Okay, so there are literally hundreds of websites that talk about oxidized cholesterol. I now realize that it is the same thing as "lipid peroxides" that Dr. Eades wrote so much about in Protein Power LifePlan. He says rancid oils have oxidized cholesterol.
From everything I've read, I can only say that there has not been a definitive list of foods that definitely have oxidized cholesterol. Any fat can oxidize and a lot of fats do actually oxidize right inside our bodies everyday due to free radicals. This is dangerous because the latest information is that the only kind of cholesterol (LDL type) to cause artery damage is oxidized (LDL) cholesterol which is why we need to ensure we eat and supplement with antioxidants (Vitamin C, E and beta carotene etc. walnuts, strawberries, blueberries, etc. flavonoids in fruit and red wine).
The studies say that processing foods that naturally contain fat will oxidize the cholesterol (fats) in the food. Dried egg noodles have dangerous oxidized cholesterol (Italian research). It has also been said that aged cheese has oxidized cholesterol and powdered eggs and aged meat. Smoking cigarettes, having stress and pollution can oxidize fats in your own body. Heat and cooking also oxidize fats (lipids). But we heat and cook everything anyway.
I will quote what I think is a balanced discussion with references here:
Other toxic effects of cooking
Heated Milk Protein
It is possible that heated milk protein may be a factor in atherosclerosis [Annand 1971, 1972, 1986].
Oxidized fats, oils, and cholesterol. Research reveals that in animal models, oxidized fats, oils, and cholesterol induce higher levels of arterial plaque (i.e., atherogenesis) than do the corresponding non-oxidized fats, oils, and cholesterol [Taylor et al. 1979, Kummerow 1993, Kubow 1993, O'Keefe et al. 1995]. The biochemical processes that make oxidized fats atherogenic are the subject of scientific controversy; however, one suggestion is that the heating of fats, oils, and cholesterol increases the levels of lipid peroxide products. The idea is that the peroxides (in combination with lipids) promote an atherogenic response [Kubow 1993].
In tests feeding high-cholesterol diets to rabbits, the consumption of scrambled or baked eggs produced increases in serum cholesterol of 6-7 times the pre-existing levels, while fried or hard-boiled eggs raised levels by 10-14 times [Pollack 1958]. Cordain [in a posting to the Paleodiet list of 10/9/1997] also reports that his research group routinely induces atherogenesis in test animals (miniature swine) by feeding oxidized fats/cholesterol.
Role of oxidized LDL cholesterol in atherogenesis. O'Keefe et al. [1995, pp. 70, 72] explain the role of oxidized cholesterol in atherogenesis as follows:
LDL cholesterol must be oxidized or glycosylated (or both) before it becomes atherogenic.(8,9) Oxidative modification of cholesterol occurs by means of oxygen free radical processes. Only after the LDL has been modified (through oxidation or glycosylation) does it activate differentiation and migration of macrophages. The scavenger receptors on the macrophages recognize oxidized LDL (but not unmodified LDL) and allow for subsequent phagocytosis. When the macrophage becomes filled with oxidized LDL cholesterol, it becomes the foam cell that is typically observed in early atherosclerotic lesions...
The oxidative modification of LDL cholesterol seems to be the final common pathway in the process of atherosclerosis.
Steinberg et al.  also report that oxidized LDL cholesterol, at high levels, is atherogenic. For a good summary of the atherogenic properties of oxidized LDL cholesterol, see Table 2 in O'Keefe et al. [1995, p. 72], and Table 1 in Steinberg et al. [1989, p. 917].
Here it should be noted that some aspects of the effects of oxidized cholesterol are controversial in the sense that a scientific consensus has not yet been reached. Readers are encouraged to consult O'Keefe et al.  and Steinberg et al.  for a detailed overview of current knowledge in this field.
The paradox of relatively high cholesterol intake and cooked meats vs. rarity of heart disease in hunter-gatherer groups
. It is also worth remarking that many other factors than lipid peroxides influence the development and/or prevention of atherogenesis, such as the amount of saturated fat, amount of mono- or polyunsaturated fat, amount of carbohydrates and insulin response, etc. Of particular note here is the example of hunter-gatherer societies, where the incidence of heart disease is extremely low (perhaps the lowest that has been seen among human groups), despite the fact that relatively large amounts of cooked meat are consumed.
(See Part 3's discussion of hunter-gatherers for a look at some of their food preparation practices; as well as another site link, Hunter-Gatherers: Examples of Healthy Omnivores, for a look at disease incidence.) This is in marked contrast to the high levels of atherosclerosis in Western diets containing cooked meat.
This divergence may be due to the differences between the type of meat (wild game) in hunter-gatherer diets--which in general is quite lean--compared to modern domesticated meats (five times less fat, and one-fifth to one-sixth as saturated [Eaton 1996]), and/or the difference may be due to a range of other factors. Of specific interest regarding the subject of oxidized cholesterol is that while hunter-gatherers eat roughly the same amount of cholesterol (480 mg) as in the modern Western diet [Eaton 1992] (from meat, presumably cooked), their serum cholesterol levels, as measured in five modern hunter-gatherer groups, averaged a very low 123.2 mg/dL [Eaton 1992].
Viewing single factors out of context can be misleading. Thus if cholesterol and/or oxidized cholesterol are in fact atherosclerotic in effect, then the implication is that there must be something else in the diets/lifestyles of hunter-gatherer groups mitigating or negating this effect.
(A good overview of the large divergences between hunter-gatherer diets and the modern Western diet can be found in Eaton . Major differences are to be found in consumption levels of saturated and polyunsaturated fats, preformed long-chain fatty acids, protein, carbohydrate, phytochemicals, etc., as well as in exercise levels.)
The general point here is to keep in mind that, before attempting to form conclusions that might be premature, it is important to view the role of any one factor in the equation of health in the context of the overall diet rather than in isolation. Depending on the situation, the benefits of a food or class of foods may mean more for the health of the body than whatever associated negatives there may be--or vice versa. That nutritional benefits from foods, whether raw or cooked, unavoidably come at the expense of costs and tradeoffs is a central issue that we will return to more than once, in different forms, as this paper proceeds.
Mayo Clin Proc 1995 Jan;70(1):69-79
Insights into the pathogenesis and prevention of coronary artery disease.
O'Keefe JH Jr, Lavie CJ Jr, McCallister BD.
Mid America Heart Institute, Kansas City, Missouri.
OBJECTIVE: To present information about risk factor clustering and the oxidation hypothesis of atherosclerosis and attempt to synthesize these facts into a clinically relevant approach to patients with or at risk for coronary artery disease (CAD). MATERIAL AND METHODS: The total cholesterol level is a relatively weak marker for the risk of CAD. The levels of both high-density lipoprotein (HDL) cholesterol and remnants of triglyceride-rich lipoproteins and the inherent susceptibility of the low-density lipoprotein (LDL) particles to oxidative modification may be as important as the total or LDL cholesterol levels. LDL cholesterol must undergo oxidative modification by means of oxygen free radical processes before it becomes atherogenic.
Patients with high levels of oxidative stress include those with risk factor clustering or insulin resistance (or both). Such patients are characterized by hypertension, truncal obesity, hypertriglyceridemia, depressed HDL cholesterol levels, and increased insulin levels. They also have increased levels of triglyceride-rich remnant lipoproteins and LDL particles that are characterized by their small dense nature and pronounced predisposition to oxidative modification. RESULTS: Biologic antioxidants seem to be promising therapy for the prevention of atherogenesis. Although long-term prospective data are not yet available, vitamin E has been shown to be effective in both animal and human models in preventing LDL oxidation
, and it may have a role in the prevention of CAD. A healthy diet of fresh fruits, vegetables, and whole grains is beneficial because it improves the lipid levels and provides high levels of natural antioxidants. The atherogenic potential of hydrogenated polyunsaturated fats is approximately equivalent to that of saturated fats. Monounsaturated fat [like Olive Oil] is inherently resistant to oxidation and may be protective against CAD.
Niacin may be effective in patients with clustered risk factors. It has been found to convert the easily oxidized small dense LDL pattern to the large buoyant oxidation-resistant particles. Hydroxymethylglutaryl-coenzyme A reductase inhibitors are well tolerated and highly effective in decreasing LDL cholesterol, but they are expensive. Estrogen has multiple potentially beneficial effects relative to cardiovascular disease. CONCLUSION: Persons with or at high risk for CAD should be identified early and aggressively treated with a program that involves lifestyle changes, alterations in dietary intake, and pharmacologic therapy.