The process of lipid peroxidation has been suggested (11) to proceed via a free radical chain reaction, as per Equations 1-6:
The susceptibility of unsaturated fatty acids to peroxidation is due to their ability to stabilize a free radical adjacent to an olefinic group. The initiation of peroxidation is thought to occur by hydrogen atom abstraction (Eqn 1), followed by reaction of the lipid radical with oxygen to form the peroxy radical (Eqn 2). The peroxidation reaction is then propagated by this radical (Eqn 3). The initial products of lipid peroxidation are mono-hydroperoxides, each having a characteristic conjugated diene system. The 9- and 13- hydroperoxides account for 96% of these while the remaining 4% is a mixture of the 8-, 10-, 12-, and 14- hydroperoxides (12). The hydroperoxides decompose to form a wide range of final products including epoxides, aldehydes, ketones, malondialdehyde, ethane, pentane, and ethene.
Ultraweak CL is associated with the lipid peroxidation chain reaction. Oxidising systems of fatty acids have been found to emit low levels of light (2,5). The excited species responsible for this CL have been suggested as singlet molecular oxygen and triplet carbonyls. Mechanisms for the generation of these excited species have been proposed (3,13), whereby singlet oxygen and excited carbonyls are formed in the termination step of lipid peroxidation by a "Russell type" mechanism. Singlet oxygen may then react with unsaturated fatty acids to produce excited carbonyls, while the quenching of triplet carbonyls by molecular oxygen may produce singlet oxygen.
A relationship between CL and lipid peroxidation in rat hepatic microsomes has been reported by Wright et al (4). These researchers found a direct correlation between the total CL measured and the formation of malondialdehyde, a major degradation product of lipid peroxidation. Other reports have confirmed a close relationship between malondialdehyde formation and CL emission (14,15). Lipid peroxidation has also been associated with the disease diabetes mellitus. Hicks et al. (16) have reported that glucose catalyses lipid peroxidation in a model system of lipids.
As a model of lipids in biological fluids or common vegetable oils, linoleic acid (LA) and methyl linoleate (ML) have been studied widely. These include investigations of antioxidants (17,18), studies of iron-chelate (10,17,19) and glucose catalysts (16), and measurement of oxidation rate constants (20). The CL of linoleic acid has also been studied by various workers (2,7). However, quantitative studies of this CL emission are few, and both the oxidation and CL of LA and ML have not been studied simultaneously before. The aim of this study is thus to correlate the CL emission with the course of oxidation.
The present study focuses on simple model systems in order to help elucidate the source of the CL. The peroxidation of linoleic acid and methyl linoleate was studied by measuring hydroperoxide (ROOH) concentration, as absorption of light at 234 nm, due to conjugated diene formation. The initiation of peroxidation is achieved at elevated temperatures, or by using the catalysts, glucose and iron (II) nitrilotriacetate. By studying both the oxidation and CL simultaneously a better understanding of the source of the light emission should be established.
21 June 1999