Evaluation of Liver and Brain Esterases in the Spotted Gar Fish ( Lepisosteus oculatus ) as Biomarkers of Effect in the Lower Mississippi River Basin

Huang, Tien L.; Obih, Patience; Jaiswal, R.; Hartley, William; Thiyagarajah, Arunthavarani

doi:10.1007/s001289900388

Cited by 34 publications

(22 citation statements)

References 14 publications

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“…Early work on fish by Kingsbury and Masters (1972) reported the presence of three carboxylesterase isozymes in rainbow trout with the detection of one polymorphism. Since then a number of researchers have examined esterase activities in fish, but the work lags significantly behind that performed in mammalian systems (Boone and Chambers, 1997;Huang et al, 1997;Sanchez-Hernandez et al, 1998;Barron et al, 1999;Al-Ghais, 2000;Wogram et al, 2001;Denton et al, 2003). This study expands the current literature on carboxylesterases in several fish species and examines the appropriateness of multiple biochemical endpoints as biomarkers of agrochemical exposure and/or susceptibility.…”

Section: Discussionmentioning

confidence: 96%

Individual variability in esterase activity and CYP1A levels in Chinook salmon (Oncorhynchus tshawytscha) exposed to esfenvalerate and chlorpyrifos

et al. 2005

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Acetylcholinesterase (AChE) activity has traditionally been monitored as a biomarker of organophosphate (OP) and/or carbamate exposure. However, AChE activity may not be the most sensitive endpoint for these agrochemicals, because OPs can cause adverse physiological effects at concentrations that do not affect AChE activity. Carboxylesterases are a related family of enzymes that have higher affinity than AChE for some OPs and carbamates and may be more sensitive indicators of environmental exposure to these pesticides. In this study, carboxylesterase and AChE activity, cytochrome P4501A (CYP1A) protein levels, and mortality were measured in individual juvenile Chinook salmon (Oncorhynchus tshawytscha) following exposure to an OP (chlorpyrifos) and a pyrethroid (esfenvalerate). As expected, high doses of chlorpyrifos and esfenvalerate were acutely toxic, with nominal concentrations (100 and 1 μg/l, respectively) causing 100% mortality within 96 h. Exposure to chlorpyrifos at a high dose (7.3 μg/l), but not a low dose (1.2 μg/l), significantly inhibited AChE activity in both brain and muscle tissue (85% and 92% inhibition, respectively), while esfenvalerate exposure had no effect. In contrast, liver carboxylesterase activity was significantly inhibited at both the low and high chlorpyrifos dose exposure (56% and 79% inhibition, respectively), while esfenvalerate exposure still had little effect. The inhibition of carboxylesterase activity at levels of chlorpyrifos that did not affect AChE activity suggests that some salmon carboxylesterase isozymes may be more sensitive than AChE to inhibition by OPs. CYP1A protein levels were ∼30% suppressed by chlorpyrifos exposure at the high dose, but esfenvalerate had no effect. Three teleost species, Chinook salmon, medaka (Oryzias latipes) and Sacramento splittail (Pogonichthys macrolepidotus), were examined for their ability to hydrolyze a series of pyrethroid surrogate substrates and in all cases hydrolysis activity was undetectable. Together these data suggest that (1) carboxylesterase activity inhibition may be a more sensitive biomarker for OP exposure than AChE activity, (2) neither AChE nor carboxylesterase activity are biomarkers for pyrethroid exposure, (3) CYP1A protein is not a sensitive marker for these agrochemicals and (4) slow hydrolysis rates may be partly responsible for acute pyrethroid toxicity in fish.

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Section: Discussionmentioning

confidence: 96%

Individual variability in esterase activity and CYP1A levels in Chinook salmon (Oncorhynchus tshawytscha) exposed to esfenvalerate and chlorpyrifos

et al. 2005

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“…Few studies have correlated exposure to Cd> with e!ects on "sh brain ChE activity. Of these, ChE activity was inhibited by in vitro exposures (Gill et al, 1991;Huang et al, 1997;Sen et al, 1995), and was increased by in vivo exposure to Cd> (Christensen, 1975;Gill et al, 1991). Following in vivo exposures, freshwater Barbus conchius exposed 48 h to 12.6 mg/liter CdCl had a signi"cant increase in brain ChE activity, 13% above control (Gill et al, 1991), and brook trout alevins (Salvelinus fontanalis; 21 days posthatch) exposed for 21 days to Cd> concentrations of 0.7 or 3.43 g/liter had ChE activities of 46 and 60%, respectively, above control (Christensen, 1975).…”

Section: Discussionmentioning

confidence: 98%

Cholinergic and Behavioral Neurotoxicity of Carbaryl and Cadmium to Larval Rainbow Trout (Oncorhynchus mykiss)

Beauvais

Jones

Parris

et al. 2001

Ecotoxicology and Environmental Safety

103

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Pesticides and heavy metals are common environmental contaminants that can cause neurotoxicity to aquatic organisms, impairing reproduction and survival. Neurotoxic effects of cadmium and carbaryl exposures were estimated in larval rainbow trout (RBT; Oncorhynchus mykiss) using changes in physiological endpoints and correlations with behavioral responses. Following exposures, RBT were videotaped to assess swimming speed. Brain tissue was used to measure cholinesterase (ChE) activity, muscarinic cholinergic receptor (MChR) number, and MChR affinity. ChE activity decreased with increasing concentrations of carbaryl but not of cadmium. MChR were not affected by exposure to either carbaryl or cadmium. Swimming speed correlated with ChE activity in carbaryl-exposed RBT, but no correlation occurred in cadmium-exposed fish. Thus, carbaryl exposure resulted in neurotoxicity reflected by changes in physiological and behavioral parameters measured, while cadmium exposure did not. Correlations between behavior and physiology provide a useful assessment of neurotoxicity.

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“…In addition to traditional chemical analysis, activity of the enzyme acetylcholinesterase (AChE) has been used for environmental monitoring programs (Burgeot, Bocquéné, Porte, Dimet, Santella, Garcia de la Parra et al, 1996;Huang, Obih, Jaiswal, Hartley, & Thiyagarajah (1997);Minier, Levy, Rabel, Bocquéné, Godefroy, Burgeot et al, 2000) because AChE inhibition in tissues of fish and other animals can be used as biomarker for organophosphorous and carbamates exposure (Escartin & Porte, 1996;Sturn, Silva de Assis, & Hansen, 1999). Inhibition of AChE is not necessarily fatal, but using a fish with a highly sensitive AChE as a sentinel species will allow the detection of lower contamination levels.…”

Section: Introductionmentioning

confidence: 99%

Brain acetylcholinesterase as a marine pesticide biomarker using Brazilian fishes

Oliveira¹,

Filho

Bastos

et al. 2007

Marine Environmental Research

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Evaluation of Liver and Brain Esterases in the Spotted Gar Fish ( Lepisosteus oculatus ) as Biomarkers of Effect in the Lower Mississippi River Basin

Cited by 34 publications

References 14 publications

Individual variability in esterase activity and CYP1A levels in Chinook salmon (Oncorhynchus tshawytscha) exposed to esfenvalerate and chlorpyrifos

Individual variability in esterase activity and CYP1A levels in Chinook salmon (Oncorhynchus tshawytscha) exposed to esfenvalerate and chlorpyrifos

Cholinergic and Behavioral Neurotoxicity of Carbaryl and Cadmium to Larval Rainbow Trout (Oncorhynchus mykiss)

Brain acetylcholinesterase as a marine pesticide biomarker using Brazilian fishes

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