Dietary lead alters fatty acid composition and membrane peroxidation in chick liver microsomes.

Inorganic Pb acetate is a pro-oxidant, and peroxidation damage to cellular membrane lipids, leading to membrane fragility and permeability, is a likely consequence of Pb poisoning. In addition to the systemic peroxidation that occurs in vivo, Pb-contaminated feedstuffs can contribute preformed peroxides. Treatments with dietary Pb that have been shown to increase tissue peroxide levels in animals may be related to the consumption of preformed peroxides from the diet. In the current study, we evaluated the possible separate effects of feed and systemic peroxides by administering equivalent doses of Pb acetatetrihydrate to chicks via either 1,500 ppm Pb in the diet or via gastric intubation. Peroxidation of lipids in hepatic microsomal membranes (assessed as malonyldialdehyde production) from birds intoxicated with Pb by either route of administration was more than double that of untreated controls. Also, both routes of Pb exposure doubled the concentration of hepatic microsomal arachidonic acid, a peroxidizable polyunsaturated fatty acid. In the data reported here, we show that tissue peroxide levels are unaffected by the method of oral Pb administration and thus, by inference, independent of peroxide content of the feed.