摘要
The prevailing hypothesis, which states that the uptake of HOCs by phytoplankton is controlled by the compound's lipophilicity (Kow) was tested. The approach taken was to determine the factors that controlled the uptake of PCBs by phytoplankton under controlled laboratory conditions, and to develop a model that would describe bioaccumulation of PCBs in phytoplankton.The results demonstrate a relationship of BAF to Kow and to phytoplankton surface properties, as well as the data presented here, support the hypothesis that the mechanism of HOC uptake is a rapid surface sorption followed by a slower transfer into lipids in the cell matrix. The work on the kinetics of uptake indicates that equilibrium is reached slowly and that the rate of uptake is of similar magnitude as phytoplankton growth under normal field conditions.Thus a critical factor that controls the bioaccumulation of HOCs reach equilibrium in phytoplankton itself.
The prevailing hypothesis, which states that the uptake of HOCs by phytoplankton is controlled by the compound's lipophilicity (Kow) was tested. The approach taken was to determine the factors that controlled the uptake of PCBs by phytoplankton under controlled laboratory conditions, and to develop a model that would describe bioaccumulation of PCBs in phytoplankton.The results demonstrate a relationship of BAF to Kow and to phytoplankton surface properties, as well as the data presented here, support the hypothesis that the mechanism of HOC uptake is a rapid surface sorption followed by a slower transfer into lipids in the cell matrix. The work on the kinetics of uptake indicates that equilibrium is reached slowly and that the rate of uptake is of similar magnitude as phytoplankton growth under normal field conditions.Thus a critical factor that controls the bioaccumulation of HOCs reach equilibrium in phytoplankton itself.
