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metabolism.
However, under pathological conditions ROS production can increase, surpassing
the
body’s detoxification capacity and thus contribute to molecular-level organic
pathology.
External
sources of free radicals include exposures to environmental toxins such
as ionizing
radiation,
ozone and nitrous oxide, cigarette smoke (including passive inhalation)
and heavy
metals,
as well as dietary intake of excess alcohol, unsaturated fat, and other
chemicals and
compounds
present in food and water.
Antioxidants
are chemical compounds that can bind to free radicals and thus prevent
them from
damaging
healthy cells. Antioxidants can be divided into enzymatic and non-enzymatic
subtypes.
Several
antioxidant enzymes are produced by the body, with the three major classes
being
catalase,
the glutathione (GSH) peroxidases, and the superoxide dismutases (SODs).
Non-enzymatic
antioxidants include the innate compound glutathione as well as antioxidant
vitamins
obtained through the diet, such as  -tocopherol
(vitamin E), ascorbic acid (vitamin C),
and  -carotene.
Measurement
Because
free radicals are unstable, and difficult to measure, traditional indices
of oxidative stress
include
downstream markers of oxidative damage to macromolecules such as lipids,
proteins and
DNA.
Oxidative stress is also indirectly assessed by estimating capacity for
antioxidant defense
in
serum, plasma, or other body fluids. Such measures include assessment
of enzymatic
antioxidant
activity, individual quantitative assessment of circulating non-enzymatic
antioxidant
levels,
and estimation of total antioxidant status (ability of antioxidants in
the blood to neutralize
a
pro-oxidant compound in vitro). Tables 1 and 2 below list a number
of commonly used
measures
of oxidative damage and antioxidant defense, their availability in biological
samples,
and
frequently used assays. These tables provide neither exhaustive catalogues
of all available
oxidative
stress measures, nor recommendations for which measures to employ.
Rather, they
provide
an overview of the types of measures commonly used in research.
Table
1. Biomarkers of oxidative damage
Table
2. Antioxidant measures
CSF=
cerebrospinal fluid; ELISA = enzyme-linked immunosorbant assay; FRAP =
ferric reducing
ability
of plasma; GC/MS = gas chromatography/mass spectrometry; HPLC = high performance
liquid
chromatography; HPLC-EC = high performance liquid chromatography with electrochemical
detection;
HPLC-MS/MS = high performance liquid chromatography/mass spectroscopy;
ORAC =
oxygen
radical absorbance capacity; RBC = red blood cell; TEAC = trolox equivalent
antioxidant
capacity;
TRAP = total radical trapping antioxidant parameter
Physiological
Mechanisms
The
single unpaired electron characteristic of free radicals contributes to
the instability and high
reactivity
of these chemical species. Interaction of free radicals with other
compounds results in
a
chain reaction of oxidation and reduction wherein uncharged molecules consecutively
lose and
gain
electrons. Changes in electron configuration ultimately can lead
to cellular damage.
Oxidation
of DNA molecules, for example, can result in mutation, and oxidation of
lipid molecules
can
result in decreased structural fluidity of these compounds thus resulting
in loss of integrity of
cellular
membranes.
Relevant Research
Findings
from experimental animal research have demonstrated that exposure to acute
psychosocial
stress might promote transient increases in oxidative damage. For
example,
exposure
of rats to acute immobilization stress has been demonstrated to increase
markers of
lipid
peroxidation in plasma (Liu, Wang, & Mori, 1994), and in myocardial
and hepatic tissue
(Davydov
& Shvets, 2001; Zaidi, Al-Qirim & Banu, 2005).
The
results of acute stress and oxidative damage research are complemented
by those from both
human
and animal research examining the association of repeated, chronic, or
sub-chronic stress
on
levels of oxidative damage. A series of rodent studies conducted
by Sahin and Gumuslu
(Gumuslu,
Sarikcioglu, Sahin, Yargicoglu & Agar, 2002; Sahin & Gumuslu, 2004;
2007a; 2007b)
revealed
that daily exposure to cold stress and/or immobilization stress over a
period of two
weeks
was associated with elevated levels of oxidized proteins and lipids in
peripheral tissues.
Similarly,
evidence from observational studies in humans supports an association of
both chronic
and
brief naturalistic stress with increased oxidative damage. Epel and
colleagues found that
more
years of giving care to an ill child and greater perceived stress each
were correlated with
increased
levels of oxidized lipids (Epel et al., 2004). When compared to a
lower stress time
period,
blood samples taken from students during academic examination week had
increased
DNA
damage, increased sensitively of lipids to oxidation, and decreased free
radical trapping
ability,
suggesting an increase in oxidative stress (Sivonova et al., 2004).
Recommended Reading
 Cherubini,
A., Ruggiero, C., Polidori, M.C., & Mecocci, P. (2005). Potential markers
of
 oxidative
stress in stroke. Free Radical Biology & Medicine, 39(7), 841-52.
Furr,
H.C. (2004). Analysis of retinoids and carotenoids: Problems resolved and
unsolved.
Journal
of Nutrition, 134, 281S-285S.
Lykkesfeldt,
J. (2007). Malondialdehyde as biomarker of oxidative damage to lipids caused
by
smoking. Clinica Chimica Acta, 380(1-2), 50-58.
Yeum,
K.-J., Russell, R.M., Krinsky, N.I., & Aldini, G. (2004). Biomarkers
of antioxidant
capacity
in the hydrophilic and lipophilic compartments of human plasma. Archives
of
Biochemistry
& Biophysics, 430(1), 97-103.
References
Davydov,
V. V., & Shvets, V. N. (2001). Lipid peroxidation in the heart of adult
and old rats
during
immobilization stress. Experimental Gerontology, 36(7), 1155-1160.
Epel,
E. S., Blackburn, E. H., Lin, J., Dhabhar, F. S., Adler, N. E., Morrow,
J. D., et al.
(2004).
Accelerated telomere shortening in response to life stress. PNAS, 101(49),
17312-17315.
Gumuslu,
S., Sarikcioglu, S. B., Sahin, E., Yargicoglu, P., & Agar, A. (2002).
Influences of
different
stress models on the antioxidant status and lipid peroxidation in rat erythrocytes.
Free
Radical Research, 36(12), 1277-1282.
Liu,
J., Wang, X., & Mori, A. (1994). Immobilization stress-induced antioxidant
defense
changes
in rat plasma: Effect of treatment with reduced glutathione. The International
Journal
of Biochemistry, 26(4), 511-517.
Sahin,
E., & Gumuslu, S. (2004). Cold-stress-induced modulation of antioxidant
defence:
Role
of stressed conditions in tissue injury followed by protein oxidation and
lipid
peroxidation.
International Journal of Biometeorology, 48, 165-171.
Sahin,
E., & Gumuslu, S. (2007a). Immobilization stress in rat tissues: alterations
in protein
oxidation,
lipid peroxidation and antioxidant defense system. Comparative Biochemistry
&
Physiology.
Toxicology & Pharmacology, 144(4), 342-347.
Sahin,
E., & Gumuslu, S. (2007b). Stress-dependent induction of protein oxidation,
lipid
peroxidation
and anti-oxidants in peripheral tissues of rats: Comparison of three stress
models
(immobilization, cold and immobilization-cold). Clinical & Experimental
Pharmacology
& Physiology, 34(5-6), 425-431.
Sivonova,
M., Zitnanova, I., Hlincikova, L., Skodacek, I., Trebaticka, J., &
Durackova, Z.
(2004).
Oxidative stress in university students during examinations. Stress, 7(3),
183-188.
Zaidi,
S. M. K. R., Al-Qirim, T. M., & Banu, N. (2005). Effects of antioxidant
vitamins on
glutathione
depletion and lipid peroxidation induced by restraint stress in the rat
liver.
Drugs
R D, 6, 157-165.
 Core-E
MainBiological
Measures Used
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