Key result
Mild oxidation of low-density lipoproteins in vitro was more potent than strong oxidation in activating platelets, whereas glycosylation alone had little effect on platelet aggregation.
Mild oxidation of LDL, rather than strong oxidation or glycosylation, appears to be the primary driver of LDL-mediated platelet activation in vitro.
Mild LDL oxidation effects on platelets should not change practice; hypothesis-generating for in vivo thrombosis mechanisms.
Low-density lipoproteins (LDL) are thought to influence directly the sensitivity of platelets, but this may only be the case when the LDL are modified by oxidation. In diabetes, LDL are known to be modified by non-enzymatic glycosylation, especially when the blood glucose concentrations are poorly controlled: platelet activation is also concomitantly increased as is the concentration of plasma lipid peroxides. In this study we found that mild oxidation of LDL in vitro is more potent than strongly oxidised LDL in terms of the activation of platelets. Glycosylation of LDL per se has little effect on the aggregation of isolated platelets.
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Meraji et al. (1992) studied this question. Mild oxidation or glycosylation of LDL vs. Strongly oxidised LDL or unmodified LDL was evaluated on Platelet activation and aggregation. Mild oxidation of low-density lipoproteins in vitro was more potent than strong oxidation in activating platelets, whereas glycosylation alone had little effect on platelet aggregation.
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