## 1 Introduction  
The human intestinal epithelium is exposed to different chemicals that we ingest with food. Among those chemicals are lipid peroxides (LOOHs) that usually form in overheated oils (fried food). LOOHs, which are by-products of pre- or auto-oxidation of polyunsaturated fatty acids (PUFAs), have been implicated in various diseases including atherosclerosis [1, 2], neurodegenerative disease [3, 4], rheumatoid arthritis [5], inflammatory bowel disease [6, 7], and colorectal cancer (CRC) [8]. Oxidation of linoleic acid (LA), the most abundant PUFA in mammals and plants, results in the formation of 13-hydroperoxyoctadecationoic acid (13-HPODE), which is rapidly decomposed by cells into toxic aldehydes and carboxylic acids [9, 10]. Lipid peroxidation products including malondialdehydedehyde (MDA) and 4-hydroxynonenal (4-HNE) have shown to modulate gene expression and contribute to CRC [11]. In addition, frying oil has shown to worsen the inflammatory condition and tumorigenesis in the colon [12]. Caco-2 cells, which are derived from human colorectal adenocarcinoma [13], have been widely used to study intestinal metabolism of molecules and drugs [14; 15]. These cells, under standard culture conditions, have the ability to become differentiated (Diff; 14-Day) and acquire mature enterocyte-like structural and functional characteristics which makes it a suitable model to study lipid peroxidation [16; 17; 18; 19; 20; 21; 22]. On the other hand, undifferentiated or poorly differentiated (PDiff; 4-Day) Caco-2 cells mimic in vivo intestinal cancer cells and could model intestinal crypt cells, as they share the proliferative phenotype and lack of microvilli cells [23; 24], which might be exposed to dietary LOOHs and contribute to disease. It has been shown that the absorption of LA, the most common dietary PUFA, by PDiff and Diff Caco-2 cells was comparable; however, the absorption of peroxid oxidized LA, 13-HPODE, by PDiff cells was less efficient compared to its absorption by Diff cells that possess brush borders [1]. It has been suggested that dietary oxidized fatty acids are absorbed by the intestine and are esterified into complex oxidized lipids that are transported in the plasma by lipoproteins [1]. Intestinal epithelial lipid transport by apolipoprotein B (ApoB) during differentiation depends on _microsomal triglyceride transfer protein_ (_MTTP_), which is suppressed by nuclear receptor 2 family 1 (_NR2F1_) in PDiff Caco-2 cells [25]. It has been demonstrated that _MTTP_ overexpression in PDiff Caco-2 cells increases triglyceride (TG) transfer activity and cholesterol esterification indicating the essential role of MTTP in lipid absorption [26]. Effects of linoleic acid on cells range from production of nitric oxide (NO) and reactive oxygen species (ROS) to protection against oxidative stress [27; 28]. In addition, dietary PUFAs are highly susceptible to peroxidation, which has been implicated in the development of colon cancer [11]. Moreover, oral consumption of frying oil in mice has shown to aggravate colon tumorigen [12]. Our recent study demonstrated alterations in the expression of inflammatory genes and reduced cell viability on annexin V staining of PDiff Caco-2 cells when treated with peroxid oxidized LA, 13-HPODE [6]. Despite these studies, the effects of dietary LOOHs on PDiff Caco-2 cells, which are sensitive to chemicals, have not been characterized fully. PDiff Caco-2 cells are used in cancer studies because their gene expression profile resembles that of human colon cancer cells [23], and might also reflect other subpopulation cell types in the human colon [29]. Of note, intestinal proliferative crypt cells might undergo programmed cell death, under stressful conditions, to remove damaged cells and protect from tumorigenesis [30] suggesting that crypt cells could initiate gut pathology.