67
The reactivation of carbamylated cholinesterase is dependent on the duration and
the temperature at which the carcass remained in the field and would therefore help
in masking carbamate poisoning (Smith et al. 1995). Secondary symptoms may
occur in some organophosphate poisoning called organophosphate-induced delayed
neuropathy (OPIDN) in which the target enzyme is brain neuropathy target esterase
(NTE), manifested by limb immobility of exposed individual (Lotti and Moretto
2005). OPIDN is symbolized by the demyelination of neurons and paralysis which
can be noticed after 20–25 days following single or recurrent exposure(s) (Grue
et al. 1997). Neurotoxic effect of organophosphate may also be mediated through
oxidative damage by producing reactive nitrogen species [such as nitric oxide
(NO•) and nitrogen dioxide (NO 2 )]. Excess (NO•) acts as a neurotoxin-promoting
neurodegenerative disorders (Di Meo et al. 2016).
Impairment of mitochondrial function plays an important role in the progress of
many neurodegenerative disorders (like Parkinson’s disease, Alzheimer’s disease),
which is related to the inhibition of complex I (CI) or ubiquinone oxidoreductase,
member of the oxidative phosphorylation system located at mitochondrial inner
membrane (Kulic et al. 2011). CI inhibitory effects were found in rats exposed to
monocrotophos (Masoud et al. 2009) and dichlorvos (Binukumar et al. 2012), which
include acute cholinergic conflict succeeded by possible intermediate syndrome and
finally OPIDN. A study reported that hens treated with chlorpyrifos showed sign of
delayed neuropathy like ataxia and locomotor disturbances with concomitant
inhibition of NTE, mitochondrial CI, and decreased ATP (adenosine triphosphate)
production, thereby supporting organophosphate-induced mitochondrial dysfunction in birds (Salama et al. 2014) which may be indirectly responsible for the
changes in behaviour due to neurological complications.
Exposure to pesticide at sublethal dose emanated to a significant hindrance in
brain cholinesterase activity in reproductively mature adults that can be correlated
to an extent behavioural alteration such as limited mobility and interrupted incubating ability; all these changes ultimately lead to considerable lower production of
fledged young (Busby et al. 1990). Studies have demonstrated that cholinesteraseinhibiting insecticides exclusively affect almost all physiological and behavioural
functions (Greaves and Letcher 2017). Behavioural changes in response to toxic
chemicals provide an insight to the population and ecological repercussion in
remote future (Raley-Susman 2014). Organophosphate may induce behavioural
alteration in avifauna by interfering thermoregulation, food consumption, sexual
behaviour, clutch size, embryonic development, mobility, seasonal behaviour,
territorial behaviour, and parental care (Grue et al. 1991, 1997). Such switch-over
in physiological and behavioural pattern has the potential to reduce the survival and
reproductive fitness of individuals, which ultimately affects the population up to
local extinction of several bird species (Grue et al. 1997). A perceptible change in a
population of white-throated sparrows (Zonotrichia albicollis) in Canada took place
after forestry spraying operations with fenitrothion (an OP) (Busby et al. 1990).
Lethargic behaviour of birds due to sublethal exposure of organophosphate and
carbamates can increase the susceptibility for predation of house sparrows (Passer
domesticus) and bobwhite quails (Colinus virginianus) (Hunt et al. 1992; Hawkes
3 Toxic Effects of Pesticides on Avian Fauna
The reactivation of carbamylated cholinesterase is dependent on the duration and
the temperature at which the carcass remained in the field and would therefore help
in masking carbamate poisoning (Smith et al. 1995). Secondary symptoms may
occur in some organophosphate poisoning called organophosphate-induced delayed
neuropathy (OPIDN) in which the target enzyme is brain neuropathy target esterase
(NTE), manifested by limb immobility of exposed individual (Lotti and Moretto
2005). OPIDN is symbolized by the demyelination of neurons and paralysis which
can be noticed after 20–25 days following single or recurrent exposure(s) (Grue
et al. 1997). Neurotoxic effect of organophosphate may also be mediated through
oxidative damage by producing reactive nitrogen species [such as nitric oxide
(NO•) and nitrogen dioxide (NO 2 )]. Excess (NO•) acts as a neurotoxin-promoting
neurodegenerative disorders (Di Meo et al. 2016).
Impairment of mitochondrial function plays an important role in the progress of
many neurodegenerative disorders (like Parkinson’s disease, Alzheimer’s disease),
which is related to the inhibition of complex I (CI) or ubiquinone oxidoreductase,
member of the oxidative phosphorylation system located at mitochondrial inner
membrane (Kulic et al. 2011). CI inhibitory effects were found in rats exposed to
monocrotophos (Masoud et al. 2009) and dichlorvos (Binukumar et al. 2012), which
include acute cholinergic conflict succeeded by possible intermediate syndrome and
finally OPIDN. A study reported that hens treated with chlorpyrifos showed sign of
delayed neuropathy like ataxia and locomotor disturbances with concomitant
inhibition of NTE, mitochondrial CI, and decreased ATP (adenosine triphosphate)
production, thereby supporting organophosphate-induced mitochondrial dysfunction in birds (Salama et al. 2014) which may be indirectly responsible for the
changes in behaviour due to neurological complications.
Exposure to pesticide at sublethal dose emanated to a significant hindrance in
brain cholinesterase activity in reproductively mature adults that can be correlated
to an extent behavioural alteration such as limited mobility and interrupted incubating ability; all these changes ultimately lead to considerable lower production of
fledged young (Busby et al. 1990). Studies have demonstrated that cholinesteraseinhibiting insecticides exclusively affect almost all physiological and behavioural
functions (Greaves and Letcher 2017). Behavioural changes in response to toxic
chemicals provide an insight to the population and ecological repercussion in
remote future (Raley-Susman 2014). Organophosphate may induce behavioural
alteration in avifauna by interfering thermoregulation, food consumption, sexual
behaviour, clutch size, embryonic development, mobility, seasonal behaviour,
territorial behaviour, and parental care (Grue et al. 1991, 1997). Such switch-over
in physiological and behavioural pattern has the potential to reduce the survival and
reproductive fitness of individuals, which ultimately affects the population up to
local extinction of several bird species (Grue et al. 1997). A perceptible change in a
population of white-throated sparrows (Zonotrichia albicollis) in Canada took place
after forestry spraying operations with fenitrothion (an OP) (Busby et al. 1990).
Lethargic behaviour of birds due to sublethal exposure of organophosphate and
carbamates can increase the susceptibility for predation of house sparrows (Passer
domesticus) and bobwhite quails (Colinus virginianus) (Hunt et al. 1992; Hawkes
3 Toxic Effects of Pesticides on Avian Fauna