In vivo iron and zinc deficiency diminished T- and B-selective mitogen stimulation of murine lymphoid cells through protein kinase C-mediated mechanism.

A. J. KLECHA; M.J. SALGUEIRO; M. WALD; J. BOCCIO; M. ZUBILLAGA; N.M. LEONARDI; G. GORELIK; G. A. CREMASCHI

BIOLOGICAL TRACE ELEMENT RESEARCH

Humana Press Inc

Lugar: USA; Año: 2005 vol. 104 p. 173 - 183

0163-4984

Zinc and iron are crucial mineral components of human diet, as theirdeficiency lead to several disorders, including alterations of the immunefunction. It has been demonstrated, both in humans and rodents, that adiminished number of lymphoid cells and a loss of lymphocyte activity accompany deprivation of these essential minerals. The aim of this work was to analyze if iron and/or zinc imbalances regulate lymphocyte activity and the intracellular signals involved in the effect. Mice from the BALB/c strain were fed with iron- and/or zinc-deficient or mineral-supplemented diets, according to the American Institute of Nutrition Rodent Diets. Levels of iron and zinc were assessed in blood, liver, or bone samples. Selective mitogen stimulation of T- and B-lymphocytes were performed. We found a diminished proliferative response in T- and B-lymphocytes from zinc- and/or iron-deficient animals with respect to controls. These effects were related to decreased mitogen-induced translocation of protein kinase C (PKC) activity to cell membranes on both celltypes from all animals fed with deficient diets. Our results demonstrate that iron and zinc deficiencies affect both T- and B-lymphocyte function by PKC-dependent mechanisms.