Following up on the zinc homeostasis story, which we discussed here earlier in the week (Think zinc), I wanted to draw your attention to Larbi et al.‘s review of the relationship between age-related zinc deficiency, heat shock protein expression, and immunological aging:

… We believe that chronic stimulation of T-cells enhances the appearance of apoptosis-resistant anergic dysfunctional cells; in humans in vivo these are predominantly specific for antigens of persistent viruses, especially CMV. Concomitantly, age-associated zinc deficiency is common and one hypothesis is that lack of zinc bioavailability contributes to impaired T-cell function. This could further compromise the integrity of T-cells under chronic antigenic stress, which can be modelled in long-term clonal cultures in vitro. Newly synthesized heat-shock proteins (HSPs) protect the cellular proteins from degradation under such conditions. In this short review we will briefly outline the role of heat-shock proteins and zinc deficiency in aging in order to finally discuss our own results in the context of a link between HSPs, aging and zinc.

Taking this argument together with the idea that decreasing Zn2+ levels are a compensatory mechanism to avoid oxidative stress, we see another example of a common theme in the biology of aging: Cells are being pulled in opposite directions along a given axis (in this case, [Zn2+]i), trying to find an optimum between two bad outcomes (in this case, immune dysfunction on the one hand, and high levels of oxidative damage on the other).

The theme arises again and again, e.g., in the balance between oncogenesis and failure to renew tissues (see p16 vs p16: Preventing cancer, limiting self-renewal and With friends like these).

The situation is common enough to deserve a memorable name…perhaps we should call this the Scylla and Charybdis scenario.