Effect of zinc deficiency in normal and tumor T lymphocyte activity by modulation of protein kinase C (PKC) isoenzymes

ANDRÉS ORQUEDA; MARÍA LAURA BARREIRO ARCOS; HORACIO TORTI; MARA ROXANA RUBINSTEIN GUICHÓN; MIRIAM RUTH WALD; ANA MARÍA GENARO; MIRIAM RUTH WALD

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 of Zn deficiency in normal and tumor T lymphocytes and the role of PKC, a crucial enzyme for lymphocyte activation. Concanavalin A-stimulated T lymphocytes or T lymphoma 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 of TPEN 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 lymphocyte growth, and that its deficiency would alter the expression of key PKC isoenzymes.