PROGRAMMED CELL-DEATH OF PERIPHERAL MYELOID PRECURSOR CELLS IN DOWN PATIENTS - EFFECT OF ZINC THERAPY

Hemopoietic stem cell differentiation represents the primary rule of s elf-renewal, proliferation, and specialization modulated by several me chanisms, including growth factors, cell interactions, and bioavailabi lity of various ions, especially Ca2+ and Zn2+. Apoptotic death, durin g normal cell turnover, has been widely studied and is recognized as a n important pathway for clonal deletion in the hemopoietic system. Mul tiparametric analyses have shown that subjects with Down syndrome show low levels of plasmic zinc associated with the presence of immature m yeloid cells in the peripheral blood. This arrangement is repaired by in vivo zinc therapy. This study presents morphological and biochemica l analyses to show that ZnSO4 therapy induces the disappearance of per ipheral myeloid precursor cells by a programmed cell death mechanism. The programmed zinc-therapy-induced cell death presumably provides a s imple way to regulate the myeloid differentiation selecting appropriat e cells.