Thermally Abused Frying Oil Potentiates Metastasis to Lung in a Murine Model of Late-Stage Breast Cancer (original) (raw)
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Cancer, 2021
This commentary refers to our recently published article “Association of long-term consumption of repeatedly heated mix vegetable oils (RHMVO) in different doses and hepatic toxicity through fat accumulation.” As highlighted in this article, longterm intake of RHMVO leads to fat accumulation in hepatocytes, oxidative stress, and lipid peroxidation. Several studies have illustrated the negative effect of RHMVO on human health. In this commentary, we considered other recent evidence reporting the carcinogenic and mutagenic potential of RHMVO. Furthermore, we emphasized the unique and easy to perform parameters to measure oxidative stress, lipid peroxidation, fat accumulation, and increased inflammation in hepatocytes to identify progression toward hepatic carcinoma. Our commentary is also intended to further highlight the necessity of developing food policies and regularity bodies as an approach to minimize the increasing trend of cancer incidence.
Deep frying cooking oils promote the high risk of metastases in the breast-A critical review
Food and Chemical Toxicology, 2020
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Journal of Neoplasms
Diets high in unsaturated fatty acids, especially those containing high levels of linoleic acid, e.g., corn oil, enhance mammary gland tumorigenesis in experimental animals. In contrast, diets high in long-chain polyunsaturated fatty acids such as eicosapentaenoic (EPA) and docosahexaenoic (DHA), e.g. menhaden oil, appear to have a suppressive effect on this tumorigenic process. Many mechanisms have been proposed to explain the tumor inhibitory action exerted by menhaden oil and other fish oils, e.g., differences in prostaglandin metabolism, energy efficiency, alterations of the immune system, changes in lipid peroxidation, etc. Fundamental to a mechanistic understanding of this phenomenon, however, is an understanding as to whether or not the tumor inhibitory activities of dietary fish oil is mediated via an inhibition of tumor cell proliferation or mediated via an enhancement of tumor cell loss. Whether the amount of dietary fat or the type of fat effects mammary tumorigenic proce...
Cytotoxic Compounds Generated in Heated Oil and Assimilation of Oil in Wistar Rats
Journal of oleo science, 2009
We have previously suggested that gluten binds with decomposition products from thermally oxidized oil during frying, and that low-molecular-weight compounds bound to browned gluten damage the liver in rats. Ten-week-old male Wistar rats were fed for 11 weeks ad libitum a diet containing 7 wt% fresh frying oil and 0.1 wt% gluten heated in/without oil at 180 for 10 h. Feces collected weekly and serum were subjected to lipid and hematological analyses, respectively. Values obtained in the analyses did not differ from those of the control group. The results show that thermally processed gluten does not influence the digestion, absorption, metabolism, and growth of rats, regardless of the cytotoxic lowmolecular-weight compounds, and that ingested fresh oil was assimilated normally. Together with the previous results, the odor of thermally processed gluten stimulated the rats' appetite, and completely assimilable fresh oil and cytotoxic low-molecular-weight compounds bound to gluten were ingested, and thus organ damage and rapid body weight increase were observed. As commercial deep-fried products are often made with repeatedly used oil with periodically added fresh oil, similar to the present experimental diet, obesity and organ damage may also occur in humans.
Effects of Oxidised Oils on Inflammation-Related Cancer Risk
Journal of Oil Palm Research
The practice of using cooking oils that are heated repeatedly is common to reduce the expenses of food preparation. However, this will result in lipid peroxidation, which generates compounds that are toxic to human health. Prolonged consumption of oxidised oils may affect lipid metabolism, which generates free radicals and products that will lead to pro-inflammatory pathways. A number of cellular, animal and clinical studies have revealed the effects of oxidised oils on inflammatory responses. By-products of lipid peroxidation, including trans, trans-2,4-decadienal (2.4-De), 4-hydroxy-2-hexenals (4-HHE) and malonaldehyde (MDA) can be found significantly in samples treated with oxidised oils. Besides, the release of inflammatory biomarkers or cytokines will be induced due to the enhanced degree of oxidative stress. Inflammation has been acknowledged to be linked to increased risk of cancer. Therefore, the consumption of repeatedly heated oils, which have higher level of oxidation may potentially lead to cancer progression. The possible cancer risk induced by the dietary intake of pro-inflammatory oxidised oils, methodology considerations and limitations of studies related to cancer risk induced by pro-inflammatory oxidised oils will be discussed in this review.
Dietary Fat and Cancer-Which Is Good, Which Is Bad, and the Body of Evidence
International Journal of Molecular Sciences, 2020
A high-fat diet (HFD) induces changes in gut microbiota leading to activation of pro-inflammatory pathways, and obesity, as a consequence of overnutrition, exacerbates inflammation, a known risk factor not only for cancer. However, experimental data showed that the composition of dietary fat has a greater impact on the pathogenesis of cancer than the total fat content in isocaloric diets. Similarly, human studies did not prove that a decrease in total fat intake is an effective strategy to combat cancer. Saturated fat has long been considered as harmful, but the current consensus is that moderate intake of saturated fatty acids (SFAs), including palmitic acid (PA), does not pose a health risk within a balanced diet. In regard to monounsaturated fat, plant sources are recommended. The consumption of plant monounsaturated fatty acids (MUFAs), particularly from olive oil, has been associated with lower cancer risk. Similarly, the replacement of animal MUFAs with plant MUFAs decreased cancer mortality. The impact of polyunsaturated fatty acids (PUFAs) on cancer risk depends on the ratio between ω-6 and ω-3 PUFAs. In vivo data showed stimulatory effects of ω-6 PUFAs on tumour growth while ω-3 PUFAs were protective, but the results of human studies were not as promising as indicated in preclinical reports. As for trans FAs (TFAs), experimental data mostly showed opposite effects of industrially produced and natural TFAs, with the latter being protective against cancer progression, but human data are mixed, and no clear conclusion can be made. Further studies are warranted to establish the role of FAs in the control of cell growth in order to find an effective strategy for cancer prevention/treatment.
Assessment of carcinogenic potential of repeated fish fried oil in mice
Molecular carcinogenesis, 2006
Our prior studies have shown that single topical treatment of repeated fish fried oil extract (RFFE), containing various polycyclic aromatic hydrocarbons (PAHs), to the dorsal epidermis of mice caused enhancement of DNA damage along with higher expression of p53 and p21WAF1 proteins and cell-cycle arrest. In the present study carcinogenic potential of repeated fish fried oil (RFFO) and RFFE was assessed. Single topical application of RFFO (100 mL/animal) and RFFE (100-500 mg/animal) to Swiss albino female mice resulted in significant induction (1.8-to 7.4-fold) of ornithine decarboxylase activity. Twice weekly topical application of methylcholanthrene (MCA) for 24 wk or single topical application of 7,12-dimethylbenzanthracene (DMBA) or RFFO or RFFE, as initiator followed by twice weekly application of 12-O-tetradecanoyl phorbol myristate acetate (TPA) as promoter for 24 wk, resulted in development of skin papillomas after 6, 7, 18, and 9 wk, respectively. The cumulative number of tumors in MCA, DMBA/TPA, RFFE (200 mg)/TPA, and RFFE (500 mg)/TPA groups were 276, 168, 34, and 58 after 24 wk while negligible or minimal initiating activity was noticed in RFFO/TPA group. No tumors were found in animals either given twice weekly topical application of RFFO or a single initiating dose of DMBA followed by twice weekly application of RFFO. Histopathology of skin of animals treated with RFFE/TPA showed marked proliferation of epidermal layers along with abnormal mitosis and multinucleated tumor appearance. Skin of animals in groups RFFO/TPA and DMBA/RFFO showed sloughing and regeneration of epidermal layers, oedema along with proliferation of fibroblasts. Histochemical localization of gglutamyl transpeptidase was found to be substantially higher in skin of mice treated with RFFO/TPA and RFFE/TPA. Animals treated with RFFO/TPA, DMBA/RFFO, and RFFE/TPA resulted in significant induction of cutaneous aryl hydrocarbon hydroxylase (AHH) (421-432%), ethoxyresorufin-O-deethylase (252-316%), and glutathione Stransferase (133-245%) activities. Animals treated with RFFO/TPA, DMBA/RFFO, and RFFE/TPA led to significant reduction in glutathione content (39-44%) with a concomitant increase in lipid peroxidation (254-492%). Animals treated with RFFO/TPA and RFFE/TPA led a significant decrease in catalase (43-69%) and superoxide dismutase (20-31%) activities while glutathione reductase activity was found to be diminished (23-51%) in RFFO, RFFO/TPA, DMBA/ RFFO, and RFFE/TPA treated groups. These results suggest that RFFE possess skin tumor initiating activity and that it may have weak promoting activity as well, which may involve free radicals. ß
Chemoprevention of Breast Cancer by Fish Oil in Preclinical Models: Trials and Tribulations
Cancer Research, 2011
Despite the perception that omega-3 fatty acids (n-3 FA) protect against breast cancer, epidemiologic studies have yielded inconsistent results. Although preclinical data have been, in general, more supportive of a protective effect of n-3 FA on breast cancer, inconsistencies still remain, which preclude definite conclusions or in-depth mechanistic investigations despite 30 years of research in this area. In this review, we discuss key variables that may account for inconsistencies of results across preclinical studies and provide recommendations for future experiments testing the chemopreventive effect of n-3 FAs in breast cancer, as part of a multiagent approach under rigorously controlled conditions. Cancer Res; 71(19); 6091-6. Ó2011 AACR.
Breast Cancer Research and Treatment, 2004
Effects of a high corn oil and a high olive oil diet on the histopathologic characteristics of rat dimethylbenz(α)anthracene-induced mammary adenocarcinomas were investigated in comparison with those of a control low-fat diet. Two experimental series (A and B) studied the influence of a high corn oil diet on the initiation and the promotion of mammary carcinogenesis, while another one (C) assessed the effects of the two dietary lipids on the promotion. Nine parameters have been analyzed and a new histologic grading method, adapted to rat tumors, has been applied in each carcinoma. High corn oil diets, particularly when acting as promoters, associated with higher-grade carcinomas than control (p p