Metabolic inhibition by transition metal ions in a slow-growing, toluene-enriched microbial population

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We studied the effects of common first-row transition metal ions, Mn(II), Fe(III), Co(II), Cu(II), Zn(II), on the respiration of a mixed microbial population enriched for toluene degradation. Dissolved oxygen consumption, i.e., respiration rate, was used to measure metabolic activity of a slow-growing consortium of toluene-enriched microorganisms. Respiration rates decreased within 30 s of exposure to the metal ions and did not measurably recover during observation times (<80 min.). Metal ion toxicity increased with metal-phosphate binding affinities, consistent with cell damage by conformational changes in the phospholipid bilayer membrane to accommodate geometry requirements of complexes with transition metal ions. Changes in normalized metabolic activity (AN) with aqueous composition were compared with an equilibrium free-ion toxicity mechanism relating the fraction of membrane phosphatic ligands affected by metal ion chemisorption to diminished metabolic activity. AN measurements agreed with model predictions that the toxicity function (AN−1−1) is proportional to the free metal ion concentration when hydrogen ions do not compete with metal ions for the phosphatic membrane sites and proportional to the square root of the free metal ion concentration if hydrogen ions effectively compete with metal ions for membrane phosphate ligands. Transition metal ion uptake and toxicity were diminished by concentrations of competing Ca(II) and Mg(II) metal ion concentrations an order of magnitude larger than concentrations of transition metal ion. The Cu(II)-EDTA complex was nontoxic compared to Cu(II) ions. Metabolic inhibition produced by Cu(II) ions was not significantly reversed by sequestering Cu(II) ions using EDTA, suggesting that membrane damage is irreversible. Published 1998 John Wiley & Sons, Inc. Environ Toxicol Water Qual 13: 249–261, 1998