69
Although organochlorines (prochloraz, endosulfan, dieldrin) are well known
for their estrogenic properties, some of organophosphates and carbamates
(toclofos-methyl, chlorpyrifos, quinalphos) are also reported to have estrogenic
potential (Andersen et al. 2002; Kitamura et al. 2010). Differentiation of avian
reproductive system is estrogen dependent; therefore, differentiation of the accessory male and female genital ducts was found to be altered by estrogen exposure
in a dose-dependent fashion (Fry 1995). Chatterjee et al. (1992) reported estrogen-like action of quinalphos exposure of which induces vaginal cornification
increased uterine wet weight in rat as established by uterotrophic assay. Gonadal
impairment may occur due to alteration in steroidogenesis in testis or ovaries of
the birds treated with anticholinesterase agents (Ray et al. 1987). Sublethal exposure of organophosphates (methyl parathion/phosphamidon/quinalphos) to wild
female of white-throated munia (Lonchura malabarica) showed significant reduction in the activity of two important steroidogenic enzymes of growing follicle,
namely, Δ53β-hydroxysteroid dehydrogenase (3βHSD) and 17β-hydroxysteroid
dehydrogenase (17βHSD) in a dose-dependent manner (Mitra 2006). These two
steroidogenic enzymes (3βHSD and 17βHSD) are the key player in the production
of oestrogen and progesterone, respectively (Civinini et al. 2001). Degenerative
changes at histological level in ovary of the treated birds include reduced thickness of membrane granulosa layer, vacuolation, and exfoliation of granulosa cells
of mature follicles (Mitra 2006). Arrested developmental process and degeneration of spermatogenic cells are observed in domestic and semi-domestic birds
after exposure to organophosphates (Mitra et al. 2011). Increased number of
degenerated germ cells in the seminiferous tubules was found in the testis of adult
male white-throated munia (L. malabarica), after exposure to sublethal dose of
methyl parathion (Maitra and Sarkar 1996). Male rose ringed parakeets (Psittacula
krameri) when ingested to graded doses of methyl parathion showed subsided
testicular function which may be caused by an upset circulating context of LH and
testosterone (Maitra and Mitra 2008). Thus, sublethal exposures of xenobiotics
adversely effect on reproduction of avian fauna that may not be related to mortality but through a direct effect on population level. Alternative pathway of organophosphate-induced reproductive impairment in different vertebrates may occur by
modifying neurotransmitter levels and thus debilitating hypothalamic and/or pituitary monitoring on reproduction (Muller et al. 1977). Possibilities also exist by
suppressing GnRH release, which may act directly by modifying gonadotropin
synthesis and secretion or indirectly by changing the pituitary cell sensitiveness to
GnRH through the mediation of gonadal steroids resulting from adjustment of
FSH and LH level by feedback mechanism (Stoker et al. 1993). According to
Rattner et al. (1984), organophosphorus insecticides depreciate reproductive function possibly by modulating secretion of luteinizing hormone and progesterone.
Rattner et al. (1982) also reported that significant decline in plasma titre of LH,
progesterone, and corticosterone was noted in female bobwhite quail following
the short-term exposure of parathion.
3 Toxic Effects of Pesticides on Avian Fauna
Although organochlorines (prochloraz, endosulfan, dieldrin) are well known
for their estrogenic properties, some of organophosphates and carbamates
(toclofos-methyl, chlorpyrifos, quinalphos) are also reported to have estrogenic
potential (Andersen et al. 2002; Kitamura et al. 2010). Differentiation of avian
reproductive system is estrogen dependent; therefore, differentiation of the accessory male and female genital ducts was found to be altered by estrogen exposure
in a dose-dependent fashion (Fry 1995). Chatterjee et al. (1992) reported estrogen-like action of quinalphos exposure of which induces vaginal cornification
increased uterine wet weight in rat as established by uterotrophic assay. Gonadal
impairment may occur due to alteration in steroidogenesis in testis or ovaries of
the birds treated with anticholinesterase agents (Ray et al. 1987). Sublethal exposure of organophosphates (methyl parathion/phosphamidon/quinalphos) to wild
female of white-throated munia (Lonchura malabarica) showed significant reduction in the activity of two important steroidogenic enzymes of growing follicle,
namely, Δ53β-hydroxysteroid dehydrogenase (3βHSD) and 17β-hydroxysteroid
dehydrogenase (17βHSD) in a dose-dependent manner (Mitra 2006). These two
steroidogenic enzymes (3βHSD and 17βHSD) are the key player in the production
of oestrogen and progesterone, respectively (Civinini et al. 2001). Degenerative
changes at histological level in ovary of the treated birds include reduced thickness of membrane granulosa layer, vacuolation, and exfoliation of granulosa cells
of mature follicles (Mitra 2006). Arrested developmental process and degeneration of spermatogenic cells are observed in domestic and semi-domestic birds
after exposure to organophosphates (Mitra et al. 2011). Increased number of
degenerated germ cells in the seminiferous tubules was found in the testis of adult
male white-throated munia (L. malabarica), after exposure to sublethal dose of
methyl parathion (Maitra and Sarkar 1996). Male rose ringed parakeets (Psittacula
krameri) when ingested to graded doses of methyl parathion showed subsided
testicular function which may be caused by an upset circulating context of LH and
testosterone (Maitra and Mitra 2008). Thus, sublethal exposures of xenobiotics
adversely effect on reproduction of avian fauna that may not be related to mortality but through a direct effect on population level. Alternative pathway of organophosphate-induced reproductive impairment in different vertebrates may occur by
modifying neurotransmitter levels and thus debilitating hypothalamic and/or pituitary monitoring on reproduction (Muller et al. 1977). Possibilities also exist by
suppressing GnRH release, which may act directly by modifying gonadotropin
synthesis and secretion or indirectly by changing the pituitary cell sensitiveness to
GnRH through the mediation of gonadal steroids resulting from adjustment of
FSH and LH level by feedback mechanism (Stoker et al. 1993). According to
Rattner et al. (1984), organophosphorus insecticides depreciate reproductive function possibly by modulating secretion of luteinizing hormone and progesterone.
Rattner et al. (1982) also reported that significant decline in plasma titre of LH,
progesterone, and corticosterone was noted in female bobwhite quail following
the short-term exposure of parathion.
3 Toxic Effects of Pesticides on Avian Fauna