Production and partial characterization of interleukin 2 induced by periodic acid oxidation of lymphocyte membranes

Murine splenocytes, when stimulated to undergo blastogenesis by H 5IO 6 oxidation, produced a lymphokine with a spectrum of properties identical to that generally ascribed to IL-2 released by lectin-stimulated cells. These included the sustained propagation of IL-2-dependent CT6 cells, as well as identical thermal and enzymatic stabilities. Cell membrane carbonyls generated in situ by the oxidation of cell membranes served as triggers for subsequent IL-2 production by the activated cells. Reduction of membrane carbonyls by NaBH 4, and their addition reaction with NaHSO 3 and NH 2OH abrogated cell activation and inhibited, but did not abolish, IL-2 production. None of the specific carbonyl reagents, e.g., NaBH 4, NaHSO 3, and NH 2OH, have by themselves induced blastogenic transformation, although they did elicit IL-2 production. It is therefore concluded that cell membrane carbonyls serve as triggers for IL-2 production by H 5IO 6-transformed cells, although an increased rate of DNA synthesis per se is not an indispensable precondition for IL-2 synthesis

Cytometric and electron microscopic studies of the direct interaction of divalent nickel with intact and chemically modified HuT-78 lymphoblasts

Cytometric and ultrastructural studies on 24 hr cultures of intact, 1.0 mM H5IO6, and 0.1 mM SeO2-oxidized HuT-78 lymphoblasts were performed after their direct, 30 min interaction with 1.0 mM NiCl2. Except for moderately depressed cell viability, divalent nickel did not alter the progression of intact and oxidized target cells through the phases of the cell cycle. Although the plasma membrane remained structurally intact, marked distortion of mitochondria structure and increased osmiophilia were an invariable attribute of all nickel-pulsed cells. Moreover, numerous electron-opaque, intracellular depositions were detected in SeO2-oxidized, nickel-pulsed cells. It is concluded that the initial state of plasma membrane, and the interaction of nickel with other trace elements, have jointly determined the response of HuT-78 cells to brief and direct, divalent nickel pulses