
gastric juice ascorbic acid concentration was inversely related to the severity
of gastritis (p = 0.01). CagA positive patients had significantly lower gastric
juice ascorbic acid concentrations than CagA negative ones (14.8 mumol/1 (IQR
7.9-52.2) versus 39 mumol/l (IQR 19.9-142.2), p = 0.05). Decreased gastric juice
dehydroascorbic acid concentrations were observed in patients with gastric
atrophy and intestinal metaplasia. Mucosal ascorbic acid concentrations were
also significantly lower in infected patients than uninfected patients (p =
0.04). CONCLUSIONS: The reduction in gastric vitamin C concentrations is related
to gastric juice pH, the severity and extent of gastritis, the presence of H
pylori, and the CagA antibody status of the individual. These findings may have
implications in H pylori associated carcinogenesis.