Kinetic Studies of the Heat-induced Cholesterol Autoxidation

• Main Authors: Da-Jung Hsu, 許大容
• Other Authors: John Tung Chien Ph. D.
• Format: Others
• Language: zh-TW
• Published: 2004
• Online Access: http://ndltd.ncl.edu.tw/handle/83954510578928247161

碩士 === 輔仁大學 === 食品營養學系 === 92 === A series of cholesterol oxidation products (COPs) are formed through oxidative degradation during intensive heating at high temperature or long-term storage. COPs are cytotoxic, and can inhibit cholesterol biosynthesis, induce carcinogenesis, mutagenicity and antherosclerosis. Intake of COPs may cause adverse effects to our health. Therefore, it is important to reduce the degree of cholesterol oxidation in food products during thermal processing or cold storage. 0.002％ of quercetin was added into cholesterol standard as an antioxidant, using paraffin/laury alcohol (LA) as solvent and ethanol as co-solvent. Cholesterol was heat at 150℃ for up to 120 min with continuous oxygen purging. In order to study the antioxidative mechanism of quercetin, the various COPs were analyzed by TLC and HPLC and were kinetically studied using non-linear regression models. Two major reaction pathways－degradation and autoxidation involved during heating of cholesterol at 150℃ in the alcohol solvent system. Among these, the autoxidation pathway includes C-7 and epoxidation routes. Results showed that the COPs concentration increased with increasing heating time. After nonlinear regression analyses on reactions in the C-7 route, the rate constants of COPs formation were observed as follows: 7-hydroperoxycholesterol (7-OOH, k1=453.5 h-1) ＞7-hydroxycholesterol (7-OH, k2=270.3 h-1)＞7-ketocholesterol (7-Keto, k3=175.5 h-1). In the solvent system containing LA, the formation of 5, 6-expoxycholesterol (5, 6-EP, k4 = 709.1 h-1) in the epoxidation route may lead to alcoholysis and the formation of Triol (5α-cholestan-3β,5,6β-triol, k6'=0.3967 h-1). Triol could further proceed dehydrogenation and formed cholestan-3β, 5α-diol-6-one (diol-6-one) (k7=5.353 h-1). For the degradation pathway, quercetin could effectively reduce the formation of COPs during the initial heating time (<30min). Thereafter, due to oxidative and thermal degradations decrease of antioxidative activity was observed when depletion of quercetin was occurred. The degradation rate constant for quercetin in presence of cholesterol at 50℃ was 3.302 h-1. The depletion of quercetin led to increase of COPs formation. Thus, kinetic studies for heating of cholesterol at 150℃ can be divided into two stages：(1) initial stage in presence of quercetin (0-60min) and (2) final stage at almost depletion of quercetin of which antioxidative activity is highly reduced (30-120min). In the initial stage, the rate constants for 7-OOH formation decreased to 1.2×10-5 h-1 from 453.5 h-1and 5, 6-EP to 0.0157 h-1 from 683.1 h-1. In the initial stage, quercetin acts as free radical scavenger, which terminates the propagation of cholesterol free radical. The scavenging rate constant for quercetin was 3.279 h-1. In the final stage, the rate constants of COPs formation were similar to those of the control, with 3.8 to 5.0 times of reduction. k1、k2 and k3 for the C-7 route were respectively 111.70 h-1, 76.77 h-1and 30.99 h-1,whereas k4 and k6' for the epoxidation route were 551.4 and 1.6313 h-1, respectively. The rate constants for thermal degradation of cholesterol (k5) was 0.656 h-1 for the control and in presence of quercetin they reduced to 0.193 h-1 in the initial stage and to 0.281 h-1 in the final stage. Except for the dehydrogenation reaction of Triol→cholestan-3β,5α,6-one, the correlation coefficients (r2) for the reactions ranged 0.82-1.00. The kinetic model developed in this study can be used to predict the concentration changes of COPs inhibited by quercetin during heating of cholesterol.