Abstract

Exposure of polyunsaturated fatty acid (PUFA)-rich culinary oils (COs) to high temperature frying practices generates high concentrations of cytotoxic and genotoxic lipid oxidation products (LOPs) via oxygen-fueled, recycling peroxidative bursts. These toxins, including aldehydes and epoxy-fatty acids, readily penetrate into fried foods and hence are available for human consumption; therefore, they may pose substantial health hazards. Although previous reports have claimed health benefits offered by the use of PUFA-laden COs for frying purposes, these may be erroneous in view of their failure to consider the negating adverse public health threats presented by food-transferable LOPs therein. When absorbed from the gastrointestinal (GI) system into the systemic circulation, such LOPs may significantly contribute to enhanced risks of chronic non-communicable diseases (NCDs), e.g. , cancer, along with cardiovascular and neurological diseases. Herein, we provide a comprehensive rationale relating to the public health threats posed by the dietary ingestion of LOPs in fried foods. We begin with an introduction to sequential lipid peroxidation processes, describing the noxious effects of LOP toxins generated therefrom. We continue to discuss GI system interactions, the metabolism and biotransformation of primary lipid hydroperoxide LOPs and their secondary products, and the toxicological properties of these agents, prior to providing a narrative on chemically-reactive, secondary aldehydic LOPs available for human ingestion. In view of a range of previous studies focused on their deleterious health effects in animal and cellular model systems, some emphasis is placed on the physiological fate of the more prevalent and toxic α,β-unsaturated aldehydes. We conclude with a description of targeted nutritional and interventional strategies, whilst highlighting the urgent and unmet clinical need for nutritional and epidemiological trials probing relationships between the incidence of NCDs, and the frequency and estimated quantities of dietary LOP intake.

Highlights

  • Since many previous investigations have focused on the potential roles of dietary lipid oxidation products (LOPs) and their fried food sources as major risk factors for the induction and development of atherosclerosis and its cardiovascular disease sequelae, and cancer, a review of these involvements and their adverse health implications are provided in Sections 4 and 5, respectively

  • A further study involved human cells collected from patients with a faulty copy of the BRCA2 breast cancer gene to investigate mechanisms associated with aldehyde-mediated cancer induction [146], and the investigators found that formaldehyde exposure leads to the degradation of cellular BRCA2 protein

  • Previously available reports that polyunsaturated fatty acid (PUFA)-laden cooking oils are ‘beneficial’ or ‘safe’ for human consumption after being employed for frying or alternative high temperature cooking purposes may be erroneous and inaccurate, since they predominantly fail to monitor or even consider any LOPs therein, nor the major public health threats posed by their human ingestion

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Summary

Introduction

An increasingly large proportion of the human population consuming Western World diets frequently ingest oxidised/peroxidised lipids, and the possibility that regular ingestion of such agents may be deleterious to human health has recently attracted a large amount of high-impacting research interest and focus [1,2,3,4,5]. Data available has provided powerful evidence that only secondary LOPs ( aldehydes and epoxy-acids), and not their primary hydroperoxide precursors, are transferred to foods during high-temperature frying practices, and that these toxins have sufficient longevity therein [12], a factor which renders them freely available for ingestion by human populations Such considerations are of major concern for home-cooking domestic consumers, and perhaps more importantly restaurant workers, who are frequently exposed to aldehyde-containing emissions arising from cooking oils during such frying episodes, or alternative high-temperature cooking practices such as those involving Chinese-style woks [14]. In view of the focus of this Commentary on lipid hydroperoxides and their aldehydic chain-cleavage products, the in vivo absorption and toxicities of dietary epoxy-fatty acids (FAs) are summarized in Section S1 of the Supplementary Materials section

Lipid Peroxidation Process
Dietary Sources of LOPs
Fried Food Sources of LOPs
Acrolein
HNE and HHE
Risk Assessments of Aldehyde Intake in Humans
Secondary Aldehydic LOPs
Atherosclerosis and Its Cardiovascular Disease Sequelae
Trans-2-Alkenals
Acrolein and Chinese Wok Cooking
Crotonaldehyde
Acetaldehyde and Formaldehyde
Impact of Fried Food Intake on Cancer Risks in Humans
Potential Mechanisms for the Toxicity and Health Effects of Dietary Aldehydes
Important Considerations for HNE and HNE
Influence of CO Consumption on Blood Plasma Levels of HNE and HHE
Haem Oxygenase-1 Expression and Dietary Marine Oil Supplementation
Cell Signalling by HHE and HNE
Aldehydes as the Dominant Carcinogens Present in Cigarette Smoke
Findings
Conclusions

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