## 1 Introduction
The basis of our research group's previously reported research findings is that SFA acylglycerols generate very little or no toxic LOPs when heated according to standard frying practices in the presence of atmospheric O2, whereas on a mole-for-mole equivalence scale, those containing PUFAs produce very high levels of these toxins when exposed to thermally facilitated peroxid oxidative assaults, as expected [12; 13; 19; 20]. However, HPM-generating MUFAs are much more resistant to oxidation than PUFAs, and hence they give rise to lower levels of only particular LOPs when heated in this manner, and generally only after exposure to prolonged thermal stressing episodes at standard frying temperatures. Therefore, the order of toxic LOP production in culinary oils is PUFAs >> MUFAs >>>>>> SFAs, and hence healthwise, PUFA-rich CFOs are generally the worst possible choice for use as frying media, especially for repeated frying episodes [13]. Indeed, the relative oxidative susceptibilities of these lipid molecules are 1:100:1200:2500 for 18-carbon chain length FAs containing 0:1:2:3 carbon-carbon double bonds (i.e., >C=C< functions), respectively [14]. Moreover, the rate of thermally-induced degradation of CHPDs or HPMs to the above series of smaller molecular fragments also increases with increasing FA unsaturation status, i.e., it is in the order linolenoyl - > linoleoyl ->> oleoylglycerols [16]. Our previously reported extensive high-resolution NMR analysis investigations of the oxidative deterioration of PUFA-rich CFOs during standard frying practices have demonstrated the heat-promoted generation of very high levels of highly toxic aldehydes, in addition to their HPM and CHPD precursors, in such products [12; 19; 20], and these results have been available to the scientific community since 1994 [19]. Indeed, samples of repeatedly used CFOs collected from domestic kittenchens, fast-food retail outlets and restaurants, have confirmed their generation at high concentrations during 'on-site' frying practices; these results have been repeatedly ratified in laboratory simulations of both deep- and shallow-frying processes [11]. We can also employ these NMR techniques to monitor the corresponding oxidative degradation of culinary oil PUFAs and MUFAs during such standard frying/cooking practices [12; 13; 19; 20]. These studies have been repeated, replicated, and further manifested by many research group laboratories worldwide, for example investigations reported in [21; 22]. Curiously, as noted above, until recently these major population public health concerns have received only limited attention from the food industry and public health researchers. Furthermore, in 1998 we first revealed that typical chemically reactive \(\alpha,\beta\)-unsaturated aldehydes produced during the thermal stressing of culinary oils according to standard frying practices are absorbed from the gut into the systemic circulation in vivo [23], where they have access and may cause damage to cells, tissues and essential organs. Further investigations performed in both animal model systems and humans have demonstrated an enhanced urinary excretion of these toxins following their ingestion [24; 25]. Aldehyde LOPs act as potent toxins since they are extremely chemically reactive. Indeed, they cause damage to critically important biomolecules such as DNA: since they are powerful electrophilic alkylating agents, \(\alpha,\beta\)-unsaturated aldehydes readily alkylate DNA base adducts, and this serves to explain their mutagenic, genotoxic and carcinogenic properties. Moreover, these secondary LOPs have the ability to form covalent adducts with many proteins via Schiff base or Michael addition reactions [12; 23], and these induce significant structural and conformational changes in these biomacromolecules which, in turn, serve to impair their biological functions. In view of these considerations, such secondary LOPs give rise to a broad spectrum of concentration-dependent cellular stresses.