Biology Reference
In-Depth Information
have long been known to be resistant to one or more pesticides (
Brown and Pal, 1971;
Georghiou and Saito, 1983
) and a much larger number of agricultural pests are also resis-
tant. The numbers identified in both groups continue to grow. Resistance to a particular
compound does not involve an entire species but only the toxicant-stressed population;
nevertheless, resistance constitutes a serious public health and economic problem.
Resistant strains are first recognized only after the parent population has been
selected by killing off many of its susceptible members. The rate at which selection pro-
gresses depends not only on the intensity of the selection pressure, but also on the dura-
tion of each generation. Therefore, it is not surprising that resistance has most often been
observed among organisms such as bacteria or houseflies, characterized by large num-
bers of individuals and a rapid rate of reproduction. However, resistance has also been
observed in species with relatively small populations and relatively slow multiplication.
Resistance of a vertebrate species to a pesticide apparently was first recognized
in the 1960s and 1970s in connection with Norway rats exposed to warfarin. This
phenomenon was first reported from Scotland (
Boyle, 1960
) and subsequently from
Denmark (
Lund, 1964, 1967
), England and Wales (
Bentley, 1969; Drummond, 1966
),
The Netherlands (
Ophof and Langeveld, 1969
), Germany (
Telle, 1971
), and the United
States, specifically North Carolina and Idaho (
Brothers, 1972; Jackson and Kaukeinen,
1972
). Resistance in rats continues to be reported and investigated on a regular basis,
for example, in France (Lasseur et al., 2005), in Germany (
Pelz, 2007
), and in China
(Wang et al., 2008).
The early literature on the resistance of mammals to warfarin was reviewed by
Lund (1967)
. Only a few points need to be recorded here. So far, resistance is known
to occur in four species; the Norway and roof rats, the house mouse, and humans.
In addition, in their original studies of coumarin compounds, Link and his students
reported marked variation in susceptibility in rabbits as a Mendelian characteristic
(
Campbell et al., 1941
). The exact mechanism of inheritance of resistance to warfarin
is not clear. In humans, the facts are consistent with transmission by a single autosomal
dominant gene (
O'Reilly et al., 1963
), but this was based on only one kindred. In rats
and mice, it seems that more than one gene is involved. The physiological basis of the
resistance in vertebrates also is not clear and may be different in different instances. It
is generally held that it involves the vitamin K cycle (
Cain et al., 1998
) and polymor-
phisms in the VKOR vitamin K epoxide reductase gene (Lasseur et al., 2005; Wang
et al., 2008). The role of CYP isoforms in anticoagulant resistance is not clear, although
it has been noted in bromadiolone resistance in the rat that several CYP isoforms are
overexpressed (
Markussen et al., 2008a,b
). In every instance studied, including humans,
resistance extended to other coumarin anticoagulants and those based on indanedione,
while susceptibility to heparin is normal.
Another early report of resistance among vertebrates involved mosquito fish col-
lected from insecticide-contaminated waters near cotton fields (
Vinson et al., 1963
).
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