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Further study revealed 2- to 500-fold levels of resistance to a variety of pesticides in
mosquito fish and five other species of fish ( Boyd and Ferguson, 1964a,b; Ferguson and
Bingham, 1966a,b; Ferguson and Boyd, 1964; Ferguson et al., 1964, 1965 ). Resistance
to chlorinated hydrocarbon pesticides was found in three species of frog ( Boyd et al.,
1963 ). The degree of resistance may be so great in some instances that resistant species
can withstand enough poison to kill their predators.
Ozburn and Morrison (1962) were the first to produce resistance to a pesticide in
a mammal by selection under laboratory conditions. In mice selected by a single intra-
peritoneal dose of DDT administered at 4 weeks of age, resistance in the ninth genera-
tion had increased by a factor of 1.7 as measured by the LD 50 . Although the factor of
1.7 is small, about half of the susceptible mice withstood a dose that was uniformly
fatal to control mice. Further study ( Ozburn and Morrison, 1965 ) revealed that the
selected and control colonies differed in their rates of oxygen consumption. The resis-
tant mice were fatter than the susceptible ones, and considerable evidence indicated
that resistance depended on preferential deposit of DDT in the fat and consequently
the avoidance of peak levels in sensitive tissues. The resistance was not specific to DDT
but extended to lindane and dieldrin ( Barker and Morrison, 1966 ). Success in the
development of resistance in mammals in the laboratory has not been uniform; appar-
ently some strains are not sufficiently heterozygous to respond to selection ( Guthrie
et al., 1971 ).
Thus many instances are known in which species or strains differ in their sus-
ceptibility to pesticides, the resistance arising through selection in the field. In other
instances, it has been possible to produce resistance in the laboratory through selection.
In many instances it has been possible to define the genetic mechanisms responsible
for observed differences in the metabolism of the pesticides in question. Except in the
case of insects, a genetic mechanism has been defined only rarely in connection with
metabolism of pesticides.
The following references are suggested on this subject: Dauterman (1994) , Evered
and Collins (1984) , Georghiou and Saito (1983) , and Hayes et al. (1990) .
CONCLUSIONS
Knowledge of the metabolism of pesticides is essential for several reasons, including the
development of more selective insecticides, and provides, in part, the fundamental basis
for science-based risk assessments for human and environmental health ( Buratti et al.,
2007; Hodgson and Rose, 2005, 2007 ). Until recently, and as a matter of necessity, this
research was carried out almost exclusively on experimental animals and the results,
particularly in the case of human health risk assessments, were extrapolated to humans.
Although much essential background will continue to be obtained from experimen-
tal animals, because of the ready availability of human hepatocytes, human cell lines,
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