Title

Plaque formation reduction with glutathione monoester in mice fed on atherogenic diet

Document Type

Article

Department

Biological and Biomedical Sciences

Abstract

Objective: To determine the role of glutathione monoester on reducing the development of plaque formation in an animal model.
Design: Laboratory control trial.
Place and duration of study: Aga Khan University, Karachi, from January 2004 to December, 2004.
Materials and methods: Twenty-four Balb/c mice were divided into 3 equal groups. First group was fed on atherogenic diet alone, while the second group received atherogenic diet plus twice weekly injections of glutathione monoester. The third group was fed on normal diet for mice. After one year, the animals were sacrificed. Blood was analyzed for lipid levels, while liver, kidney, spleen, heart and aorta were removed to study morphological changes.
Results: In the groups of mice receiving atherogenic diet (with and without glutathione monoesters), there was significant increase in levels of total cholesterol (p=0.011) and LDL cholesterol (p=0.001) compared to levels of these lipids in mice on normal diet. However, a significant decrease in levels of triglycerides (p=0.01) was observed in the group receiving atherogenic diet along with glutathione monoester. Supplementation with glutathione monoester had the most pronounced effect only on triglyceride levels. Atherosclerotic plaques were seen in heart and/or aorta of mice receiving atherogenic diet. However, such plaques were either totally absent or if seen in an animal, were extremely small and diffuse in the group receiving glutathione monoester along with atherogenic diet. Mice on normal diet had no evidence of any plaque formation. Cholesterol granuloma was seen in liver of mice on atherogenic diet alone. In mice receiving atherogenic diet plus glutathione monoester, no cholesterol granuloma was found in liver. There were no remarkable morphological changes in spleen and kidney in the three groups of mice.
Conclusion: Glutathione monoester appears to inhibit or reduce the development of plaque formation in mice.

Comments

Eprint is not available

Publication

Journal of the College of Physicians and Surgeons Pakistan

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