Mechanism of toxicity of zinc to the marine diatomNitzschia closterium

The effect of zinc on cell division, photosynthesis, ultrastructure, respiration, ATP levels, mitochondrial electron-transport chain (ETC)-activity, total thiols and glutathione in the marine diatomNitzschia closterium (Ehrenberg) W. Smith was investigated. Although 65µg Zn 1^–1 halved the cell division rate, photosynthesis and respiration were unaffected by zinc concentrations up to 500µg Zn 1^–1. Most of the zinc associated with the cells was bound at the cell surface, with only 3 to 4% of this extracellular zinc penetrating the cell membrane. Once inside the cell, zinc exerted its toxicity at a number of sites. Increased ATP production and ETC activity were observed in zinc-treated cells. Zinc also enhanced cellular thiols (SH) and total glutathione, and zinc toxicity was reversible by the addition of thiol compounds such as cysteine. Zinc-thiol binding may be a detoxification mechanism for the cell. It is suggested that increased ATP production may provide the energy required for increased glutathione synthesis at the expense of other energy-requiring processes including cell division. The mechanisms of toxicity of ionic zinc and copper toN. closterium were compared.