The relatively recent introduction and use of an intravenous form of a vitamin E preparation (E-Ferol) has been associated with the development of an unusual syndrome and fatalities among low birth weight (<1,500 g), premature infants in neonatal intensive care units. We have observed an inhibitory effect by this vitamin E preparation on the in vitro response of human lymphocytes to phytohemagglutinin (PHA). E-Ferol suppressed the expected response to low doses of PHA. However, this suppression was not due to the α-tocopherol acetate (vitamin E) component, because α-tocopherol acetate by itself was not inhibitory; in fact, it often enhanced the PHA response. Because a mixture of polysorbate 80 and polysorbate 20 is used as a carrier in E-Ferol, these components were also tested and were found to be responsible for the suppression, especially the polysorbate 80. Concurrent with this suppression of PHA-induced mitogenesis was a decrease in the percentage of T11 lymphocytes.

Serum thiobarbituric acid (TBA) reactivity for lipoperoxidation products was assessed at diagnosis in children with T-cell and common acute lymphocytic leukemia (ALL) and T-lymphoblastic lymphoma. Comparisons were made among these groups and with healthy controls. Mean TBA reactivity (mumol malondialdehyde/L serum) was increased (P less than 0.01) in the T-cell leukemia group versus common ALL and T-lymphoblastic lymphoma patients and controls, respectively. The increase in lipoperoxidation products in T-cell ALL appeared to bear a positive relation to peripheral leukocyte counts, and was accompanied by increased serum prostaglandin E2 (PGE2) levels in most representative cases. Indomethacin added to a childhood T-cell ALL line (SUP-T3), at a concentration known to inhibit prostaglandin synthesis in vitro (i.e., 3 micrograms/mL), effected significant increases in the numbers of natural killer (NK; Leu-11+ and Leu-19+) cells (P less than 0.01) and B-lymphocytes (P less than 0.05), and significant decreases in cell viability (P less than 0.01). Indomethacin may be a useful agent for enhancing the antileukemic immune response in T-cell ALL.