Section 9
Chapter 8,527

Effect of chronic iron overload on iron status, lipid peroxidation, cell proliferation, and DNA damage

Whittaker, P.; Wamer, W.; Calvert, R.J.

Journal of Trace Elements in Experimental Medicine 5(4): 227-236


ISSN/ISBN: 0896-548X
Accession: 008526393

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The relationship of dietary carbonyl Fe overload to lipid peroxidation and single strand DNA breakage in liver and intestinal mucosa was investigated using a rat model. Control animals received a standard American Institute of Nutrition diet, and treated animals were supplemented with 2.5% carbonyl Fe for 2, 4, 6, or 9 weeks. Alkaline elution rate, a sensitive indicator of DNA damage, was assesed at each interval with liver nonheme Fe and lipid peroxides. Liver thymidine kinase activity was monitored at week 9. Liver nonheme Fe (mu-g/g) increased from 1,100 to 4,700 in the treated rats compared to 30 and 43 in controls. Although undetected in the serum, lipid peroxidation, measured by the thiobarbituric acid reaction, was significantly greater in the mucosa of treated rats. Liver lipid peroxidation (nmol of malondialdehyde reactive substance/g) increased from 31.4 to 51.8 in treated rats compared to 13.4 and 10.2 in controls. Liver cell suspensions and intestinal mucosa showed no significant increase in alkaline elution rate. Fe overload increased liver Fe directly with lipid peroxidation (r = 0.88). Thymidine kinase activity rose with liver nonheme Fe and correlated directly with lipid peroxidation (r = 0.94). These results suggest that dietary Fe overload induces lipid peroxidation and may indicate cell proliferation in hepatic cells, without causing a correspondingly significant increase in DNA damage.

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