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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Available from: Janice E Chambers, Oct 05, 2015
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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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    ABSTRACT: Tropical coastal ecosystems, including the Great Barrier Reef (GBR) of Australia are increasingly threatened by pollution; yet few studies have investigated the sensitivity of GBR species to these pollutants. Here we exposed juveniles of the tropical reef fish Acanthochromis polyacanthus (spiny damselfish) to three concentrations of the insecticide chlorpyrifos (CPF) and measured (i) muscle cholinesterase (ChE) activity; (ii) hepatic glutathione-S-transferase (GST) activity; and (iii) coenzyme Q (CoQ) redox balance, after 6h and 96h of exposure. After 96h, muscle ChE activity was significantly inhibited by 26%, 49% and 53% when fish were exposed to 1, 10 or 100μg/L CPF, respectively. Muscle ChE characterization revealed three types of ChEs, including two atypical forms. Hepatic CoQ antioxidant form significantly increased at 10μg/L after 6h of exposure, potentially demonstrating an early response to CPF-induced oxidative stress in liver. Hepatic GST was not affected by CPF exposure.
    Marine Pollution Bulletin 09/2011; 65(4-9):384-93. DOI:10.1016/j.marpolbul.2011.08.020 · 2.99 Impact Factor
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    • "The World Health Organization (WHO) classifies methyl parathion as an extremely hazardous pesticide. Like other organophosphate insecticides, methyl parathion is a cholinesterase inhibitor in mammals and fish (Boone and Chambers, 1996; Hai et al., 1997; Aguiar et al., 2004). Moreover, in a previous study we demonstrated that 2 mg L − 1 of MPc (1/3 of 96 h-LC 50 ) has a high oxidative-stress-inducing potential in the neotropical fish matrinxã, Brycon cephalus, generating free radicals and inducing changes to the "
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    ABSTRACT: Methyl parathion (MP), an organophosphate widely applied in agriculture and aquaculture, induces oxidative stress due to free radical generation and changes in the antioxidant defense system. The antioxidant roles of selenium (Se) were evaluated in Brycon cephalus exposed to 2 mg L(-1) of Folisuper 600 BR (MP commercial formulation - MPc, 600 g L(-1)) for 96 h. Catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione S-transferase (GST), reduced glutathione (GSH) and lipid peroxidation (LPO) levels in the gills, white muscle and liver were evaluated in fish fed on diets containing 0 or 1.5 mg Se kg(-1) for 8 weeks. In fish treated with a Se-free diet, the MPc exposure increased SOD and CAT activities in all tissues. However, the GPx activity decreased in white muscle and gills whereas no alterations were observed in the liver. MPc also increased GST activity in all tissues with a concurrent decrease in GSH levels. LPO values increased in white muscle and gills and did not change in liver after MPc exposure. A Se-supplemented diet reversed these findings, preventing increases in LPO levels and concurrent decreases in GPx activity in gills and white muscle. Similarly, GSH levels were maintained in all tissue after MPc exposure. These results suggest that dietary Se supplementation protects cells against MPc-induced oxidative stress.
    Comparative Biochemistry and Physiology Part C Toxicology & Pharmacology 01/2009; 149(1):40-9. DOI:10.1016/j.cbpc.2008.06.012 · 2.30 Impact Factor
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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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    ABSTRACT: The organophosphate azinphos methyl (AzMe) and the carbamate carbaryl are the insecticides mostly used in the irrigated valley of Río Negro and Neuquén, Patagonia, Argentina. Juvenile rainbow trout were exposed to AzMe and carbaryl and the sensitivity of skeletal muscular cholinesterase (ChE) and the time course of inhibition and recovery were evaluated. EC50 values demonstrated that AzMe was a stronger in vivo inhibitor of muscular ChE (1.05+/-0.23 microg/L) than carbaryl (270+/-62.23 microg/L). Muscular ChE was significantly less sensitive to both insecticides than brain ChE. EC50 values obtained for muscular ChE were closer than those for brain ChE to the respective pesticide lethal concentrations, pointing out the relevance of the muscular enzyme in determining acute toxicity. The recovery process of ChE activity after carbaryl exposure (500 microg/L) was fast, whereas no significant recovery was observed with AzMe (1 microg/L) after 21 days in uncontaminated media. Brain and muscular ChE were inhibited and showed a significant but not complete recovery after three consecutive 48-h exposures to AzMe (1 microg/L) followed by a recovery period of 7 days. This scheme mimics the periodical application of the insecticides in the region and suggests a certain probability of a sustained ChE inhibition under field conditions, affecting fish development and survival.
    Comparative Biochemistry and Physiology Part C Toxicology & Pharmacology 10/2007; 146(3):308-13. DOI:10.1016/j.cbpc.2007.04.002 · 2.30 Impact Factor
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