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in Rats1
* Clinical Nutrition Research, Department of Public Health and Caring Sciences/Geriatrics, and ** Department of Medical Cell Biology, Faculty of Medicine, Uppsala University, Sweden
2To whom correspondence should be addressed.
 |
ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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) and PGF2-metabolite
(15-K-DH-PGF2), respectively, in blood, urine and liver.
Samples were collected from control rats (n = 6)
and from rats supplemented with vitamin E in the diet for 3 wk
(n = 8, 20 g/kg diet of DL--tocopherol hydrogen succinate). Plasma
-tocopherol concentration and antioxidative capacity were greater in
the vitamin E-supplemented rats than in the control rats (17.9
± 1.7 vs. 50.4 ± 10.4 µmol/L, P < 0.001 and 181 ± 6 vs. 275 ± 27 µmol/L trolox equivalents, P < 0.001). Urine 8-iso-PGF2 tended
to be lower in the vitamin E-supplemented rats (0.72 ± 0.40
vs. 0.34 ± 0.19 nmol/mmol creatinine, P = 0.056). Urine 15-K-DH-PGF2 was lower due to vitamin E supplementation (0.97 ± 0.38 vs. 0.56 ± 0.21 nmol/mmol
creatinine, P < 0.05), as was liver-free
8-iso-PGF2 concentration (0.47 ± 0.11 vs. 0.18
± 0.04 nmol/g, P < 0.001). Supplementation
with vitamin E did not affect plasma 8-iso-PGF2 or 15-K-DH-PGF2 concentrations, liver total 8-iso-PGF2 or plasma malondialdehyde levels. Thus,
vitamin E supplementation reduced urine basal levels of biomarkers of
both nonenzymatic and enzymatic lipid peroxidation. In liver, vitamin E
reduced the basal level of free 8-iso-PGF2 but not total 8-iso-PGF2.
KEY WORDS: • vitamin E • lipid peroxidation • F2-isoprostane • prostaglandin • rats
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Peroxidation of
unsaturated fatty acids can proceed through nonenzymatic free
radical-catalyzed pathways or through processes that are enzymatically
catalyzed. Several methods have been developed to assess nonenzymatic
lipid peroxidation, but most of these methods have their own
shortcomings and limitations (de Zwart et al. 1999
, Gutteridge and Halliwell 1990
).
Recently, a group of prostaglandin
(PG)3
F2-like compounds,
F2-isoprostanes, produced by free
radical-induced peroxidation of arachidonic acid independent of the
cyclooxygenase pathway, was discovered (Morrow et al. 1990
). F2-isoprostanes are formed in situ
in phospholipids (Morrow et al. 1992a
) and are then
released into circulation and excreted in the urine (Roberts and Morrow 1997
). 8-Iso-prostaglandin F2
(8-iso-PGF2) is the most abundant
F2-isoprostane, exerts potent biological activity
(Morrow et al. 1990
) and has been suggested as a
potential marker for oxidative injury (Morrow and Roberts 1999
, Roberts and Morrow 1997
). Levels of
8-iso-PGF2 in body fluids are elevated
in animal models of oxidative injury (Awad et al. 1994a
,
Basu 1999
, Basu and Eriksson 1998
and
1999
, Burk et al. 1995
, Mathews et al. 1994
, Morrow et al. 1992a
and
1992b
, Nanji et al. 1994b
) and in several
diseases and conditions that are proposed to be associated with free
radical-induced oxidative injury in humans such as smoking
(Morrow et al. 1995
, Reilly et al. 1996
),
diabetes mellitus (Davi et al. 1999
, Gopaul et al. 1995
), vascular reperfusion (Delanty et al. 1997
, Reilly et al. 1997
), hypercholesterolemia
(Davi et al. 1997
) and liver cirrhosis (Pratico et al. 1998a
).
Cyclooxygenase-2, an isoform of cyclooxygenase, is induced in
macrophages, epithelial cells and fibroblasts by several
pro-inflammatory stimuli leading to release of prostaglandins
(Fu et al. 1990
, Mitchell et al. 1993
,
Vane and Botting 1995
, Xie et al. 1991
).
15-Keto-13,14-dihydro-PGF2
(15-K-DH-PGF2), a major metabolite of the
primary PGF2, is increased in inflammatory
response and can be used as an index of lipid peroxidation through the
cyclooxygenase pathway (Basu 1998c
and
1999
, Basu and Eriksson 1998
and
1999
).
Highly specific and sensitive radioimmunoassays for the measurement of
both 8-iso-PGF2 and
15-K-DH-PGF2 were recently developed,
validated and used as biomarkers of oxidative injury and inflammatory
response (Basu 1998b
and 1998c
).The use
of these radioimmunoassays is an excellent approach for simultaneous
measurement of nonenzymatic and enzymatic lipid peroxidation in vivo.
Both 8-iso-PGF2 and
15-K-DH-PGF2 levels in urine and plasma are
increased in animal models of hepatotoxicity (Basu 1999
)
and experimental septic shock (Basu and Eriksson 1998
and 1999
).
Vitamin E is a chain-breaking antioxidant with the particular
function of preventing lipid peroxidation in membrane systems. The aim
of this study was to investigate if enrichment of the diet with vitamin
E could suppress basal levels of both
F2-isoprostanes and PGF2
metabolite in rats by its influence on nonenzymatic and enzymatic lipid
peroxidation. We measured 8-iso-PGF2 as an
index of nonenzymatic lipid peroxidation and
15-K-DH-PGF2 as a biomarker of enzymatic lipid
peroxidation in plasma, urine and liver. Malondialdehyde and
antioxidant status in the circulation were also monitored.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Male Sprague-Dawley rats (6-wk-old, about 200 g) were
purchased from B & K Universal (Sollentuna, Sweden). The rats had free
access to tap water and food. They were subjected to a 12 h
light/12 h dark schedule. Powdered food was prepared from commercial
food pellets (R36; Lactamin AB, Stockholm, Sweden) containing total
lipids 4%, protein 18.5%, carbohydrates 55.7% and fibers 3.5% and
supplemented with vitamin E at 63 mg/kg and vitamin K and
cholecalciferol at 10 mg/kg and 37.5 µg/kg, respectively. For vitamin
E treatment, DL--tocopherol hydrogen succinate (Merck,
Darmstadt, Germany) was blended into the powdered food at a
concentration of 20 g/kg diet, which equals ~2 g/(kg body wt/d).
Control rats received powdered food without vitamin E supplementation.
Both control (n = 6) and vitamin E-treated rats
(n = 8) received powdered food for 3 wk.
Sample collection.
Urine samples were collected in petri dishes. The rats were then weighed and surgical anesthesia was induced with ether. During laparotomy, livers were excised and blood samples were drawn from the abdominal aorta. The rats were killed by heart puncture. Blood samples were collected in heparinized glass vials and plasma was prepared by centrifugation at 1930 x g for 8 min. All samples were immediately stored at -20°C during the experiment and thereafter at -70°C until analysis. The animal experimental procedure was approved by the Animal Ethics Committee of the Medical Faculty of Uppsala University.
Preparation of liver tissues.
Liver samples were weighed, diluted with 3 vol of phosphate buffer and homogenized under cold conditions. The homogenate was centrifuged at 1680 x g and 4°C for 10 min, and the supernatant was stored frozen at -0°C until further preparation within 1 wk. The homogenate was hydrolyzed by incubation with 3 vol of 3 mol/L KOH at 37°C for 60 min. Extraction with 3 vol of ethyl acetate was performed after acidification to pH 3–4 with HCl. Extracts were then centrifuged at 1680 x g and 4°C for 10 min, and the supernatant was evaporated under nitrogen. Samples were finally rediluted in <5% ethanol and phosphate buffer and stored frozen at -70°C until analysis within 2–8 wk.
Radioimmunoassay of 8-iso-PGF2.
The plasma, urine and liver samples were analyzed for
8-iso-PGF2 by a newly developed radioimmunoassay
(Basu 1998b
). An antibody was raised in rabbits by
immunization with 8-iso-PGF2 coupled to bovine serum
albumin at the carboxylic acid by the 1,1'-carbonyldiimmidazole method.
The cross-reactivity of the antibody with
8-iso-15-keto-13,14-dihydro-PGF2,
8-iso-PGF2ß, PGF2,
15-keto-PGF2, 15-keto-13,14-dihydro-PGF2,
TXB2, 11ß-PGF2, 9ß-PGF2
and 8-iso-PGF3 was 1.7, 9.8, 1.1, 0.01, 0.01, 0.1, 0.03,
1.8 and 0.6%, respectively. The detection limit of the assay was about
23 pmol/L. Unextracted plasma and urine samples of various volumes and
dilutions were used in the assay. The levels of
8-iso-PGF2 in urine were adjusted for creatinine
concentration and were measured by a colorimetric method using IL test
creatinine 181672–00 in a Monarch 2000 centrifugal analyzer
(Instrumentation Laboratories, Lexington, MA). In the liver
samples, free 8-iso-PGF2 was analyzed after extraction
and the total amount (sum of free and esterified) of
8-iso-PGF2 was analyzed after hydrolysis and extraction.
Radioimmunoassay of 15-keto-13,14-dihydro-PGF2.
The plasma and urine samples were analyzed for
15-K-DH-PGF2 by a newly developed radioimmunoassay
(Basu 1998c
). An antibody was raised in rabbits by
immunization with 15-K-DH-PGF2 coupled to bovine serum
albumin at the carboxylic acid by the 1,1'-carbonyldiimmidazole method.
The cross-reactivity of the antibody with PGF2,
15-keto-PGF2, PGE2, 15-keto-13,14
dihydro-PGE2,
8-iso-15-keto-13,14-dihydro-PGF2,
11ß-PGF2, 9ß-PGF2, TXB2
and 8-iso-PGF3 was 0.02, 0.43, <0.001, 0.5, 1.7,
<0.001, <0.001, <0.001 and 0.01%, respectively. The detection limit
of the assay was about 45 pmol/L. Unextracted plasma and urine samples
of various volumes and dilutions were used in the assay. The levels of
15-K-DH-PGF2 in urine were adjusted for creatinine
concentration.
Measurement of malondialdehyde.
Malondialdehyde levels in plasma samples were measured using HPLC with
fluorescence detection as described by Öhrvall et al. (1994)
. A
thiobarbituric acid reaction was carried out by mixing 200 µL of
plasma sample with 750 µL of 0.15 mol/L phosphoric acid, 300 µL of
water and 250 µL of 42 mmol/L thiobarbituric acid. The reaction
mixture was incubated in a boiling water bath for 60 min and then
cooled on ice. The malondialdehyde-thiobarbituric acid complex was
extracted with methanol, and 20 µL of the sample was injected into an
HPLC column (Lichrospher 100 RP-18, 250 x 4 mm). The mobile phase
contained methanol/50 mmol/L phosphate buffer (2:3). Fluorescence was
measured with an excitation wavelength of 532 nm and an emission wave
length of 553 nm.
Measurements of antioxidants.
Plasma -tocopherol was assayed by using HPLC with fluorescence
detection (Öhrvall et al. 1993
). Briefly, 500 µL
of plasma was extracted with 500 µL of ethanol containing 0.05 g/L of
butylated hydroxytoluene and 2 mL of hexane. Supernatant (20 µL) was
injected into an HPLC column (LiChrospher 100 NH2 250 x 4 mm).
Fluorescence was measured with an excitation wavelength of 295 nm and
an emission wavelength of327 nm.
Plasma antioxidant capacity was measured as trolox equivalents by a
modified chemiluminescence assay described by Öhrvall et al. (1997)
. The technique is based on measurement of light emission when
the chemiluminescent substrate luminol is oxidized by hydrogen peroxide
in a reaction catalyzed by horseradish peroxidase. Suppression of the
light output by antioxidants is related to the antioxidant capacity of
the sample. Uricase was used to eliminate the urate content in the
sample resulting in an antioxidant capacity value without urate.
Statistics.
Data are presented as means ± SD. All variables were continuous and on an interval scale. Significant differences between groups were determined with unpaired Student’s t test. Variables with skewed distributions were log-transformed before analyses. Variables that were not normally distributed after transformation were analyzed with Mann Whitney’s nonparametric test. P < 0.05 was regarded as significant. The statistical analyses were performed using the statistical software package JMP (SAS Institute, Cary, NC).
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). The plasma -tocopherol concentration and the antioxidative
capacity of plasma samples were greater in the rats supplemented with
vitamin E for 3 wk compared to the control rats (P < 0.001). Plasma malondialdehyde concentrations did not differ between
groups.
|
level tended to be lower in
the vitamin E-supplemented rats compared to the controls
(P = 0.056, Fig. 1A
). However, plasma 8-iso-PGF2 did not differ
between the groups (Fig. 1B
). Free
8-iso-PGF2 concentration in the liver was
significantly lower in the vitamin E-supplemented rats than in the
controls (P < 0.001, Fig. 2A
), whereas the total 8-iso-PGF2 hepatic
concentration did not differ between groups (Fig. 2B
).
|
|
were similar to those on
8-iso-PGF2. Urine
15-K-DH-PGF2 was significantly lower in the
vitamin E-supplemented rats than in the control rats (P
< 0.05, Fig. 3A
), while the plasma concentration was not affected by vitamin E
treatment (Fig. 3B
).
|
|
DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Nonenzymatic formation of isoprostanes through free
radical-catalyzed peroxidation of arachidonic acid or enzymatic
formation of prostaglandins, mainly PGF2,
through oxidation catalyzed by cyclooxygenase are found to be unique
indicators of in vivo oxidative stress and inflammation, respectively
(Basu 1998b
and 1998c
).
8-Iso-PGF2, a major
F2-isoprostane, increases during free
radical-mediated arachidonic acid oxidation in experimental animal
studies (Awad et al. 1994a
, Basu 1999
,
Basu and Eriksson 1998
and 1999
,
Burk et al. 1995
, Mathews et al. 1994
,
Morrow et al. 1992a
and 1992b
,
Nanji et al. 1994b
) and in human studies (Davi et al. 1997
and 1999
, Delanty et al. 1997
, Gopaul et al. 1995
, Morrow et al. 1995
, Pratico et al. 1998a
and 1997, Reilly et al. 1996
). The primary
PGF2 increases not only during inflammation
(Basu and Eriksson 1998
and 1999
) and
hepatotoxin-induced oxidative injury (Basu 1999
),
but also during physiological control of luteolysis and parturition in
various species (Basu and Kindahl 1987
, Basu et al. 1987
). To our knowledge, however, little is known about the
effect of vitamin E on levels of F2-isoprostanes
and PGF2 formation in vivo.
The levels of plasma 8-iso-PGF2 in the present
study did not differ between control rats and the vitamin
E-supplemented rats in contrast to the levels of urinary
8-iso-PGF2, which did differ between the two
groups. The 8-iso-PGF2 in plasma does not
decrease after vitamin E supplementation as in the urine probably
because of the difference in the kinetics of formation and
availability. The half-life of plasma
8-iso-PGF2 is very short, and 8-iso-PGF2
metabolizes rapidly and is efficiently excreted into the urine
(Basu 1998a
). We contend that urinary levels of
8-iso-PGF2 reflect an earlier event of the biosynthesis
and availability of 8-iso-PGF2 in the body compared to
plasma levels measured at the same time (Basu 1998a
).
Levels of both free and esterified 8-iso-PGF2 were also
measured in liver. The free 8-iso-PGF2 levels are very
low in liver, since isoprostanes initially are formed from arachidonic
acid esterified to phospholipids from which they subsequently are
released preformed, presumably by phospholipases (Morrow et al. 1992a
). By hydrolysis of the liver, it is possible to detect
the sum of free and esterified 8-iso-PGF2 levels.
Vitamin E supplementation suppressed free but not total
8-iso-PGF2 levels compared to controls. The cause for
these different effects of vitamin E on 8-iso-PGF2
levels in the liver is unclear.
There are only a few earlier animal studies investigating the effect of
vitamin E on F2-isoprostanes (Awad et al. 1994b
, Nanji et al. 1994a
, Palmer et al. 1998
, Pratico et al. 1998b
). In apolipoprotein
E-deficient mice, supplementation with vitamin E (2000
IU/kg diet) significantly reduced
F2-isoprostane generation in urine, plasma and vascular
tissue (Pratico et al. 1998b
). Inverse correlations were
also seen between plasma vitamin E and F2-isoprostane
levels in the urine, plasma and vascular tissues. Vitamin E dietary
supplementation to streptozotocin-diabetic rats decreased the
levels of plasma and liver total 8-iso-PGF2
(Palmer et al. 1998
). However, plasma levels of
8-iso-PGF2 in the nondiabetic control rats and in
diabetic rats fed a higher dose of vitamin E (500 mg/kg diet) were
below the detection limit (0.03 nmol/L). In the same study, a
dose-dependent decrease in plasma 8-iso-PGF2
concentration was demonstrated when comparing a vitamin E-deficient
diet, a standard diet with a small amount of vitamin E (75.9 mg/kg
diet), and a vitamin E-supplemented diet (250 mg/kg diet). Vitamin
E deprivation has also been related to increased basal levels of
8-iso-PGF2 in both plasma and tissues of normal rats
(Awad et al. 1994b
) and in plasma in an animal model of
alcoholic liver injury (Nanji et al. 1994a
). The changes
in levels of 8-iso-PGF2 in relation to the content of
vitamin E in the diet may be important to consider when comparing the
effects on oxidative stress in different animal studies. The dose used
in our study (20 g/kg diet, which equals to ~2 g/kg body weight) is
in the upper range of vitamin E doses used in animal studies. In safety
studies of vitamin E intake (reviewed in Kappus and Diplock 1992
),
adverse effects were rarely observed with dosages up to 2 g/kg body
weight in rats. It was concluded that there was no evidence of adverse
toxic effects nor mutagenic, carcinogenic or teratogenic effects even
at high doses of vitamin E. Controls and vitamin E-supplemented
rats in this study both gained weight, and there was no difference in
the final body weight between the groups. The antioxidant capacity and
-tocopherol level in plasma were greater in the vitamin
E-supplemented rats than in controls.
Plasma malondialdehyde did not differ between groups, and the
concentration of malondialdehyde did not correlate with levels of
8-iso-PGF2 in plasma (r = -0.35,
P = 0.23, n = 14). This is in
agreement with previously reported results from an animal study where
8-iso-PGF2 was measured with the same radioimmunoassay
(Basu 1999
). These different responses between two
biomarkers of lipid peroxidation may be because they reflect different
stages of the lipid peroxidation process.
Whether vitamin E has other functions, apart from its antioxidant
properties by scavenging of free radicals and reacting with active
forms of oxygen, has not yet been established. We showed that the basal
levels of the PGF2 metabolite
15-K-DH-PGF2 in urine were decreased due to vitamin E
supplementation with a simultaneous suppression of urinary
8-iso-PGF2. In an earlier animal experimental study of
hepatotoxicity (Basu 1999
), both the inflammatory
response, as measured by 15-K-DH-PGF2, and oxidative
injury, as measured by 8-iso-PGF2, were increased. The
oxidative injury was increased before an increase in the inflammatory
response could be seen, suggesting that the
cyclooxygenase-dependent inflammatory response possibly could be a
secondary effect of oxidative injury and a conceivable link between
inflammation and oxidative stress (Basu 1999
). The
simultaneous noninvasive measurement of 8-iso-PGF2 and
15-K-DH-PGF2 is a promising approach for studies,
investigating the possible roles of lipid peroxidation under normal
conditions and in the pathology of human diseases.
In summary, dietary supplementation with the antioxidant vitamin E
decreased basal levels of free 8-iso-PGF2 in rats. Thus,
vitamin E supplementation may have a possible effect on free
radical-induced oxidative injury. A decrease in the basal levels of
15-K-DH-PGF2 in urine after vitamin E supplementation
also shows a possible effect of vitamin E on
cyclooxygenase-catalyzed prostaglandin formation.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: 8-iso-PGF2, 8-iso-prostaglandin F2; 15-K-DH-PGF2,
15-keto-13,14-dihydro-prostaglandin F2; PG, prostaglandin.
Manuscript received June 23, 1999. Initial review completed July 23, 1999. Revision accepted September 9, 1999.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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