ZINC DEFICIENCY ACCOMPANIES HYPOTHYROIDISM IN MICE ALTERING PROLIFERATION AND INTRACELLULAR SIGNALING. ZINC SUPPLEMENTATION REVERSES IMMUNOSUPPRESSION IN HYPOTHYROID MICE.

BARREIRO ARCOS MARIA LAURA; CREMASCHI GRACIELA; STERLE HELENA; CAYROL FLORENCIA; PAULAZO ALEJANDRA; DIAZ FLAQUE MARIA CELESTE; KLECHA ALICIA

Buenos Aires, Mar del Plata

Congreso; LXI Reunión Científica Anual de la Sociedad. Argentina de Investigación Clínica; 2016

Zinc (Zn) is essential for all highly proliferating cells, especiallythose of the immune system. Zn deficiency (ZnD) affectsthe functioning of many proteins crucial for intracellular signalsin immunocompetent cells. Furthermore, it is required for optimalactivity of many hormones, including thyroid hormones (TH). Also,it was demonstrated that hypothyroidism leads to immunosuppression,but alterations of Zn levels were not studied. Our aimwas to evaluate the effect of ZnD on lymphocyte function both invitro and in vivo, and its impact in hypothyroid status. Reversionof these effects by Zn supplementation was studied as well. Forin vitro assays, cells were cultured in the absence or presence ofspecific intra-(TPEN) or extracellular (DTPA) Zn chelators. ZnD invivo was evaluated in lymphocytes from mice fed a reduced Zndiet and hypothyroidism by propylthiouracil treatment. Both Znchelators significantly inhibited proliferative responses of T cells,stimulated with the T cell-mitogen ConA. To ascertain the inductionof apoptosis, caspase-3 activity, cell binding of annexin V / propidiumiodide, nuclear condensation and DNA fragmentation wereevaluated. In all cases, a remarkable induction of apoptosis wasobserved in cells treated with chelators (p