Table 1.
Mechanism | Reference |
---|---|
Prevention of LDL and cell membrane oxidation | 20, 60–65, 68 |
Prevention of LDL Glycation | 95 |
Prevention of diabetes development | 80, 81 |
Reduction of macrophage oxidative stress | 73 |
Promotion of macrophage RCT | 69, 73 |
Normalisation of endothelial function | 58, 75 |
Metabolism of homocysteine thiolactones+ | 96–98 |
Prevention of LCAT oxidative inactivation | 99 |
Disposal of toxic apoptosis products | 93 |
Prevention of apoptosis | 94 |
Reduction of monocyte macrophage inflammatory response | 101, 102 |
A physiological role for PON1 in the detoxication of homocysteine thiolactone (HCTL) has recently been challenged with the discovery that biphenyl hydrolase-like protein has a catalytic efficiency towards HCTL 7.7 × 104 M−1 s−1 greater than PON1 indicating it to be the physiological detoxicant [100].