Literature DB >> 10765936

Abnormalities of erythrocyte membrane fluidity, lipid composition, and lipid peroxidation in systemic sclerosis: evidence of free radical-mediated injury.

R Solans1, C Motta, R Solá, A E La Ville, J Lima, P Simeón, N Montellà, L Armadans-Gil, V Fonollosa, M Vilardell.   

Abstract

OBJECTIVE: To elucidate whether oxidative injury occurs in systemic sclerosis (SSc) and whether it affects the erythrocyte membrane (EM) properties.
METHODS: EM fluidity and lipid composition (cholesterol:phospholipid molar ratio [C:PL], fatty acid composition) were studied in 52 patients with SSc and in 53 subjects without SSc (32 with primary Raynaud's phenomenon [RP] and 21 healthy subjects [controls]). Fluidity was measured as the fluorescence anisotropy of the hydrophobic fluorescent probe DPH (1,6-diphenyl-1,3,5-hexatriene). Lipid peroxidation products were determined as thiobarbituric acid-reactive substances (TBARS).
RESULTS: EM fluidity was significantly lower in SSc patients than in primary RP patients and controls (P < 0.001). The EM C:PL molar ratio was significantly higher in SSc patients than in primary RP patients and controls (P < 0.05). Levels of EM polyunsaturated n6 fatty acids (PUFA n6) were significantly lower in SSc patients than in primary RP patients and controls (P < 0.001). TBARS were significantly increased in SSc patients compared with primary RP patients and controls (P < 0.001). Multiple regression analyses indicated that the reduced EM fluidity was partly due to its greater C:PL molar ratio, lower PUFA n6 content, and higher TBARS levels. EM fluidity was lower among patients with nailfold capillary loss (P < 0.001) and digital ischemic ulcers (P < 0.05). EM lipid peroxidation products were higher among patients with pulmonary involvement (bibasal pulmonary fibrosis [P < 0.05] and reduced levels of diffusing capacity for carbon monoxide [P < 0.001]) and among patients who were positive for anti-topoisomerase I antibodies (P < 0.05) or negative for anticentromere antibodies (P < 0.001).
CONCLUSION: Our findings support the idea that oxidative injury occurs in SSc and that, through lipid peroxidation, it induces structural and functional changes of the EM that may contribute to the development of the microvascular abnormalities that are seen in the disease.

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Year:  2000        PMID: 10765936     DOI: 10.1002/1529-0131(200004)43:4<894::AID-ANR22>3.0.CO;2-4

Source DB:  PubMed          Journal:  Arthritis Rheum        ISSN: 0004-3591


  18 in total

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Review 2.  Microvascular damage in systemic sclerosis: detection and monitoring with biomarkers.

Authors:  Laura K Hummers
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3.  Lipid peroxidation and trace elements in systemic sclerosis.

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5.  Effect of a high-altitude expedition to a Himalayan peak (Pumori, 7,161 m) on plasma and erythrocyte antioxidant profile.

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7.  Abnormalities in the regulators of angiogenesis in patients with scleroderma.

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8.  Radical oxygen species production induced by advanced oxidation protein products predicts clinical evolution and response to treatment in systemic sclerosis.

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9.  17β-Estradiol Directly Lowers Mitochondrial Membrane Microviscosity and Improves Bioenergetic Function in Skeletal Muscle.

Authors:  Maria J Torres; Kim A Kew; Terence E Ryan; Edward Ross Pennington; Chien-Te Lin; Katherine A Buddo; Amy M Fix; Cheryl A Smith; Laura A Gilliam; Sira Karvinen; Dawn A Lowe; Espen E Spangenburg; Tonya N Zeczycki; Saame Raza Shaikh; P Darrell Neufer
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Review 10.  Molecular biomarkers in interstitial lung diseases.

Authors:  Angelo De Lauretis; Elisabetta A Renzoni
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