Increased levels of lipid oxidation products in low density lipoproteins of patients suffering from rheumatoid arthritis
Introduction
Lipidperoxidation products of arachidonic acid, e.g. prostaglandines (Bergström and Sjövall, 1957, Bergström et al., 1962), thromboxanes (Hamberg et al., 1975), prostacyclines (Moncada et al., 1976, Moncada et al., 1978) and leukotrienes (Borgeat and Samuelsson, 1979, Murphy et al., 1979, Oerning et al., 1980) are well known potent physiological active compounds in humans and animals. Jasmonic acid, derived by lipid peroxidation of linolenic acid is a comparable potent active compound in plants (Vick and Zimmerman, 1987). In contrast only very little is known about the physiological role of lipid peroxidation products of linoleic acid: Moch et al. (Moch et al., 1990) recognized that 9-Hydroxy-10,12-octadecadienoic (9-HODE), derived by lipid peroxidation of linoleic acid followed by enzymic reduction, has comparable inflammatory potence to leukotrienes. Ku et al. (Ku et al., 1992) reported, that 9-HODE and the isomeric 13-hydroxy-9,11-octadecadienoic acid (13-HODE), but also cholesteryl-9-HODE induce the release of interleukin 1β from macrophages.
Comparing the lipid peroxidation products of myocardial infarcted tissue of a porcine heart with the surrounding non infarcted tissue of the same heart we recognized that the content of 9-HODE was increased for a factor of about 20 (Dudda et al., 1996).
9- and 13-HODE are also main lipid peroxidation products observed after injury of tissue. Hereby hydroxy acids of linoleic acid outweighed those of arachidonic acid for a factor of four, indicating a major involvement of linoleic acid in the LPO process (Herold and Spiteller, 1996). This observation stimulated us to investigate samples of patients suffering from other diseases in which increased amounts of lipid peroxidation products were reported by measurement of thiobarbituric acid reactive substances (TBARS). One of these diseases is rheumatism.
Lunec et al. (Lunec et al., 1981) found increased concentrations of conjugated dienes and fluorescent lipid peroxidation products in the serum and synovial fluid of patients with inflammatory joint diseases. By measuring MDA with the thiobarbituric acid test Muus et al. (Muus et al., 1979) detected, that the MDA concentration in the plasma correlates with disease activity. Selley et al. (Selley et al., 1992) found 4-hydroxy-2-nonenal in plasma and synovial fluid of patients with rheumatoid arthritis (RA) and osteoarthritis. In addition a loss of vitamin E in synovial fluid of rheumatic patients was observed (Fairburn et al., 1993). We report in this paper on the observation of a strong increase of 9- and 13-HODE and enhanced levels of aldehydic compounds in the LDL of patients suffering from RA.
Section snippets
Materials
N-Methyl-N-trimethylsilyltrifluoroacetamide (MSTFA) was obtained from Machery and Nagel (Düren, Germany). All other chemicals were purchased from Fluka (Neu Ulm, Germany). Solvents were destilled before use.
Methods
Blood samples of healthy individuals were obtained from the red cross blood service in Bayreuth. Samples of patients suffering from RA were provided from the hospital in Bayreuth. All patients (with exception of patient no. 8) showed typical signs of RA, considering the revised criteria from
Results
Most of the LOOHs produced during lipid peroxidation (LPO) of LDL are reduced enzymically to their hydroxy derivatives under catalysis by glutathione-dependent peroxidases (Lehmann et al., 1992). Thus determination of LOOHs and LOHs is required to obtain a true picture of the amount of LPO. This is achieved when the total content of LOOHs and LOHs is determined together by reduction of the mixture of hydroperoxides by catalytic hydrogenation (Nikkari et al., 1995), which not only reduces the
Discussion
Reactive oxygen species (ROS) play an important role in the pathology of a wide range of inflammatory diseases (Blake and Lunec, 1990). The involvement of these ROS in the pathogenesis of human rheumatoid diseases is based on the work of McCord (McCord, 1974) who showed that the decreased viscosity of synovial fluid from the joints of patients with RA could also be produced by exposing synovial fluid of hyaluronate (the glycosaminoglycan responsible for most of the synovial fluid viscosity) to
Abbrevations
13-HODE, 13-hydroxy-9,11-octadecadienoic acid; 13-HPODE, 13-hydroperoxy-9,11-octadecadienoic acid; 15-HPETE, 15-hydroperoxy-5,8,11,13-eicosatetraenoic acid; 9-HODE, 9-hydroxy-10,12-octadecadienoic acid; 9-LOH, 9-hydroxy octadecanoic acid; 9-LOOH, 9-hydroperoxy octadecanoic acid; AMPA, ammoniummolybdatophosphorus acid; BHT, butylated hydroxytoluene; CH cyclohexane; DMARD, disease-modifying anti-rheumatic drugs; EDTA, ethylene diamine tetra acetic acid; EE, ethylacetate; GC, gas chromatography;
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