Oxidant and Anti-Oxidant Systems of Synovial Fluid from

Patients with Knee Post-Traumatic Arthritis

Alina Osta -l-owska,1 Sl--awomir Kasperczyk,1 Aleksandra Kasperczyk,1 Ludmil--a S -l-owińska,2
Marek Marzec,3 Tomasz Stol--tny,4 Bogdan Koczy,4 Ewa Birkner1
1
Department of Biochemistry, Medical University of Silesia in Katowice, Jordana 19, 41–808 Zabrze, Poland
2
Department of Biophysics, Medical University of Silesia in Katowice, Jordana 19, 41–808 Zabrze, Poland
3
Department of Orthopaedics, Silesian Hospital of Rheumatology, Szpitalna 11, 43–450 Ustroń, Poland
4
Department of Orthopaedics, District Orthopaedic Hospital, Bytomska 62, 41–940 Piekary Slaskie, Poland

Received 2 June 2006; accepted 9 November 2006

Published online 22 February 2007 in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jor.20357

ABSTRACT: It has been suggested that patients with knee post-traumatic arthritis (PA), associated
or not to haemarthrosis (HA), display altered oxidant and anti-oxidant systems in their synovial
fluid. This study aimed to establish whether this is really the case. Synovial fluid samples were
obtained by transdermal arthrocentesis from 69 patients with PA (36 of them had HA) and 22
control subjects. The activities of synovial fluid zinc-copper superoxide dismutase (ZnCuSOD) and
manganese superoxide dismutase (MnSOD) isoenzymes, catalase (CAT), glutathione peroxidase
(GPX), glutathione reductase (GR) and glutathione-S-transferase (GST) enzymes, and malondial-
dehyde (MDA) concentration and synovial fluid viscosity were measured in the study groups.
Patients with PA had significantly increased activities of all antioxidant enzymes, except CAT, and
MDA concentration than did the controls. However, synovial fluid viscosity was found to be de-
creased in the study group, mainly in the HA subgroup. Results suggest that excessive free radicals
production may exist in synovial fluid of PA patients and may contribute to knee joint destruction.
ß 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:804–
812, 2007
Keywords: knee post-traumatic arthritis; anti-oxidant enzymes; malondialdehyde;
synovial fluid viscosity

INTRODUCTION but it can be converted to more harmful species,

hydroxyl radical (.OH) and hydrogen peroxide
Acute post-traumatic articular effusion, partially (H2O2). The first step of this reaction cascade is
post-traumatic hemarthrosis (HA) is found more very often catalyzed by the enzyme NADPH
commonly in the knee than in any other joint in oxidase:6,7
the human body.1,2 Clinical experiences and
epidemiologic studies have shown that the knee NADPH þ 2 O2 ! NADPþ þ 2 O

2

joint injury (i.e., ruptured anterior cruciate liga- Superoxide anion radicals dismutase either
ment) frequently leads to progressive joint damage spontaneously or in the presence of superoxide
that causes the clinical syndrome of post- dismutase (SOD) into hydrogen peroxide and
traumatic arthritis (PA).3–5 Some investigators oxygen according to:
have focused on oxidative stress in PA. Disruption
of cells through trauma, and the accompanying HO2 þ O
þ
2 H ! H2 O2 þ O2
phagocytes activation, can lead to an increase in
and
production of reactive oxygen species (ROS) and
subsequent exacerbation of articular cartilage HO2 þ HO2 ! H2 O2 þ O2 :
damage initiated by trauma. The initial radical
formed generally is superoxide anion radical (O.
A univalent reduction of hydrogen peroxide to
2 ),
hydroxyl radical is assumed to be caused in the
presence of Fe(II) or Cu(I) as the result of the so-
Correspondence to: Alina Ostałowska (Telephone: þ48 32
272 23 18; E-mail: aostalowska@slam.katowice.pl) called Fenton reaction:
ß 2007 Orthopaedic Research Society. Published by Wiley Periodicals,
Inc. Fe2þ þ H2 O2 !OH þ
OH þ Fe3þ :

804 JOURNAL OF ORTHOPAEDIC RESEARCH JUNE 2007


These ROS are capable of degrading many of the
components of the knee joint, including collagen,
proteoglycans, and hyaluronan.8–10
Fortunately, several lines of anti-oxidant
defense exist both intra- and extracellulary to
protect the knee joint against damage from ROS
and other oxidants. Defense against ROS is
provided by scavengers and detoxifying reactions,
catalyzed meanly by anti-oxidant enzymes SOD,
catalase (CAT), and glutathione transformation
enzymes, including glutathione peroxidase (GPX),
glutathione reductase (GR), and glutathione-S-
transferase (GST).11,12
We hypothesized that patients with knee post-
traumatic arthritis, associated or not to hemarthro-
sis, display altered oxidant and anti-oxidant sys-
tems in their synovial fluid. This study was designed
with the following objectives: (1) to examine poten-
tial changes in anti-oxidant enzymes activities—
ZnCuSOD and MnSOD isoenzymes and CAT, and
glutathione transformation enzymes—GPX, GR,
and GST in post-traumatic arthritic synovial fluid
of the knee joints; and (2) to estimate their relation-
ships to degree of lipid peroxidation in synovial fluid
(SF) evaluated by malondialdehyde (MDA) concen-
tration, synovial fluid viscosity, and presence of
hemarthrosis (color of synovial fluid) in the knee
joint.
MATERIALS AND METHODS
Patient Characteristics
SF samples were obtained from 91 patients with the
knee joints exudates treated in the Department of
Orthopaedic Surgery, Special Hospital No. 4 in Bytom,
Poland. Sixty-nine of these patients had been diagnosed
as having PA based on clinical, laboratory, and ultra-
sonographic findings (mean age, 35 years; mean disease
duration, 3 weeks). Thirty-six of them had PA with
hemarthrosis (HA), whereas 33 patients had PA without
hemarthrosis (non-HA). Twenty-two patients selected
from these who had atraumatic and asymptomatic
normal knees (mean age, 40 years) were classified as
controls. In addition, this group consisted of patients
without obesity (BMI less than 30), who did not work in
professions related to excessive load of the knee joints
(e.g., drivers of trucks), and did not practice injurious
sports (e.g., soccer, skiing), and so far not diagnosed and
not treated for osteoarthritis, post-traumatic, inflam-
matory, or another knee joint pathology. The final
verification of the study groups were carried out after
preliminary analysis of SF, including a visual examina-
tion of color, turbidity, viscosity, test by Ropes, volume,
and biochemical parameters. SF samples collected from
the control subjects showed criteria of the normal
synovial fluid.13,14
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KNEE POST-TRAUMATIC ARTHRITIS 805
Patients and controls with any history of smoking, and
alcohol habits and signs of malignant tumors, diabetes,
serious liver, kidney, or heart insufficiency, or other
systemic diseases that might cause an increase in
oxidations were not included in the study. None of the
patients and the controls had received systemic or
intraarticular drugs within 6 weeks preceding the
collection of synovial fluid samples. Eleven patients and
eight controls were excluded from the study.
The study was approved by Medical Ethics Committee
of the Silesian Medical University (NN-013-283/03).
Sample Preparation
SF samples were obtained with needle aspiration or
during knee arthroscopy, and next divided into two
equal portions. The first SF sample was drawn into a
test tube without an anticoagulant, and the second SF
sample was collected into a test tube containing
K3EDTA as an anticoagulant, immediately placed on
ice and centrifuged at 3,000g for 30 min. Supernatant
was separated and stored at
768C until analysis but no
longer than 4 weeks. Activities of anti-oxidant enzymes,
MDA concentration, and SF viscosity in the study
groups were determined.
Assay
In the test tube without an anticoagulant, color,
turbidity, and volume of synovial fluid was examined
before centrifugation.
Execution Color of Synovial Fluid
Color of SF was determined indirectly. Data are shown
as: 0, colorless or clearly yellow; 1, yellow; 2, amber
or xanthochromatic; 3, rinsing meaty; 4, bloody, red, or
red-tinged.
Execution Test by Ropes (Mucin Clot Test)
The mucin clot test is a semiquantitative indicator of the
amount of hyaluronic acid determined by measurement
of precipitation knocked out by acidification with acetic
acid (addition of five drops of 5% acetic acid into 3 ml of
SF). The precipitate formed is graded according to the
following scale: 0, compact reaction (a tight ropy clot in a
clear solution); 1, compact/floccular reaction (a soft clot
with a turbid solution); 2, floccular reaction (a friable
clot in a cloudy solution); 3, floccular/turbidity reaction
(flocculent material in a cloudy solution); 4, turbidity
reaction (turbid supernatant with no evidence of clot).
Assay for SF Viscosity
In the test tube containing K3EDTA—before centrifuga-
tion—the SF viscosity was measured using a cone-late
viscometer Brookfield DV-IIþ at 378C. Data are shown
as cP (N  s  m
2).
JOURNAL OF ORTHOPAEDIC RESEARCH JUNE 2007

806 OSTAŁOWSKA ET AL.
Determination of MnSOD and ZnCuSOD Activity
The activity of above isoenzymes of SOD in SF was
determined by the Oyanagui method.15 Superoxide
anion radical, produced in the reaction of xanthine with
O2 catalyzed by xanthine oxidase, reacts with hydro-
xylamine producing nitric ion. Nitric ion combines with
naphthalene diamine and sulfaniline acid producing a
colored product; concentration of this mixture is propor-
tional to the amount of produced O.
2 . Enzymatic
activity is expressed as nitric unit (NU) in each ml of
SF (NU/ml). One NU means 50% of inhibition by SOD of
nitric ion production in this method. SOD isoenzymes—
MnSOD and ZnCuSOD—were assayed in synovial fluid,
using potassium cyanide (KCN) as the an inhibitor of the
ZnCuSOD by the Oyanagui method.
Determination of CAT Activity
CAT activity in SF was analyzed with the use of Aebi
kinetic method.16 Before CAT was assayed, the SF was
diluted 100 times with Tris/HCl buffer, pH 7.4. Kinetics
of the reaction were determined out in a quartz tank;
2.5 ml of substrate were mixed consisting of 50 mM Tris/
HCl buffer with pH ¼ 7.4 and perhydrol with 50 ml of
SF. After 10 s, absorbance was measured at 240 nm and
the kinetic changes of absorbance were marked every
30 s for 2 min. Enzymatic activity was not presented
in SF.
Determination of GPX Activity
GPX activity in SF was assayed by the Paglia and
Valentine kinetic method.17 GPX catalyses reaction
between reduced glutathione (GSH) and H2O2. The
product of this reaction—oxidized glutathione (GSSG)—
was recovered back to GSH using nicotinamide adenine
dinucleotide phosphate (NADPHþHþ) catalyzed by GR.
Decrease in absorbance was measured at 340 nm.
Activity of GPX was determined as the quantity of mmol
of NADPHþHþ used to recover GSH in 1 min converted
to 1 l of SF (IU/l).
Determination of GR Activity
GR activity in SF was also assayed by the kinetic
method.18 The decrease of the concentration of
NADPHþHþ after reduction of GSSG back to GSH
was measured. Activity of GR was determined as the
quantity of mmol of NADPHþHþ used to recover GSH in
1 min converted to 1 l of SF (IU/l).
Determination of GST Activity
Activity of GST in SF was analyzed by the Habig
and Jakoby kinetic method using 1-chloro-2,3-
dinitrobenzene.19 GST reacted with 1-chloro-2,3-dini-
trobenzene producing thioether. Increase in absorbance
was measured at 340 nm. Activity of GST was
determined as the quantity of mmol of thioether
produced in 1 min in 1 l of SF (IU/l).
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Determination of MDA Concentration
MDA concentration in SF was measured fluorometri-
cally as 2-thiobarbituric acid-reactive substance
(TBARS) by the Ohkawa method.20 SF sample was
mixed with 8.1% sodium dodecyl sulfate, 20% acetic
acid, and 0.8% 2-thiobarbituric acid. The method was
modified by adding sodium sulphate (100 mmol/l) and
BHT (3,5-diisobutylo-4-hydroxytoluen) (2.5 mmol/l).
After vortexing, SF sample was incubated 1 h in 958C
and butanol-pirydine 15:1 (v/v) was added. The mixture
was shaken 10 min and then centrifuged. Butanol-
pirydine layer was measured fluorometrically at 552 nm
(515 nm excitation). TBARS value is expressed as MDA
equivalent. Tetraethoxypropane was used as the stan-
dard. Data are shown as mmol MDA/l SF (mmol/l).
Statistical Analysis
Statistical analysis was performed with Statistica
6.0 PL software. Statistical methods included mean
and standard error of mean (SEM). Shapiro-Wilk’s test
was used to verify normality and Levene’s test to verify
homogeneity of variances. Statistical comparisons were
made by t-test, t-test with separate variance estimates,
or Mann–Whitney U test. Chi-square or Fisher test was
used to analyse sex. Yates’ correction for continuity was
used if needed. Spearman non-parametric correlation
was calculated. A value of p < 0.05 was considered to be
significant.
RESULTS
Table 1 depicts characteristics of the study
population. The study population did not differ in
sex. The HA subgroup was the youngest and the
controls was the oldest.
The mean  SD ZnCuSOD and MnSOD activit-
ies of SF were significantly higher in the study
group (þ115% and þ146%, respectively, p < 0.001)
as well as for both, the HA subgroup (þ147% and
þ137%, respectively, p < 0.001), and the non-
HA subgroup (þ85% and þ156%, respectively,
p < 0.001) when compared with the control subjects
(Fig. 1). ZnCuSOD and MnSOD activities of SF did
not differ between the study subgroups. The
mean  SD level of MDA in the PA group was
significantly higher than in the controls (þ40 %,
p < 0.001). MDA concentration in SF was signifi-
cantly higher in the HA subgroup than in the non-
HA subgroup (þ38%, p < 0.001) (Fig. 1).
Also, the mean  SD activities of GPX, GST, and
GR were significantly higher in the PA group than
in the control subjects for both the HA subgroup
and the non-HA subgroup (Fig. 2). In the study
group, the SF activities of above enzymes were
significantly higher (þ903%, þ369%, and þ120%,
respectively, p < 0.001), in the HA subgroup
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KNEE POST-TRAUMATIC ARTHRITIS 807

Table 1. Age, Sex, and Color of Synovial Fluid (Scale 0–4) in the Post-Traumatic Arthritis (the PA Group), and Separately in the PA with Hemarthrosis (the

Compared HA
p Level When
about þ1,089%, þ391%, and þ133%, respectively

to Non-HA
( p < 0.001), and in the non-HA subgroup about

0.009

<0.001
0.195
þ699%, þ344%, and þ105%, respectively ( p <
0.001). The mean  SD activity of GPX was sig-
nificantly higher in the HA subgroup than in the
p Level When non-HA subgroup (þ49%, p ¼ 0.001), and the
Compared to mean  SD activity of GR was significantly higher
Control

<0.001
0.985
0.122
in the HA subgroup than in the non-HA subgroup
(þ14%, p ¼ 0.005), and the mean  SD activity of
GST was higher in the HA subgroup but not
statistically significant.
The mean  SD viscosity of synovial fluid was
(Mean  SEM)

significantly lower in the study group (
80%,

39.6  2.26

1.42  0.18
Subgroup
Non-HA

p < 0.001) as well as for both, the HA subgroup

21/12

(
85%, p < 0.001), and the non-HA subgroup

(
74%, p < 0.001) when compared with the control
subjects (Fig. 3). Also, the SF viscosity was
statistically significantly lower by about
44% in
p Level When

the HA subgroup when compared with the non-HA

Compared to

subgroup ( p ¼ 0.012). The mean  SD test by Ropes

<0.001
Control
0.017
0.642

was incorrect in the study group, mainly the most

incorrect in the HA subgroup (3.44  0.12 in the HA
subgroup, and 2.85  0.16 in the non-HA subgroup
vs. 0.62  0.13, p < 0.001) (Fig. 3).
(Mean  SEM)
HA Subgroup
HA Subgroup), PA without Hemarthrosis (the Non-HA Subgroup), and Control Subjects

The mean  SD activities of all anti-oxidant

31.8  2.23

3.11  0.14

enzymes significantly positively correlated with

28/8

the test by Ropes (R ¼ 0.30–0.61), color of SF

(R ¼ 0.43–0.66, except Mn-SOD) and significantly
negatively correlated with the SF viscosity (R ¼

0.33–
0.64). Patients’ age significantly negative-
p Level When
Compared to

ly correlated with GPX and GST activities (R ¼

Control

<0.001
0.167
0.254

0.26, and
0.25, respectively). No relationships

between patients’ age and ZnCuSOD and MnSOD
activities, MDA concentration, or SF viscosity were
observed in the study group (Table 2).
(Mean  SEM)
35.6  1.65

2.30  0.15
PA Group

DISCUSSION
49/20

Different theories for the production of reactive

oxygen species in synovial fluid have been pro-
posed by several researchers.21–26 However, we
Control Group
(Mean  SEM)

0.62  0.11

also suggested a simple scheme of the generation

41.0  3.5

of individual ROS (Fig. 4).

19/3

One source of oxidants generated at the site of

inflammation such as post-traumatic knee is
phagocytosis. Inflammation induces an influx of
polymorphonuclear leukocytes or macrophages
Color of synovial fluid

into the synovium and the SF, which produce O.

No. of men/women

2
via the phagocytic isoform of NADPH oxidase.27,28
For the production of ROS, it has been proposed
Age (years)

that movement of an inflamed joint generates

Variables

sufficient pressure to cause transient ischemia of

the superficial synovial membrane.29,30 Ischemia
and reperfusion can lead to the articular cartilage

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808 OSTAŁOWSKA ET AL.

Figure 1. MnSOD and ZnCuSOD activities and MDA concentration of SF in control

group and the PA group, separately in the non-HA subgroup and the HA subgroup. For
experimental details, see Materials and Methods.

injury and are serious complications in PA.
Xanthine dehydrogenase (XOD), which normally
utilizes NADþ as electron acceptor, is converted by
proteolytic cleavage under the conditions of ische-
mia/reperfusion into xanthine oxidase (XO).31
Xanthine oxidase generates O.
2 by converting
hypoxanthine into xanthine, and xanthine into
uric acid. Under normal conditions, XO accounts
for only a minor proportion of total ROS production.
During the ischemic period, excessive ATP con-
sumption leads to the accumulation of the purine
metabolites, which upon subsequent reperfusion
and influx of oxygen are metabolized by XO to yield
massive amounts of O.
2 and H2O2.

Figure 2. GR, GST, and GPX activities of SF in control group and the PA group,
separately in the non-HA subgroup and the HA subgroup. The experimental details are
described in Materials and Methods.

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KNEE POST-TRAUMATIC ARTHRITIS 809

Figure 3. SF viscosity and test by Ropes in control group and the PA group, separately
in the non-HA subgroup and the HA subgroup. For experimental details, see Materials
and Methods.

Reoxygenation also stimulates NADPH oxidase
activity in chondrocytes.6,32 Studies by Wientjes
and Segal33 and other researchers34–38 using in
vitro models on chondrocytes cultures revealed
that, under unstressed conditions, articular carti-
lage cells produce both O.
2 and H2O2 in synovial
fluid, probably through the activation of NADPH
oxidase.
Erythrocytes may also have a role. Hemoglobin
can be liberated into SF from disrupted erythro-
cytes. This heme-containing protein is potentially
dangerous in that it can accelerate peroxidation of
lipids in the presence of H2O2. By the other hand,
the excess H2O2 can cause degradation of the heme
rings of hemoglobin, releasing from the protein
iron ions that are capable of stimulating .OH
formation.6,39–41 Zardeneta et al.42 suggest that
denatured hemoglobin may contribute redox active
iron that can catalyze a reaction, leading to the
formation of damaging ROS. Such a process may
represent one of the earliest molecular events
involved in the pathogenesis of PA.38,43
Findings from the present study demonstrate
that synovial fluid samples from patient with PA
are more prone to lipid peroxidation owing to
impaired anti-oxidant defense system. Pro-
oxidant–anti-oxidant imbalance in PA may be
due to the decreased synovial fluid viscosity.
Tulamo et al.43 found that the SF concentration of
hyaluonic acid can be used as a diagnostic marker
for chronic PA. Takahasi et al.44 and Grootveld
et al.21 found that exposition of hyaluronan on ROS,
notably .OH, potentially results in decreased high
molecular weight hyaluronan. Indeed, .OH may
inhibit cartilage proteoglycan synthesis, e.g., by
interfering with ATP synthesis, in part by inhibit-
ing the glycolytic enzyme glyceraldehyde-3-
phosphate dehydrogenase in chondrocytes.45–48
Alpaslan et al.49 found that intraarticular use of
hyaluronan significantly decreased concentration

Table 2. Correlations between Patient’s Age, Color of SF, Test by Ropes, SF Viscosity and MDA Concentration,
MnSOD, ZnCuSOD, GPX, GR, and GST Activities of SF in the Study Populationa

Variable Age MDA MnSOD ZnCuSOD GPX GR GST

Age — NS NS NS
0.26 NS
0.25
Color of SF
0.31 0.65 NS 0.52 0.62 0.58 0.43
Test by Ropes
0.33 0.44 0.30 0.48 0.58 0.61 0.54
Viscosity 0.31
0.34
0.45
0.33
0.64
0.53
0.42
NS, no statistical significance.
a
Spearman correlation
R, p < 0.05.

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810 OSTAŁOWSKA ET AL.
Figure 4. Scheme of the generation of different ROS in post-traumatic arthritic
synovial fluid of the knee joints. The enzymes that catalyze the individual reactions are
also provided in the figure.
of 2-thiobarbituric acid-reactive substance in SF.
This would suggest that membrane lipids are only
one of the possible targets of oxidative damage, and
compounds of SF such as hyaluronic acid would be
more susceptible to oxidative stress.
The production of ROS in synovial fluid is
difficult to detect because ROS are extremely
labile.50 Under normal circumstances, ROS are
eliminated by detoxifying reactions, catalyzed
meanly by anti-oxidant enzymes: ZnCuSOD and
MnSOD isoenzymes, CAT, and glutathione trans-
formation enzymes, including GPX, GR, and GST.
The first line of defense against ROS are both SOD
isoenzymes, which remove O.
2 by catalyzing
the dismutation reaction. CAT protects cells
and tissues by directly decomposing H2O2. The
glutathione transformation enzymes eliminate
H2O2 in reaction catalyzed by GPX. In SF,
these anti-oxidant enzymes often coexist.49 The
absence or dysfunction of some of these anti-
oxidant enzymes make the components of the joint
cavity vulnerable to oxidative damage.51
We hypothesized that patients with knee post-
traumatic arthritis, associated or not to hemar-
throsis, display a decreased anti-oxidant system.
Meanwhile, the anti-oxidant system, measured
by activities of anti-oxidant enzymes, was found
to be significantly higher in SF from PA patients
compared to the control subjects. In addition to
being in contrast to our hypothesis, it is also in
JOURNAL OF ORTHOPAEDIC RESEARCH JUNE 2007
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contrast to many reports which have found
decreased anti-oxidant enzymes’ activities in SF
from knee PA. It is possible that the difference in
results in anti-oxidant system between our studies
and those in others reports is due to differences in
the stage of disease between studies. Chronic
joint diseases may deplete anti-oxidant defenses,
whereas acute post-traumatic arthritis may upre-
gulate them.49,52 The samples used in the present
study represent an acute PA with inflammatory
exudates in the knee joints, especially in HA
subgroup.
Conflicting data are presented in the literature
about concentration of anti-oxidants’ enzymes in
post-traumatic SF. Schumacher13 found that there
was no SOD, and no or low CAT in synovial fluid
from arthritic joints. Terĉiĉ and Boziĉ14 found
similar results as well as decreased SOD, CAT,
and GPX activities in synovial fluid from patients,
as compared to normal synovial fluid. In another
study,51 it was suggested that these anti-oxidant
enzymes are rarely present in extracellular fluids,
such as SF, which contain little or no CAT activity,
and only low activities of SOD isoenzymes and
GPX. There is also very little GR and GST.51 In
contrast, Sumii et al.53 found that high levels of
ROS in synovial fluid can induce high activity of
SOD isoenzymes locally to protect articular carti-
lage from the harmful effects of the ROS.6,31,53,54
Ostalowska et al. found52 similar results as well as
DOI 10.1002/jor

increased activities of anti-oxidant enzymes in SF
from patients with the secondary type of osteoar-
thritis of the knee joint (KOA). All patients from the
secondary KOA subgroup had a history of knee
post-traumatic arthritis.
By contrast with the intracellular presence,
CAT is significantly less prominent in human
extracellular fluids. Blood plasma, tissue fluid,
cerebrospinal fluid, synovial fluid, and seminal
plasma contain little or no catalase activity.
In the present study, we did not find activity of
catalase in the investigated SF samples. However,
it seems possible that lack of CAT activity
could result from the existence of other mecha-
nisms of anti-oxidizing defense of synovial fluid,
with decomposing hydrogen peroxide without
participation of CAT, e.g., at participation of
glutathione peroxidase.
In conclusion, we suggest that patients with
knee post-traumatic arthritis, associated or not to
hemarthrosis, display altered oxidant and anti-
oxidant systems in their synovial fluid. Concurrent
with the increased lipid peroxidation, measured by
MDA concentration, was a tendency for changed
anti-oxidant systems with increased anti-oxidant
enzyme activities, suggesting a potential adapta-
tion to the increased ROS in synovial fluid from
knee PA.
ACKNOWLEDGMENTS
This work is supported by the Medical University of
Silesia (NN-2-179/05). We thank Dr. Sławomir Kożuch
and Dr. Janusz Stelmaszyński (Department of Ortho-
paedic Surgery, Special Hospital No. 4 in Bytom) for
providing specimens of synovial fluid from patients with
the knee joints exudates, and Dr. Ludmiła Słowińska
(Department of Biophysics, Medical University of
Silesia) for her help in the synovial fluid viscosity
determinations.
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