Oxidative damage in rat tissue following excessive L-tryptophan and atherogenic diets

N. Ronen, E. Livne, B. Gross

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

Abstract

Numerous reports were published on the connection between diets containing excessive L-tryptophan and the development of Eosinophilia Myalgia Syndrome. It has been also demonstrated that some cell functions depend on fatty acid composition which can result in increased lipid peroxidation in cells such as macrophages and other inflammatory cells. The purpose of the present study was to investigate the combined effects of an atherogenic diet enriched with tryptophan on lipid peroxidation in rats. 3-week-old CD-1 female rats were fed (3 weeks) control or atherogenic diets and the same diets supplemented with 0.4% or 1.0% L-tryptophan. Liver and skeletal muscle samples from all groups were taken for histology, autoradiography and for determination of lipid peroxidation. Infiltration of cells into fascia of muscle was observed following tryptophan or atherogenic diet consumption. However, no change in 3H-thymidine incorporation into DNA was observed by autoradiography. A significant increase of lipid peroxidation was detected in muscle following consumption of L-tryptophan-rich diets, with no significant difference from control in animals treated with atherogenic diets. Contrastly, a reduced lipid peroxidation was detected in liver of animals treated with excessive tryptophan as well as in animals fed on L-tryptophan and atherogenic diet or atherogenic diet alone. Our results indicated that excessive dietary tryptophan, when consumed with an atherogenic diet, increased lipid peroxidation in muscle but not in liver. Consumption of these feeding diets with or without supplementation of tryptophan resulted in reduced lipid peroxidation in muscle as well as in liver.

Original languageEnglish
Pages (from-to)497-505
Number of pages9
JournalAdvances in Experimental Medicine and Biology
Volume467
StatePublished - 1999
Externally publishedYes

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