Time Course of Inhibition of Cholinesterase and Aliesterase Activities, and Nonprotein Sulfhydryl Levels Following Exposure to Organophosphorus Insecticides in Mosquitofish (Gambusia affinis)

Department of Biological Sciences, Mississippi State University, Mississippi 39762, USA.
Fundamental and Applied Toxicology 02/1996; 29(2):202-7. DOI: 10.1093/toxsci/29.2.202
Source: PubMed


Cholinesterase (ChE) in brain and muscle was quickly inhibited during a 48-hr in vivo exposure to chlorpyrifos (0.1 ppm), parathion (0.15 ppm), and methyl parathion (8 ppm) in mosquitofish (Gambusia affinis). ChE remained inhibited during a 96-hr nonexposure period. Brain ChE reached peak inhibition by 12 hr after exposure to
parathion and chlorpyrifos and by 4 hr after exposure to methyl parathion. All insecticides caused greater than 70% ChE inhibition
by 4 hr in muscle. There was no recovery of ChE after 4 days of nonexposure in either brain or muscle. Hepatic aliesterases
(AliE) were quickly and greatly inhibited (>70% by 4 hr) after exposure to parathion and chlorpyrifos but not after exposure
to methyl parathion. Exposure to methyl parathion required 24–36 hr to inhibit hepatic AliE to the same level as that following
parathion and chlorpyrifos exposures at 4 hr. Exposure to all insecticides eventually resulted in greater than 80% inhibition
of AliE. None of the test groups treated with insecticides showed any signs of significant recovery of AliE during the 4 days
of nonexposure. Nonprotein sulfhydryl (NPSH) concentrations were lower than controls after 24 hr of exposure and 96 hr after
recovery for all compounds. Exposure to methyl parathion lowered NPSH concentrations greater than the other compounds. Hepatic
AliE appear capable of affording some protection of ChE from inhibition following parathion or chlorpyrifos exposures, but
considerably less protection against methyl parathion.

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    • "There is often an apparent discrepancy between the low or patchy detection of CPF in the environment and biomarker indications of exposure in living organisms. This inconsistency is likely due to low-level of chronic exposures, as the non-reversible binding of CPF induces ChE inhibition with exposure duration (Boone and Chambers, 1996; Fulton and Key, 2001). In fact, decreases in ChE activity in living organisms might be one of the few ways to effectively detect exposure to OPs such as CPF. "
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    • "Cholinesterase (ChE) inhibition has been widely used as a biomarker of OP and CB exposure in aquatic organisms including fish (Edwards and Fisher, 1991; Gruber and Munn, 1998; Monserrat et al., 2002; Abdel-Halim et al., 2006). Contrary to what happens in other vertebrates, the correlation between ChE inhibition and mortality in fish has not been fully established (Boone and Chambers, 1996; Ferrari et al., 2004a). Some fish species are able to tolerate a high degree of brain ChE inhibition without lethal consequences (Chambers and Carr, 1995; Pathiratne and George, 1998; Fulton and Key, 2001; Varò et al., 2003; Ferrari et al., 2004a), whereas in other species survival is affected (Coppage, 1972). "
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