OBJECTIVES: Despite the evidence that both homocysteine and cysteine are important risk factors for vascular disease and atherosclerosis no information are reported about their effective amount in plaque and on the relationship with the other low molecular weight thiols. DESIGN AND METHODS: We used capillary electrophoresis to measure thiols in both carotid plaque specimens and plasma samples from 37 patients undergoing carotid endarterectomy. RESULTS: Pearson's correlation shows that intraplaque homocysteine, cysteine and cysteinylglycine levels are related to their plasma concentrations. The distribution of intraplaque GSH and Glu-Cys was higher than that of the same thiols in plasma, whereas the other thiols were significantly less prevalent in plaque than in plasma. Intraplaque haemoglobin and GSH levels were correlated, thus suggesting their common origin from erythrocytes lysis. CONCLUSION: Data suggest that increased levels of intraplaque glutathione may induce important effects on plaque fate by perturbing the normal LMW thiol redox state.
OBJECTIVES: Despite the evidence that both homocysteine and cysteine are important risk factors for vascular disease and atherosclerosis no information are reported about their effective amount in plaque and on the relationship with the other low molecular weight thiols. DESIGN AND METHODS: We used capillary electrophoresis to measure thiols in both carotid plaque specimens and plasma samples from 37 patients undergoing carotid endarterectomy. RESULTS: Pearson's correlation shows that intraplaque homocysteine, cysteine and cysteinylglycine levels are related to their plasma concentrations. The distribution of intraplaque GSH and Glu-Cys was higher than that of the same thiols in plasma, whereas the other thiols were significantly less prevalent in plaque than in plasma. Intraplaque haemoglobin and GSH levels were correlated, thus suggesting their common origin from erythrocytes lysis. CONCLUSION: Data suggest that increased levels of intraplaque glutathione may induce important effects on plaque fate by perturbing the normal LMWthiol redox state.