Cadmium-resistance mechanism in the bacteria Cupriavidus metallidurans CH34 and Pseudomonas putida mt2.

Cupriavidus metallidurans CH34 and Pseudomonas putida mt2 were used as cadmium (Cd)-resistant and -sensitive bacteria, respectively, to study Cd uptake, sorption, intracellular accumulation, metallothionein (MT) induction, and bioremediation potential of both isolates. According to this research work, Cd had a stimulatory effect on the growth of CH34 cells (OD578 = 1.43) compared with mt2 cells (OD578 = 0.8). Addition of N,N'-dicyclohexylcarbodiimide (DCCD) and 2,4-dinitrophenol (DNP) along with Cd resulted in more cell growth in mt2 (OD578 = 0.71) compared with CH34 (OD578 = 0.34). DCCD and DNP inhibited this active uptake only in CH34 but not in mt2. Greater Cd interaction with the cell surface was observed in mt2 cells compared with CH34 cells. Intracellular Cd accumulation was interrupted by DCCD and DNP in CH34 (only 1.81 ± 0.04 μg L(-1) at 5 h) but not in mt2 (24.41 ± 0.01 μg L(-1) at 5 h). Intracellular Cd uptake was observed in even killed mt2 cells (7.11 ± 0.05 μg L(-1) at 5 h) compared with CH34 cells (2.50 ± 0.08 μg L(-1) at 5 h). This result showed that the Cd accumulation mechanism in CH34 is ATPase-dependent, whereas in mt2 uptake mechanism is not ATPase-dependent because mt2 ATPase was not inhibited by DCCD and DNP. CH34 removed 93 mg L(-1) of Cd after 8 days from original industrial effluent, which was more than Cd removal by CH34 from distilled water (i.e. 90 mg L(-1) after 8 days). mt2 was able to remove 80 mg L(-1) of Cd after 8 days from original industrial effluent, which was more than Cd removal by mt2 from distilled water (i.e. 77 mg L(-1) after 8 days). Cd did not induce any MT in CH34, but it did so in mt2 (14 kDa), which was thought to be a Cd-resistance mechanism operative in mt2.