As indicated earlier, carrier transport (both
facilitated diffusion and active transport) is
saturable and follows the Michaelis-Menten
kinetics. The maximal rate of transport is
dependent on the density of the transporter
in a particular membrane, and its rate constant (Km), i.e. the substrate concentration
at which rate of transport is half maximal,
is governed by its affinity for the substrate.
Genetic polymorphism can alter both the
density and affinity of the transporter protein for different substrates and thus affect
the pharmacokinetics of drugs. Moreover,
tissue specific drug distribution can occur
due to the presence of specific transporters
in certain cells. .
Vesicular transport (endocytosis,
exocytosis)
Certain substances with very large or impermeable molecules are transported inside the cell
(endocytosis) or extruded from it (exocytosis)
by enclosing their particles into tiny vesicles.
A binding protein located on the membrane
complexes with the substance and initiates
vesicle formation (Fig. 2.6). The vesicle then
detaches from the membrane and may remain
stored within the cell, or it may release the
substance in the cytoplasm, or it may move to
the opposite membrane fuse with it to release
the substance across the cell (exocytosis).
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