EFFECT OF ZINC DEFICIENCY IN NORMAL ANDTUMOR T LYM¬PHOCYTE ACTIVITY BY MODULATION OF PROTEIN KINASE C (PKC) ISOENZYMES

A ORQUEDA; M.L. BARREIRO ARCOS; H TORTI; R. RUBINSTEIN; M. WALD; A.M. GENARO; G.A. CREMASCHI

Madrid, España

Congreso; 2nd Iberoamerican Congress on Neuroimmunomodulation; 2007

Neuroimmunomodulation International Society

Zinc deficiency has known effects on immune responses but the mechanisms involved are being studied. Here we study the effect ofZn deficiency in normal and tumorT Iymphocytes and the role of PKC, a crucial enzyme for Iymphocyte activa­tion. Concanavalin A-stimulated T Iymphocytes or T Iympho­ma cells (LBC and BW 5147) were cultured in the absence or presence of specific intra-(TPEN) or extracellular (DTPA) Zn chelators and the proliferation, PKC activity and PKC isoen­zymes pattern were evaluated. Both TPEN and DTPA inhibited normal and LBC cell proliferation, effect reverted by Zn ad­dition.On BW they also inhibited growth to a lesser extent, actions not modified by exogenous Zn. DTPA lowered intra­cellular Zn content, effect impaired by Zn addition, as meas­ured by atomic absorption spectroscopy. Proliferative actions ofTPEN were accompanied by a decreased in PKC activation. Also, a decrease in PKC a and q isoforms both in normal T and LBC cells treated with the chelators was found. However, only on normal lymphocytes an increase in the atypical PKC z isoform was observed. These results show that Zn plays a role in normal and tumor Iymphocyte growth, and that its defi­ciency would alter the expression of key PKC isoenzymes.