<<snip>>
protein oxidation could play an important role in the pathogenesis of
rheumatoid arthritis as does lipid peroxidation.
<<snip>>
<<snip>>
The presence of molecular markers of in vivo lipid peroxidation was
demonstrated in osteoarthritic cartilage
<<snip>>

Arthritis Rheum. 2005 Sep 6;52(9):2799-2807 [Epub ahead of print]
Related Articles, Links

The presence of molecular markers of in vivo lipid peroxidation in
osteoarthritic cartilage: A pathogenic role in osteoarthritis.

Shah R, Raska K Jr, Tiku ML.

University of Medicine and Dentistry of New Jersey, New Brunswick.

OBJECTIVE: To investigate the role of oxidative functions in human
osteoarthritic (OA) chondrocytes and to investigate the presence of in
vivo molecular markers of lipoxidation in OA cartilage. METHODS: An in
vitro model of cartilage collagen degradation was used. Lipid
peroxidation activity and overall oxidative function in OA chondrocytes
were monitored by cis-parinaric acid and dichlorofluorescein assays,
respectively. In vivo molecular markers of lipoxidation in normal and
OA cartilage were studied using immunohistochemistry to detect the
presence of malondialdehyde and hydroxynonenal adducts. RESULTS: Human
OA chondrocytes showed a robust amount of (3)H-proline-labeled collagen
degradation upon stimulation with lipopolysaccharide and calcium
ionophore A21387, as compared with that in untreated OA chondrocytes.
Primary OA chondrocytes showed both spontaneous and inducible levels of
lipid peroxidation activity. However, lipid peroxidation activity was
already maximally elevated in more than 50% of the OA chondrocyte
samples. Overall, spontaneous and inducible oxidative activities were
observed in all OA samples. Immunohistochemical analysis of control OA
tissue sections that were not treated with monoclonal antibody showed
little immunoreactivity. OA cartilage sections treated with monoclonal
antibodies showed specific immunoreactivity on the cartilage surface,
at sites of OA lesions, at the pericellular matrix, and at intra- and
intercellular matrices. Normal cartilage sections showed faint surface
reactivity. CONCLUSION: Our observations suggest that human OA
chondrocytes demonstrate spontaneous and inducible cell-associated
lipoxidative and nonlipoxidative activity. Lipoxidative activity
appears to be enhanced in OA chondrocytes. The presence of molecular
markers of in vivo lipid peroxidation was demonstrated in OA cartilage,
suggesting its role in the pathogenesis of the disease.

PMID: 16145669 [PubMed - as supplied by publisher]

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Cell Biochem Funct. 2005 Sep 2; [Epub ahead of print] Related Articles,
Links

Investigation of protein oxidation and lipid peroxidation in patients
with rheumatoid arthritis.

Baskol G, Demir H, Baskol M, Kilic E, Ates F, Karakukcu C, Ustdal M.

Department of Biochemistry and Clinical Biochemistry, Erciyes
University, Faculty of Medicine, Kayseri, Turkey.

We aimed to determine the importance of neutrophil activation and the
source of oxidative stress in the pathogenesis of rheumatoid arthritis
(RA) by quantification of advanced oxidation protein products (AOPP)
and total thiol levels as markers of oxidative protein damage,
malondialdehyde (MDA) levels as a marker of lipid peroxidation and
myeloperoxidase (MPO) activity as a marker of neutrophil activation in
patients with RA. Fifty-seven rheumatoid arthritis patients were
included in the study and sub-grouped according to disease activity
(active, n = 31; inactive, n = 26) and compared with healthy controls
(n = 25). Serum MPO activity, AOPP, MDA, and thiol levels were measured
by an enzymic spectrophotometric method. Serum MPO activity (p <
0.001), AOPP (p < 0.001), MDA (p < 0.001) and levels of thiol (p <
0.002), were higher in the patient group than the controls. Active and
inactive RA groups were compared with the control group and there were
significant differences between each parameter. MPO activity, AOPP, MDA
and thiol levels were significantly higher in both active and inactive
RA patients than the controls. On the other hand, when a comparison was
made between active and the inactive stage, a statistically significant
difference was present only in MDA (p < 0.05) and AOPP levels (p <
0.05). There was also a significant positive correlation between all
parameters. These data strongly suggest that neutrophils, which
constitute the most important source of chlorinated oxidants due to
their high MPO content, may be involved in serum AOPP formation and
therefore the production of a novel class of pro-inflammatory mediators
of oxidative stress in RA patients and that protein oxidation could
play an important role in the pathogenesis of RA as does lipid
peroxidation. Copyright (c) 2005 John Wiley & Sons, Ltd.

PMID: 16142689 [PubMed - as supplied by publisher]

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