Open AccessAbnormalities of erythrocyte membrane fluidity, lipid composition, and lipid peroxidation in systemic sclerosis: Evidence of free radical–mediated injury
Author(s) -
Solans Roser,
Motta Claude,
Solá Rosa,
La Ville Agnes E.,
Lima Joan,
Simeón Pilar,
Montellà Nuria,
ArmadansGil Lluis,
Fonollosa Vicent,
Vilardell Miquel
Publication year - 2000
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/1529-0131(200004)43:4<894::aid-anr22>3.0.co;2-4
Subject(s) - tbars , membrane fluidity , lipid peroxidation , medicine , polyunsaturated fatty acid , phospholipid , endocrinology , diphenylhexatriene , thiobarbituric acid , chemistry , fatty acid , oxidative stress , biochemistry , membrane
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.