To the Editor.
—In the August Archives (1981;141:1169-1171), Yasaka et al reported an increase in lipid peroxidation (as measured by serum malondialdehyde levels) after ingestion of paraquat, a bipyridinium compound widely used as a herbicide. The authors suggested that the serum malondialdehyde may have originated from passage of the blood through the lung or, possibly, from the liver, which has the capacity to generate reactive oxygen species in response to paraquat. In addition, it was suggested that levels of serum malondialdehyde might provide a useful indicator of the efficacy of therapeutic modalities involving free radical scavenging agents. The accompanying editorial by Fairshter (1981;141:1121-1122) addressed some of the difficulties inherent in studies involving activated oxygen species, lipid peroxidation, and the use of the malondialdehyde level as an end point of lipid peroxidation.However, several additional aspects of this initial report deserve comment in order that subsequent research be more meaningful. First,