Original Contribution
COENZYME Q
10
ENRICHMENT DECREASES OXIDATIVE DNA DAMAGE IN
HUMAN LYMPHOCYTES
M. TOMASETTI,* G. P. LITTARRU,* R. STOCKER,
†
and R. ALLEVA*
*Institute of Biochemistry, Faculty of Medicine, University of Ancona, via Ranieri, 60131 Ancona, Italy;
†
Heart Research
Institute, Camperdown, Sidney, New South Wales, Australia
(Received 1 March 1999; Revised 26 April 1999; Accepted 28 May 1999)
Abstract—Ubiquinol-10, the reduced form of coenzyme Q
10
, is a powerful antioxidant in plasma and lipoproteins. It
has been suggested that endogenous ubiquinol-10 also exerts a protective role even towards DNA oxidation mediated
by lipid peroxidation. Even though the antioxidant activity of coenzyme Q
10
is mainly ascribed to ubiquinol-10, a role
for ubiquinone-10 (the oxidized form), has been suggested not only if appropriate reducing systems are present. To
investigate whether the concentration of ubiquinol-10 or ubiquinone-10 affects the extent of DNA damage induced by
H
2
O
2
, we supplemented in vitro human lymphocytes with both forms of coenzyme Q
10
and evaluated the DNA strand
breaks by Comet assay. The exposure of lymphocytes to100 MH
2
O
2
resulted in rapid decrease of cellular
ubiquinol-10 content both in ubiquinol-10-enriched and in control cells, whereas -tocopherol and -carotene concen-
tration were unchanged. After 30 min from H
2
O
2
exposure, the amount of DNA strand breaks was lower and cells’
viability was significantly higher in ubiquinol-10-enriched cells compared with control cells. A similar trend was
observed in ubiquinone-10-enriched lymphocytes when compared with control cells. Our experiments suggest that
coenzyme Q
10
in vitro supplementation enhances DNA resistance towards H
2
O
2
-induced oxidation, but it doesn’t inhibit
directly DNA strand break formation. © 1999 Elsevier Science Inc.
Keywords—Ubiquinol-10, Ubiquinone-10, Coenzyme Q
10
Supplementation, DNA damage, Comet assay, Hydrogen
peroxide, Lymphocytes, Liposomes, Free radicals
INTRODUCTION
Oxidative damage to DNA can result from free radical
attack after exposure to ionizing radiation or to agents
such as H
2
O
2
that can produce active oxygen species.
The hydroxyl radical is thought to be responsible for
most of the damage, such as strand breaks and the
formation of oxidized bases. Endogenous damage to
DNA, caused by oxygen free radicals liberated during
normal respiration, may be significant in the etiology of
cancer [1]. DNA damage can account for the genetic
changes that occur at the different stages in the progres-
sion from anaplastic growth to metastasis [2], and there-
fore, dietary factors that reduce the impact of free radical
attack are likely to protect against cancer. Antioxidants,
largely of dietary origin, may limit DNA damage by
scavenging free radicals and hence protect against mu-
tagenesis and cancer [1].
Coenzyme Q
10
has long been known to be a compo-
nent of the mitochondrial respiratory chain [3]. Recently,
its reduced form (ubiquinol-10) has also been shown
serve as a potent antioxidant, protecting phospholipids
from peroxidation [4]. Recent investigations suggest that
the endogenous content of coenzyme Q
10
might protect
membrane proteins and DNA against oxidative damage
mediated by lipid peroxidation [5– 6]. Although the an-
tioxidant activity of coenzyme Q
10
in systems as lipopro-
teins [7,8] or plasma [9], is mainly ascribed to ubiquinol-
10, an antioxidant role for ubiquinone-10 appears
feasible even if appropriate reducing systems are not
present.
The aim of this study was to investigate the role of in
vitro supplementation with both the reduced and oxi-
dized forms of coenzyme Q
10
(i.e., ubiquinol-10 and
ubiquinone-10, respectively) in the prevention of DNA
oxidative damage in lymphocytes exposed to H
2
O
2
.
Address correspondence to: Marco Tomasetti, Institute of Biochem-
istry, School of Medicine, University of Ancona–via Ranieri-60131,
Ancona, Italy. Tel./Fax: +390 735-592755; E-Mail: ralleva@jth.it.
Free Radical Biology & Medicine, Vol. 27, Nos. 9/10, pp. 1027–1032, 1999
Copyright © 1999 Elsevier Science Inc.
Printed in the USA. All rights reserved
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