Certain proteins from the blood of Arctic and Antarctic fishes may make it possible to store blood platelets at cold temperatures, report researchers at the University of California, Davis. The scientists hope their discovery will extend the shelf life of stored platelets in blood banks and lower the possibility of bacterial growth during storage. The results of the study, conducted by Fern Tablin, an associate professor in the UC Davis School of Veterinary Medicine, and John Crowe, a UC Davis professor of cellular and molecular biology, appear in the August issue of the Journal of Cellular Physiology. A patent is pending on this new technique for treating platelets, and the technology has been licensed for commercialization to A/F Protein of Boston. Platelets, shaped like thin disks, are the smallest of the cells in blood and circulate through the bloodstream. Essential for blood to clot, platelets are important in controlling bleeding and also are widely used in transfusions for patients with leukemia and other forms of cancer. "This is a very important piece of work because it indicates that there is the potential for storing platelets at temperatures cold enough to prevent bacterial growth," said Dr. Morris Blajchman, an authority in hematology and transfusion medicine at McMaster University in Hamilton, Ontario. "If it works, this technique could both significantly increase the supply of platelets as well as decrease the number of deaths due to bacterial infections from platelet transfusions," he said. According to Blajchman, who is also a medical officer for the Canadian Red Cross, bacterial contamination of platelets is the most common problem associated with transfusions, significantly affecting approximately one in every 2,000 transfusion recipients. Deaths associated with bacteria-contaminated platelet units may be three to four times greater than the current rate of AIDS from transfused blood, he said. Another specialist with experience in cryobiology and blood preservation, Dr. Harrold Meryman, director of the Transfusion and Cryopreservation Research Program at the Naval Medical Center in Bethesda, Md., expresses more caution regarding the potential for clinical application. "It would be a stretch of faith to presume that this will result in clinically useful platelet storage," said Meryman. "It will be critically important to know, for example, something about platelet function following storage with the antifreeze glycoprotein as well as to know more about the mechanism of the effect." Red blood cells can be refrigerated for up to 42 days or frozen for up to 10 years. Platelets on the other hand, must be stored at 72 degrees F. Unfortunately, the warm temperatures required for platelet storage also foster bacterial growth and the platelets must be discarded after five days. At cool temperatures -- less than 59 degrees F -- platelets change shape from disks to spheres and undergo changes that mimic the events that happen during clotting. Once they have undergone these changes, they are no longer useful for transfusion purposes. The UC Davis scientists discovered a way to prevent this. They became interested in the effect of polar fish proteins because previous research in their laboratories, published in the Proceedings of the National Academy of Sciences, had indicated that these proteins -- known as "antifreeze glycoproteins" -- prevent leakage in liposomes (artificially-produced microscopic spheres sometimes used to transport drugs into diseased cells). Like platelets, liposomes are encased in membranes and are prone to leaking their cellular contents as they change from the liquid to the solid state at cool temperatures. Crowe, an authority on membrane stability, and Tablin, a platelet expert, speculated that the antifreeze glycoproteins might also stabilize the platelets at low temperatures, preventing the shape change and leakage. To test this, they first measured the point at which human platelets moved from the fluid to the solid state -- much like bacon grease solidifying as the frying pan cools. Next, Tablin and Crowe maintained human platelets in test tubes with varying concentrations of the antifreeze glycoproteins and stored them for 21 days at 39 degrees F, then rapidly warmed them. They then analyzed the platelets for signs of shape change and activation and tested the ability of the cells to respond to chemicals that normally activate them during clotting. The researchers found that the antifreeze glycoproteins inhibited the shape change and activation of platelet cells that normally accompanies storage at very cool temperatures. This inhibiting effect increased in proportion to the concentration of the antifreeze glycoproteins. "We were floored that this worked," said Crowe. He and Tablin still aren't sure why the platelets change shape and activate at cool temperatures or why the antifreeze glycoproteins prevent those changes. They conjecture that the activation is related to the leakage across the membrane. The mixture of liquid and solid states that coexist in the platelets' membranes as they pass through the phase transition may be responsible for this hypothesized leakage. "We are very hopeful that the results of this study will greatly improve the storage conditions for platelets," Tablin said. "Our data indicate that treatment with antifreeze glycoproteins will extend the shelf life of platelets from five days to more than three weeks, with 80 percent of the platelets remaining active and usable." The researchers said that future research is needed to demonstrate that the antifreeze glycoproteins can be washed away from the platelets before transfusion, that the treated platelets are functional first in research animals and later in humans, and that the platelets truly can be stored for extended periods at cold temperatures. Tablin and Crowe's study was funded by the Office of Naval Research. -pb- EDITOR'S NOTE: Reporters can reach Morris Blajchman in Hamilton, Ontario at (905) 521-2100 Ext. 6274 and Harrold Meryman in Bethesda, Md. at (301) 295-3769.