Tuesday, July 3, 2007

More in Vitamin C

Natural killer cell activity
An in vivo effect of ascorbic acid on enhancement of
human natural killer cell activity has been reported
at a dosage of 60 mg per kg body weight (Vojdani &
Ghoneum, 1993).
19.10.8 Regulation of the complement
component C1q
When guinea pigs were fed tissue-saturating amounts
of vitamin C, plasma C1q concentrations were signifi -
cantly higher than in those animals fed only enough
ascorbate for adequate growth and for the prevention
of scurvy (Haskell & Johnston, 1991). When healthy
men and women were given 500 mg ascorbate three
times daily with meals for 4 weeks, their plasma C1q
levels were not signifi cantly altered (Johnston, 1991).
Hence, signifi cantly enhanced C1q production may
occur only during activation of the immune system,
and not in healthy, non-infected individuals.
19.10.9 Enhancement of lymphocyte blastogenesis
Using cultured spleen cells from an inbred strain of
rat that does not synthesize vitamin C, Oh & Nakano
(1988) observed that ascorbic acid enhanced
lymphocyte blastogenesis through inhibition of the
biosynthesis of immunosuppressive histamine.
19.10.10 Enhancement of interferon
The participation of vitamin C in protection against
some viral infections may be in the enhancement of
interferon biosynthesis as demonstrated in vivo and
in vitro. The level of circulating interferon induced
in mice by inoculation with leukaemia virus was enhanced
by the addition of ascorbate to the drinking
water (Siegel, 1974). Ascorbate also enhanced the interferon
levels produced by cultured human embryo
fi broblasts in response to Newcastle Disease virus
(Dahl & Degré, 1976; Karpin´ ska et al., 1982).
19.10.11 Regulation of cytokines
Vitamin C has an indirect effect on lymphocyte proliferation
through its action on cytokines, as shown in
vitro by Cunningham-Rundles et al. (1993). Ascorbic
acid suppressed proliferation response to interleukin-
2, suggesting a basis for the vitamin’s inhibitory effect
on mitogen-induced lymphocyte proliferation. In
contrast, ascorbic acid enhanced the proliferative
response to interferon-γ, without inhibiting the
production of interferon-γ that accompanied the response
to infl uenza A (Table 19.4).
19.10.12 Clinical application to immunodeficiency diseases
Anderson (1981) administered a single oral daily dose
of 1 g sodium ascorbate to three children suffering
from chronic granulomatous disease as a supplement
to prophylactic trimethoprim–sulphamethoxazole
therapy for 2 years. In all three patients, introduction
of ascorbate to the therapeutic regimen resulted in the
correction of defective neutrophil motility and increased
activity against staphylococci. These responses
were accompanied by a decrease in the frequency of
infection and increased weight and growth rate.

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