By G. Winkelmann

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Contribution of PKC to the activation of human neutrophils by zinc The results obtained from the study of the contribution of PKC to the activation of human neutrophils by zinc shows that the PKC specific inhibitor Go¨6983 inhibited the response of neutrophils to zinc in a concentration-dependent manner. At 500 nM, Go¨6983 provided a complete inhibition of zinc-induced luminol oxidation (Fig. 6). 6 A 2 0 5 3 62 98 3 o6 98 G +G o6 * 12 5 nc ( n zi nc zi 20000 0 The results obtained in the present study clearly demonstrate that zinc activates human neutrophils’ oxidative burst in vitro.

According to Csermely et al. (1988), zinc activates PKC in T-lymphocytes and causes a translocation to the plasma membrane, a central event in the activation of PKC. Zinc-induced NADPH oxidase activation has already been described (Benoni et al. 1998; Kauppinen et al. 2008; Noh and Koh 2000; Suh et al. 2008; Takeyama et al. 1995). Inclusively, Noh and Koh (2000) reported that zinc induces and activates NADPH oxidase in cortical neurons and astrocytes in a PKC-dependent manner. Our results are in agreement with those obtained by Noh and Koh (2000) since the PKC specific inhibitor Go¨6983 decreased the response of neutrophils to zinc in a concentration dependent manner.

Acknowledgments Marisa Freitas acknowledges Fundac¸a˜o para a Cieˆncia e Tecnologia (FCT) and Fundo Social Europeu (FSE) her PhD grant (SFRH/BD/28502/2006). -activated K? channel is essential for innate immunity. Nature 427:853–858 Babior BM (1999) NADPH oxidase: an update. Blood 93:1464–1476 123 Biometals (2010) 23:31–41 Benoni G, Cuzzolin L, Marrella M, Crivellente F, Adami A, Bertaso C, Velo G, Milanino R (1998) Neutrophil behavior following exposure to in vivo or in vitro zinc in normal and acutely-inflamed rats: studies on lysozyme secretion, superoxide anion release and platelet adhesion.

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Biometals by G. Winkelmann

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