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Effect of Dietary Iron Overload on Lipid Peroxidation, Prostaglandin Synthesis and Lymphocyte Proliferation in Young and Old Rats^1,2,

USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111

The effect of dietary iron overload on lipid peroxidation (LP), prostaglandin (PG) synthesis and lymphocyte proliferation was examined in young and old F344 rats. Rats 4 and 19–22 mo old were fed AIN-76 diet for 11–12 wk supplemented with 2.5% carbonyl iron obtained from two sources (Type A and B). Animals supplemented with Type A iron showed reduced food intake and weight gain associated with marked increases in extrahepatic and hepatic iron concentration. Rats receiving Type B iron had food intakes and body weights similar to those of controls but exhibited small increases in tissue iron concentration. Old control rats compared to young had significantly higher conjugated dienes (CD) in hepatic microsomes. Feeding Type A iron diets induced a significantly higher level of CD in hepatic microsomes from old rats compared to young rats. Iron overloaded rats also showed highly correlated (r = 0.94) increases in the urinary excretion of thiobarbituric acid-reactive substances and PG metabolites indicating increased in vivo LP and PG synthesis. Mitogen-stimulated PGE₂ synthesis in young rats was increased at 4 wk in association with enhanced T-cell proliferation stimulated by Concanavalin A. Lymphocyte proliferation was significantly lower in old than in young control or iron-treated rats. The lack of efficacy of Type B vs. Type A iron appears due to a larger particle size and lower bioavailability. In conclusion, iron overloading increases in vivo LP and PG metabolism. Furthermore, the mitogenic response to Concanavalin A in young rats is enhanced after 4 wk of iron overloading.

KEY WORDS: • iron • lipid peroxidation • prostaglandin E₂ • immune system • rats

¹ This study was supported by USDA Contract #53-3K06-5-10.

² Presented in part at the 1987 meeting of the Federation of the American Societies for Experimental Biology.

³ Present address: Institute of Biochemistry, College of Medicine, National Taiwan University, Taipei, Taiwan 10018.

⁴ Address correspondence and reprint requests to: Mohsen Meydani, DVM, Ph.D., USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111. Telephone (617) 556-3126; FAX (617) 556-3295.

Manuscript received 31 January 1989. Revision accepted 27 September 1989.