Distribution and Effects of Chemicals in Communities and Ecosystems - Organic Pollutants: An Ecotoxicological Perspective - page 80

Peripheral
tissues

1
v

Redistribution

Liver

Gut

C L

1
V max

R U

R M

1
K m

Metabolism and
excretion

1
s

(a) (b)

fIgure 4.2 (a) A bioaccumulation model for terrestrial organisms. A kinetic model for
liver. R U , rate of uptake from the gut; R M , rate of metabolism in liver; C L , concentration of
pollutant in liver. The arrows indicate the routes of transfer of pollutant within the animal.
The rates of uptake and metabolism are expressed in terms of kilograms of body weight. The
final elimination of water-soluble products (metabolites and conjugates) is in the urine. (b)
Lineweaver-Burke plot to estimate the bioaccumulation factor; V max and v are expressed as
milligrams of pollutant metabolized per kilogram of body weight per day; S is expressed as
the concentration of pollutant, ppm by weight (either in terms of grams of liver or milligrams
of hepatic microsomal protein) (from Walker 1987).

that are good substrates for monooxygenases, hydrolases, etc., can be metabolized
relatively rapidly even though they, as a group, have relatively low metabolic capac-
ity (Chapter 2). So, in this case metabolism as well as diffusion is an important fac-
tor determining rate of loss. By contrast, many polyhalogenated compounds are only
metabolized very slowly by fish, so metabolism does not make a significant contribu-
tion to detoxication, and loss by diffusion is the dominant mechanism of elimination.
Some further aspects of detoxication by fish need to be briefly mentioned. When
fish inhabit polluted waters, exchange diffusion occurs until a steady state is reached,
and no net loss will occur by this mechanism unless the concentration in water falls.
When a recalcitrant pollutant is acquired from prey, digestion can lead to the tissue
levels of that pollutant temporally exceeding those originally existing while in the
steady state. Here, diffusion into the ambient water may provide an effective excre-
tion mechanism in the absence of effective metabolic detoxication. Seen from an
evolutionary point of view, the requirements of fish for metabolic detoxication would
appear to have been limited on the grounds that loss by diffusion would often have
prevented tissue levels becoming too high. The poor metabolic detoxication sys-
tems of fish relative to those of terrestrial omnivores and herbivores are explicable
on these grounds (Chapter 2). However, the advent of refractory organic pollutants,
which combine high toxicity with high lipophilicity, has exposed the limitations of
existing detoxication systems of fish. The very high toxicity of compounds such as
dieldrin and other cyclodiene insecticides to fish was soon apparent, with fish kills
occurring at very low concentrations in water (see Chapter 5) and metabolically
resistant strains of fish being reported in polluted rivers such as the Mississippi.