Soybean oil heating or cooking is a very complicated process. In order to better understand the composition of the volatile compounds from soybean oil during heating process, volatile profiling was carried out through vacuum‐assisted headspace solid‐phase microextraction combined with GC‐MS. As a result, a total of 72 volatile compounds were detected and identified during this process, including aldehydes (27), alcohols (14), ketones (10), furans (6), aromatic compounds (9), acids, and esters (6). And the forming temperature of each volatile was determined. Results show most of volatile aldehydes and alcohols were formed at 120°C leading to release off‐flavor largely, which was considered as a critical temperature point for the formation of soybean oil flavor during the whole heating process. Meanwhile, ketones and furans were formed at 150°C, and acids were detected at 180°C. The content of most volatile compounds increased significantly with the temperature raised. Simultaneously, results of principal component analysis demonstrate that flavor characteristics of soybean oil have a big difference between higher and lower temperature in the heating process.
Effects of ultrasound on pH, intermediate products, browning, glycin and glucose contents, reducing power, and antioxidant activity of a glycin-glucose solution were examined. Results showed that the ultrasonic treatment at the intensity of 17.83 W/cm 2 for 50 min resulted in the increases of the solution's absorbance at 294 and 420 nm and the antioxidant activity from approximately 0% to 2.40%, 1.19%, and 18.62%, respectively. At the same time, 21% reduction in glycin and 92% in glucose were observed. Gas chromatography/mass spectrum analysis showed that the ultrasonic treatment induced a Maillard reaction in the model system producing substances including 2,5-dimethyl-pyrazine, trimethyl-pyrazine, (Z)-9-octadecenamide, 1,2-benzenedicarboxylic acid, and mono (2-ethylhexyl) ester. This study indicated that ultrasound, especially at higher intensities, could potentially be employed as a means to promote the Maillard reaction in the glycin-glucose solution.
Molasses, the main byproduct of sugar production, is a well-known source of phenolic compounds. In this study, the effect of sugarcane molasses extract on the formation of N-(carboxymethyl)lysine (CML) and N-(carboxyethyl)lysine (CEL) was investigated in glucose-lysine model reaction systems. Results showed that sugarcane molasses extract significantly and dose dependently inhibited the formation of CML and CEL in model reaction systems. The antiglycation activities of sugarcane molasses extract were not only brought about by its antioxidant activities but also associated with its trapping abilities of reactive carbonyl species, such as glyoxal (GO) and methylglyoxal (MGO), the key intermediate compound for the formation of CML and CEL. Besides, the presence of sugarcane molasses extract effectively reduced the extent of browning. The present study emphasized the potential health effects of sugarcane molasses and the possibility of using byproducts as effective ingredients to reduce dietary Maillard reaction end products.
A new analytical method allowing the simultaneous quantification of Nε-(carboxymethyl)lysine (CML), lysine, and reducing sugars (glucose, lactose, and galactose) is described. It is based on high performance anion-exchange chromatography with pulsed amperometric electrochemical detection. This method demonstrated a low limit of quantification (0.385 to 0.866 mg/L), excellent linear correlation (R(2)>0.997), and desired calibration range (3.125 to 25 mg/L). In addition, lactose-lysine solutions containing sulfite (4 to 400 mmol/L) were heated at 110°C for 2h. The results showed that sulfite inhibited the formation of CML and promoted the consumption of reducing sugars and lysine in the Maillard reaction model. The method proved to be useful for simultaneous analysis of CML, lysine, and reducing sugars (glucose, galactose, and lactose) in the Maillard reaction system. Moreover, sulfite was an effective inhibitor of CML formation.
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