Canolol formation

Formation of Canolol during Heating of Canola Seeds. 320... 

FORMATION OF CANOLOL DURING HEATING OF CANOLA SEEDS... 

FIG U RE 17.4 Influence of temperature during roasting on formation of canolol and content of tocopherols. 

FIGURE 17.6 Correlation between oil temperature during pressing and formation of canolol. 

For the production of virgin canola oil, the application of heat during the whole processing chain from the pre-treatment of the raw material to the pressing is not allowed. Thus, the requirements for the formation of canolol in the raw material are not given. 

FIGURE 17.8 Formation of canolol during roasting of canola seeds and its effect on the oxidation stability of the resulting oil in the Rancimat test at 120°C. 

At higher contents of canolol in the oil, a good correlation with the oxidation stability using the Rancimat test was found. If the temperature load was <15 min at 180°C, a decrease in the oxidation stability was observed due to the low formation of canolol. With increasing temperature load, the oxidation stability increased from 4 to 7 h, before the oxidation stability decreased again as a result of a temperature load of more than 45 min at 180°C. At a low temperature load, less canolol is formed so that the temperature is sufficient to impair the oxidation stability of the oil. Only when the content of canolol in the oil from roasted seeds increases does oxidative stability improve. If the temperature load is too high, the impairment of the oil is faster, then the formation of canolol can improve the oxidation stability. 

In a study by Kuwahara et al. (2004), the effect of canolol on peroxynitrite-medi-ated mutagenicity in bacteria was analysed. In DNA, purine nucleotides are vulnerable to oxidation and to adduct formation by peroxynitrite, whereby 8-oxoguanine and 8-nitroguanine are two of the major products (Salgo et al., 1995 Szab6 and Ohshima, 1997 Burney et al., 1999 Niles et al., 2006). Moreover, peroxynitrite can cause deoxyribose oxidation and DNA strand breaks (Kennedy et al., 1997). 

Particularly interesting is the observation made by Cao et al. (2008) that canolol is able to inhibit the inflammatory process in gastric mucosa and the subsequent formation of gastric tumours by repressing the expression of inflammatory cytokines. In this context it should be determined if canolol can also inhibit tumour development in those experimental models of liver and intestinal cancer, in which carcinogenesis is preceded or accompanied by inflammation. 

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