Zinc deficiency accompanies hypothyroidism in mice altering proliferation and intracellular signaling. Zinc supplementation reverses immunosuppression in hypothyroid mice

PAULAZO MA; STERLE, H A; BARREIRO ARCOS ML; DÍAZ FLAQUÉ MC; CAYROL MF; CREMASCHI, G A; KLECHA AJ

Mar del Plata

Congreso; LXI Reunión anual SAIC, LXIV Reunión anual SAI, XLVIII Reunión anual SAFE, VII Reunión anual NANOMEDAR, V Congreso Nacional AACYTAL; 2016

SAIC, SAI, SAFE, NANOMEDAR, AACYTAL

Zinc (Zn) is essential for all highly proliferating cells, espe-cially those 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 immunosup-pression, 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 / prop-idium iodide, nuclear condensation and DNA fragmentation wereevaluated. In all cases, a remarkable induction of apoptosis wasobserved in cells treated with chelators (p