Complexation of Cadmium and Copper by Fluvial Humic Matter and Effects on Their Toxicity



The effects of humic acids and fulvic acids isolated from the River Arno (Italy) on the bioavailability and toxicity of cadmium and copper were assessed in relation to changes in their speciation. Measurements of the complexing capacity of solutions containing these organic ligands were carried out by a titration procedure followed by DPASV and toxicity tests were carried out using lysosomes isolated from rat liver. The complexing capacity of the physiological medium containing about 13 mg/L of humic acids, expressed as ligand concentrations, was 0.30 and 0.072 μmol/L for cadmium and copper respectively; the corresponding conditional stability constants were 4.2 × 1011 and 1.3 × 108 (mol/L)-1. The complexing capacities of the solution containing the same amount of fulvic acids were 0.33 and 0.164 μmol/L for cadmium and copper respectively, the conditional stability constants were 3.2 × 1011 and 2.4 × 107 (mol/L)-1.

The humic acids reduced the toxicity of cadmium by about 5 times: the EC50 changed from 4.4 to 20.4 μmol/L. The dose effect curve of copper presented a bi-sigmoid trend and two EC50 values can be determined: The EC50(1) in the presence of humic acids changed from 2.0 to 3.1 μmol/L, while the EC50(2) increased from 22.3 to 45.3 μmol/L. The fulvic acids reduced the cadmium toxicity by about the same amount as humic acids, from 4.4 to 18.6 μmol/L, but they had no effect on copper toxicity. Analysing the chemical speciation of cadmium and copper in the presence of humic components and under toxicity test conditions we can say that the appreciable decrease of EC50 is not related to changes in their speciation; we can hypothesize that this is due to different processes, as well as to blocking of the lysosomal membrane. On the basis of the shape of the dose-effect curves obtained for cadmium and copper respectively, we can say that the toxic effects of the two metals are different and we can hypothesize that copper could exercise its toxic activity by inhibiting the ATP-driven proton pump and the function of the Cl- selective channel.