Chondroitin 4-sulphate (C4S), a basic component of the extracellular matrix of the artery wall, inhibited copper-induced low density lipoprotein (LDL) oxidation by prolonging the lag time and reducing the rate of propagation. LDL oxidation was assessed by monitoring conjugated dienes and low level chemiluminescence. A possible initial key reaction in LDL oxidation, the reduction of copper(II) to copper(I) by LDL, was decreased in the presence of C4S. Moreover, C4S protected tryptophan residues of Apo-B-100 in the early stage of LDL oxidation and during the subsequent propagation phase. The presence of the sulphate group in position 4 of N-acetylgalactosaminyl residues of C4S is crucial for protective activity. In fact, the structurally related chondroitin 6-sulphate, also present in tissues, had no effect on LDL oxidation. These data suggest that C4S may contribute to protect LDL against oxidation in arterial intima.
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Albertini et al. (1997) studied this question.
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