Alteration induced by zinc deficiency in normal and tumor T lymphocyte activity through the differential modulation of protein kinase C (PKC) isoenzymes.

A. ORQUEDA, M.L. BARREIRO ARCOS, H. TORTI, M. WALD, A.M. GENARO AND G.A. CREMASCHI

Buenos Aires, Argentina

Congreso; XXII Latinoamerican and First Ibero-American Congress of Physiological Sciences; 2006

Sociedad Argentina de Fisiología

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 an  role in normal and tumor lymphocyte growth, and that its deficiency would alter the expression of key PKC isoenzymes.