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Effect of autoxidized methyl linoleate on glutathione peroxidase
Abstract:
To determine the effect of several oxidation stages of autoxidized methyl linoleate (AOML) on glutathione peroxidase (GSH-Px), several experiments were carried out. In the first experiment, GSH-Px was prepared from gastrointestinal tract and liver which were excised from mice, and the effects of AOML rich in hydroperoxides (HP) and that rich in the decomposition products of HP on the activity of GSH-Px were compared. The results indicate that GSH-Px indiscriminately metabolized both types of AOML without strict recognition of the specificity of the substrate. In the second experiment, it was noted that the inhibitory rate of GSH-Px by in vitro incubation with various AOML closely correlated with POV of the sample esters, but did not correspond with the toxicity revealed by intraperitoneal injection or intragastric feeding. In the next experiment, mice were given AOML with a low vitamin E diet for 45 days, and an increase of GSH-Px activity in gastrointestinal tract in proportion to the POV of the administered oil occurred, but the level in liver remained unchanged. On the contrary, the increase of GSH-Px activity by intraperitoneal injection of AOML in mice was marked in liver, but not in gastrointestinal tract. From these results, most of the orally administered AOML seemed to be reduced in the mucosa of the gastrointestinal tract. However, the marked increase of fluorescence in the lipid fraction of heart and kidney by oral administration of AOML suggested that the damage caused by it was not limited to gastrointestinal tract but was spread through the whole body.
Insights
Autoxidized methyl linoleate (AOML) affects glutathione peroxidase (GSH-Px) activity differently depending on administration route. Oral AOML primarily impacts the gastrointestinal tract, while injected AOML affects the liver, with systemic damage observed.
Area of Science:
- Biochemistry
- Toxicology
- Nutrition
Background:
- Autoxidized methyl linoleate (AOML) is a complex mixture of oxidation products.
- Glutathione peroxidase (GSH-Px) is a key antioxidant enzyme.
- Understanding AOML's interaction with GSH-Px is crucial for assessing its biological effects.
Purpose of the Study:
- To investigate the impact of different oxidation stages of AOML on GSH-Px activity.
- To compare the effects of orally administered versus injected AOML on GSH-Px.
- To evaluate the systemic distribution and damage caused by AOML.
Main Methods:
- Preparation of GSH-Px from mouse gastrointestinal tract and liver.
- Incubation of GSH-Px with AOML at various oxidation levels.
- Assessment of GSH-Px activity and Peroxide Value (POV).
- Administration of AOML to mice with varying vitamin E intake and via different routes (oral, intraperitoneal).
- Analysis of fluorescence in lipid fractions of organs.
Main Results:
- GSH-Px metabolized both hydroperoxide-rich and decomposition product-rich AOML indiscriminately.
- In vitro inhibition of GSH-Px correlated with AOML's POV, not its toxicity.
- Oral AOML increased GSH-Px in the gastrointestinal tract (dose-dependent on POV) but not the liver.
- Intraperitoneal AOML increased GSH-Px in the liver but not the gastrointestinal tract.
- Systemic damage was indicated by increased fluorescence in heart and kidney lipids after oral AOML administration.
Conclusions:
- GSH-Px exhibits non-specific metabolism of AOML.
- Oral AOML is largely reduced in the gastrointestinal tract.
- AOML-induced damage extends beyond the gastrointestinal tract, affecting the whole body.
- Vitamin E status may influence GSH-Px response to AOML.