After all, it has already oxidized. The oxidative stress from it is a thing of the past, or is it?
Will it cause further oxidation and even be a seed that begins another round of lipid peroxidation?
And if not, what harm does it cause to just leave the oxidized LDL alone in a foam cell that is part of the necrotic core in plaque?
The reason I ask is I've always assumed the oxidized LDL to be a source of lipid peroxidation. thinking that as long as it exists, there would continue to be a source of lipid peroxidation, long after a person has stopped taking PUFAs in his diet. Now I'm questioning this assumption so I'm asking this.
Thanks for your reply.
Will it cause further oxidation and even be a seed that begins another round of lipid peroxidation?
And if not, what harm does it cause to just leave the oxidized LDL alone in a foam cell that is part of the necrotic core in plaque?
The reason I ask is I've always assumed the oxidized LDL to be a source of lipid peroxidation. thinking that as long as it exists, there would continue to be a source of lipid peroxidation, long after a person has stopped taking PUFAs in his diet. Now I'm questioning this assumption so I'm asking this.
Thanks for your reply.