12Toxicity of Food Frying

12.1 Introduction

The main purpose of frying is to produce high‐quality foods with good consumer acceptability. However, not all acceptable foods are safe. The early work of Custot (1959) and Nolen et al. (1967) showed that frying fats may not be used repeatedly. Experiments were based on animal models that used dietary frying fats. Changes in serum biochemistry and fat depositions were commonly observed. Food chemists were keenly interested in the new toxic compounds produced during frying. It was found that the initial products of fat oxidation were hydroperoxides, epoxides, and hydroxides. These products caused significant toxic effects in experimental animals. Horton et al. (1987) found that lipid peroxidation products are toxic. Kubow (1990) also found that dietary lipid oxidation products are toxic, increasing atherosclerosis. Marnett (1991) showed that these oxidation products are produced by free radical reactions.

In order to study the mechanisms of certain chronic diseases caused by oxidized lipids, cell culturing and model studies were performed. Marnett (1999) showed that lipid oxidation products react with DNA to form toxic compounds that are unable to proceed with normal metabolic reactions. He reported that the principal compounds involved in the reaction were deoxyguanine and deoxyadenosine, forming adducts such as pyrimidopurinone.

A large variety of oxidized or newly formed compounds found in both frying fats and fried foods have been evaluated ...

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