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Protection from Cold Injury by Deferoxamine, an Iron Chelator

Surgical Research Center, Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut Source of Support: Office of Naval Research, United States Department of the Navy

Dan Lu, M.D.

Surgical Research Center, Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut Source of Support: Office of Naval Research, United States Department of the Navy

John C. Russel, M.D.

Surgical Research Center, Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut Source of Support: Office of Naval Research, United States Department of the Navy

Jaisimha Lyengar, M.D., F.A.C.A.

Surgical Research Center, Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut Source of Support: Office of Naval Research, United States Department of the Navy

Dipak K. Das, Ph.D.

Surgical Research Center, Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut Source of Support: Office of Naval Research, United States Department of the Navy

The presence of hydroxl radical (OH^-) has been implicated in the pathogen esis of cold injury. Since iron is known to catalyze the OH^- formation respon sible for cellular injury, this study was designed to examine whether an iron chelator such as deferoxamine can salvage a tissue from cold injury. Cold inju ry was induced in the hind limbs of rabbits. The experimental group received 0.6 mM of deferoxamine through the femoral vein prior to cooling of the limbs. Deferoxamine reduced the tissue injury, as evidenced by the decreased release of lactate dehydrogenase, a nonspecific marker for cellular injury. In addition, this drug inhibited OH ^- formation and lipid peroxidation when examined by monitoring the formation of conjugated dienes and malonaldehyde, presump tive markers for lipid peroxidation. Rewarming of the cooled limbs was also as sociated with the loss of membrane phospholipids, with the corresponding accumulation of lysopho-sphoglycerides and free fatty acids, especially linoleic and arachidonic acids. Deferoxamine prevented the loss of phospholipids and inhibited the accumulation of amphipathic lipid products. These results indi cates that deferoxamine salvaged the tissue from cold injury, possibly by prevent ing the formation of OH^- presumably by chelating iron, thus protecting the phospholipids from free radical attack.

Angiology, Vol. 43, No. 9, 781-790 (1992)
DOI: 10.1177/000331979204300908


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