High Cholesterol Symptoms And Causes

oxidized cholesterol, what is it?

What is more, antioxidant compounds, including probucol, probucol analogs, vitamin E, coenzyme Q, diphenylphenylenediamine, and butylated hydroxytoluene were investigated in the scope of atherosclerosis and oxLDL in various animal models. Mostly, the results of these investigations were successful (Witztum and Steinberg, 2001). The oxidative modification hypothesis was suggested by Steinberg and Chisolm groups (Hessler et al., 1979; Henriksen et al., 1981; Steinberg and Witztum, 2002). This is because high cholesterol can lead to the formation of plaque in your arteries, which can eventually cause them to narrow and harden. This can lead to blood clots, which can block blood flow to your heart and potentially cause a heart attack. In terms of dairy, in my last video, I talked about the potential dangers of ghee, which made me wonder about UHT milk, which stands for ultra-high temperature processing, to make little half-and-half no-refrigeration-needed coffee creamers.

However, there are still unresolved issues, including the identity of the physiological oxidizing agents, the characteristics of naturally occurring OxLDL species, and the importance of lipid oxidation for the formation of foam cells and atherogenesis. Furthermore, the use of poorly defined OxLDL preparations in various studies led to irreproducible, and at times conflicting data on the biological activities and proposed mechanisms. There is thus a need for sell the standardization of OxLDL preparations and development of criteria to define and classify the various preparations based on a more robust analytical methodology than TBARS assay, which is fraught with numerous pitfalls. Some of the potential candidates include the analysis of one or more oxidized PAPC products by LC/MS, measuring the epitopes of modified Apo B by specific monoclonal antibodies, and the quantitation of modified lysine residues of Apo B.

It was first identified by expression cloning of the cDNA library of bovine aortic endothelial cells (247). Expression of LOX-1 in CHO cells resulted in binding and degradation of OxLDL comparable to that in cells expressing SRA receptors. The binding was effectively inhibited by OxLDL but not by native LDL or acLDL (193, visit the website 247). The human homolog isolated in the same study from human lungs was shown to have similar properties. In vivo, LOX-1 receptor was shown to be most abundant in vascular-rich organs, such as lungs, placenta, and brain (247). It was also identified in thoracic and carotid arteries, including atheromatous regions (247).

oxidized cholesterol, what is it?

The sn-1 alkyl analogs of LPA were shown to be more prevalent in the mildly oxidized LDL, and are 20 times more potent than the acyl analogs in platelet activation (257). In addition to promoting chemokine expression by endothelial cells, LPA stimulates the uptake of OxLDL itself through upregulation of scavenger receptor super fast reply A in macrophages (41), and increases monocytes migration at low concentrations (83). It was also shown to stimulate SMC proliferation through the activation of the transcription factor Egr-1 (48). Similarly, targeted disruption of CD36 in apoE knockout mice resulted in 45% 75% decrease in lesion formation (63).

If you’re concerned about your cholesterol levels, talk to your doctor, who can help you understand your risk factors and develop a plan to keep your heart healthy. Egg powder in processed foods is good for shelf life, but it may not be so good for human life. Some examples of packaged foods with egg products include some pastas, many baked goods, and mayonnaise. So, even people who stay away from eggs out of the egg carton may still be exposed unwittingly through processed foods if they don’t read the ingredients label.

After all, oxidized LDL is still a promising object for further investigations that have the potential to clarify the unknown parts of the atherogenic process. In this review, we discuss the role of oxLDL in atherosclerosis development on different levels. Another bioactive lysophospholipid that is present in OxLDL is lysophosphatidic acid (LPA). This compound is generated from LPC by the action lysophospholipase D (autotaxin) (290), and is a well-known mitogen that acts through specific G-protein coupled receptors. Seiss et al. (257, 259) demonstrated the accumulation of LPA during the oxidation of LDL, as well as in atherosclerotic lesions, and identified it as the factor responsible for platelet activation by OxLDL, although the receptor responsible for this effect remains elusive.

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