We sought to elucidate the mechanisms underlying the aerobic dechlorination of the persistent organic pollutants hexachlorobenzene (HCB) and pentachlorophenol (PCP). We performed genomic and heterologous expression analyses of dehalogenase genes in Nocardioides sp. PD653, the first bacterium found to be capable of mineralizing HCB via PCP under aerobic conditions. The hcbA1A2A3 and hcbB1B2B3 genes, which were involved in catalysing the aerobic dechlorination of HCB and PCP, respectively, were identified and characterized; they were classified as members of the two-component flavin-diffusible monooxygenase family. This was subsequently verified by biochemical analysis; aerobic dechlorination activity was successfully reconstituted in vitro in the presence of flavin, NADH, the flavin reductase HcbA3, and the HCB monooxygenase HcbA1. These findings will contribute to the implementation of in situ bioremediation of HCB- or PCP-contaminated sites, as well as to a better understanding of bacterial evolution apropos their ability to degrade heavily chlorinated anthropogenic compounds under aerobic conditions.
The median lethal dose of pesticide in acute oral toxicity, used as a conservative index in avian risk assessment, varies by the species with differences of less than one order of magnitude, depending on body size, feeding habit, and metabolic enzyme activity. The profiles of pesticide metabolism in birds with characteristic conjugations are basically common to those in mammals, but less information is available on their relevant enzymes. The higher toxicity of some pesticides in birds than in mammals is due to the lower activity of avian metabolic enzymes. The bioaccumulation in birds is limited for very hydrophobic pesticides resistant to metabolic degradation. Several in silico approaches using the descriptors of a pesticide molecule have recently been employed to estimate the profiles of acute oral toxicity and bioaccumulation.