Environmental Engineering Reference
In-Depth Information
thermodynamic processes, such as partitioning into the organism as well as kinetic
processes related to rates of diffusion, transport, etc. This means that the critical
body burden associated with the threshold of toxicity is not reached until sometime
after exposure is initiated. This has been demonstrated for CPY (Giesy et al.
1999
)
and other organophosphorus insecticides (Bogen and Reiss
2012
). The relationship
between time of exposure and toxicity is reciprocal, with shorter exposures at
greater concentrations resulting in the same level of response as lesser concentra-
tions for longer durations. This reciprocal relationship was demonstrated in studies
of effects of CPY on
Daphnia magna
exposed to CPY for varying durations (Naddy
et al.
2000
). For example, continuous exposures to 0.25
g L
−1
CPY resulted in
100% mortality in 5 d, while exposures for 1 d followed by transfer to clean water
resulted in only 17% mortality, and then only after 16 d (Naddy et al.
2000
). Whether
this is the result of a delayed (latent) response or other causes, including regenera-
tion of AChE activity, is uncertain; however, given the recovery observed in other
Crustacea (below), the latter is a more plausible explanation. Where multiple epi-
sodic exposures occur, recovery from toxic effects between exposures can affect
responses of exposed organisms. This was demonstrated in the greater response of
D. magna
exposed to the same concentration of CPY for 1 × 12 h compared to ani-
mals exposed for 2 × 6 h, 3 × 4 h, or 4 × 3 h with a 24-h interval between pulses
(Naddy and Klaine
2001
). Here, the interval between exposures likely provided
time for detoxifi cation and excretion of CPY, recovery of the target enzyme AChE
by dephosphorylation (k
3
in Fig.
4
in Solomon et al.
2014
), and/or synthesis of new
AChE (Naddy and Klaine
2001
).
Recovery of AChE inhibited by CPY has been observed in arthropods and fi sh.
After exposure of
D. magna
to the 24-h LC
50
concentration, whole-body activity of
AChE (50% of unexposed control at time of removal to uncontaminated water)
recovered to control activity within 24 h when animals were moved to clean water
(Barata et al.
2004
). After exposures of larvae of the midge
Kiefferulus calligaster
to 0.38, 1.02, or 1.26
μ
g L
−1
CPY for 3 d, concentration-dependent depression of
activity of AChE as great as 90% was observed (Domingues et al.
2009
). When
transferred to fresh medium for a further 3 d, AChE activity returned to control
values. Similar recovery of activity of AChE was observed in the shrimp (
Paratya
australiensis
) exposed to CPY for 96 h at concentrations from 0.001 to 0.1
μ
g L
−1
and then moved to clean medium for 48 h or 7 d (Kumar et al.
2010
). Complete
recovery was dependent on exposure concentration and recovery time. Recovery
after a 7-d exposure to 0.025
μ
g L
−1
,
recovery was not complete within 7 d. Whether this recovery resulted from dephos-
phorylation of AChE or synthesis of new AChE is not known. However, it is clear
that recovery occurs and that recovery times are of the order of 1 to ~7 d.
Studies of fi sh exposed to CPY suggest that recovery of AChE in fi sh takes longer
than in arthropods. No recovery of brain- or muscle-AChE was observed within a 4-d
period in mosquitofi sh (
Gambusia affi nis
) exposed to 100
μ
g L
−1
occurred in 7 d, but after exposure to 0.1
μ
g CPY L
−1
for 24 h (Boone
and Chambers
1996
). This exposure resulted in 70% inhibition of these enzymes. In
another study of the same species, exposure to 297
μ
g CPY L
−1
for 96 h resulted in
80% inhibition of brain-AChE (Kavitha and Rao
2008
), but activity had recovered to
control levels after 20 d in clean water. AChE activity in the brain of Nile tilapia,
μ
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