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Mechanisms and Biomarkers (WG 4) page 31
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Polyphenols and flavonoids quercitin,
kaempferol chlorogenic acid and pcoumaric
acid
Biomarkers of oxidative stress and injury.
deficiency causes neurodegeneration
(Traber et al., 1987). In the absence of
regenerating antioxidants such as vitamin
C and glutathione this vitamin can behave
as a pro-oxidant (Stocker, 1999).
In vitro studies indicate potent
antioxidant, metal-chelating, and RS
scavenging properties of these plant.
products (Salah et al., 1995). Can act as
pro-oxidants in the presence of Fe 3+ or
Cu 2+ ions (Rahman et al., 1989). Sparse
data on absorption and bioavailability but
uptake from tea and wine supports a role
for these compounds in the protective
function of these beverages, and other
sources like tomatoes. (Weisburger,
1995; Goldberg, 1995).
The perceived wisdom that antioxidants protect against cancer and cardiovascular diseases is
based on the well demonstrated fact that free radicals and RS are constantly produced in the
human body. Their removal by endogenous mechanisms and dietary antioxidants is never
complete, nor is the repair of damaged cellular components. This supports the notion that
these diseases are largely the consequence of long-term exposure to RS which are major
contributors to the age-related development of these conditions. It then follows that
biomarkers of oxidative damage should be significant indicators of intermediate risk in both
conditions. It is well established that free radical damage to LDL-lipids is associated with the
development of atherosclerosis, which is a risk factor of myocardial infarction,stroke, and
general vascular disease (Steinberg and Lewis, 1997). End products of lipid peroxidation can
bind to DNA to yield mutagenic lesions (El Ghissassi et al., 1995), and several RS can react
directly with DNA to cause oxidative mutations (Kasai, 1997). It should be noted that radical
oxidation of proteins may play a crucial role in the progression of many diseases. However,