Acetylcholinesterase inhibition and increased food consumption rate in the zebrafish, Danio rerio, after chronic exposure to parathion

Roex, Erwin; Keijzers, Rineke; Gestel, Cornelis A.M. van

doi:10.1016/s0166-445x(03)00100-0

Cited by 111 publications

(53 citation statements)

References 29 publications

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“…It could be found that after additional 8 days of elimination, the ChE activities in liver and brain kept on reducing, but those in gill and muscle increased slightly, which confirmed studies by other researchers (Straus and Chambers, 1995;Sancho et al, 1997). Roex et al (2003) reported that AChE inhibition in zebrafish after chronic exposure to parathion was correlated with exposure concentration, but not with exposure time. Straus and Chambers (1995) revealed that after 4-h exposure to chlorpyrifos or parathion AChE specific activities were greatly depressed in five tissues (brain, gill, liver, muscle, and plasma) of fingerling channel catfish.…”

Section: Cholinesterase Activity Assaysupporting

confidence: 87%

“…The activities of cholinesterase (ChE), including both acetylcholinesterase (AChE, EC 3.1.1.7) and butyrylcholinesterase (BuChE, EC 3.1.1.8), have been commonly used as biomarker for pollution evaluation and risk assessment (Christensen, 1975;Shaw and Panigrahi, 1990;Aljafari et al, 1995;Roex et al, 2003). AChE plays an important role in the function of nerve impulse transmission (Smallman and Mansingh, 1969) and its inhibition causes an accumulation of acetylcholine (ACh) in synapses and in neuromuscular junctions, which can result in nerve dysfunction even death of organisms (Peakall, 1992;Roex et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…AChE plays an important role in the function of nerve impulse transmission (Smallman and Mansingh, 1969) and its inhibition causes an accumulation of acetylcholine (ACh) in synapses and in neuromuscular junctions, which can result in nerve dysfunction even death of organisms (Peakall, 1992;Roex et al, 2003). Although the role of AChE in neurotransmission is well documented, however, the physiological role of BuChE remains unclear (Hoffmann et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Methylmercury accumulation, histopathology effects, and cholinesterase activity alterations in medaka (Oryzias latipes) following sublethal exposure to methylmercury chloride

Liao

Shi

et al. 2006

Environmental Toxicology and Pharmacology

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Section: Cholinesterase Activity Assaysupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Methylmercury accumulation, histopathology effects, and cholinesterase activity alterations in medaka (Oryzias latipes) following sublethal exposure to methylmercury chloride

Liao

Shi

et al. 2006

Environmental Toxicology and Pharmacology

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“…Regarding serum AchE results demonstrated in Table (1), revealed that there was a significant inhibition of AchE in the exposed fish during the chronic exposure in comparison to the control group fish. Also, the inhibition of AchE is correlated with that of exposure concentration, but not with exposure time as reviewed by Roex et al (2003). Data are represented as means ± SE (n = 10).…”

Section: Resultsmentioning

confidence: 99%

Vitamin E as antioxidant in female african catfish (Clarias gariepinus) exposed to chronic toxicity of atrazine

Kadry

Amer

Marzouk

et al. 2012

Egypt. J. of Aquatic Biolo. and Fish.

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The present study was planned aiming to investigate the effects of atrazine herbicide exposure on stress biomarkers acetylcholinesterase activity (AchE) and cortisol, oxidative stress responses and the histopathological changes in liver of female Clarias gariepinus and the ameliorative effect of vitamin E supplementation (240mg/kg diet) on the degree of atrazine sublethal toxicity (1.37mg/l) for 6 weeks. Chronic exposure to atrazine revealed a marked inhibition in the activity of AchE. But, significant increase of serum cortisol level was recorded. Moreover, atrazine exposure was associated with a marked induction of oxidative damage in liver tissue as evidenced by increased level of lipid peroxidation (LPO) and reduced glutathione (GSH) content. Atrazine exposure also led to a significant increase in the activities of catalase (CAT) and superoxide dismutase (SOD).Furthermore, histopathological examination of the liver of exposed fish showed dilatation and congestion of blood vessels, fatty degeneration, necrosis and pyknotic nuclei of hepatocytes. However, fish fed diet supplemented with vitamin E exhibited protective effect by minimizing the atrazine-induced toxicity, through measured values more or less similar to the control group fish.

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“…The majority of information on brain and muscle AChE comes from inhibition of the enzyme, mainly through pesticide toxicity (Fernandez-Vega et al, 2002). When the enzyme is inhibited, ACh is not hydrolyzed in nerve synapses and neuromuscular junctions, causing build-up of ACh at these sites and leading to overstimulation of brain and muscular tissue (Roex et al, 2003). Because these previous studies were based on enzyme inhibition, the details of enzyme activation are little known in fish, although AChE activation likely affects ACh concentration in the synaptic cleft.…”

Section: Introductionmentioning

confidence: 99%

NTPDase and acetylcholinesterase activities in silver catfish, Rhamdia quelen (Quoy & Gaimard, 1824) (Heptapteridae) exposed to interaction of oxygen and ammonia levels

et al. 2009

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The effects of various levels of oxygen saturation and ammonia concentration on NTPDase (ecto-nucleoside triphosphate diphosphohydrolase, E.C. 3.6.1.5) and acetylcholinesterase (AChE, E.C. 3.1.1.7) activities in whole brain of teleost fish (Rhamdia quelen) were investigated. The fish were exposed to one of two different dissolved oxygen levels, including high oxygen (6.5 mg.L -1 ) or low oxygen (3.5 mg.L -1 ), and one of two different ammonia levels, including high ammonia (0.1 mg.L -1 ) or low ammonia (0.03 mg.L -1 ) levels. The four experimental groups included the following (A) control, or high dissolved oxygen plus low NH 3 ; (B) low dissolved oxygen plus low NH 3 ; (C) high dissolved oxygen plus high NH 3 ; (D) low dissolved oxygen plus high NH 3 . We found that enzyme activities were altered after 24 h exposure in groups C and D. ATP and ADP hydrolysis in whole brain of fish was enhanced in group D after 24 h exposure by 100% and 119%, respectively, compared to the control group. After 24 h exposure, AChE activity presented an increase of 34% and 39% in groups C and D, respectively, when compared to the control group. These results are consistent with the hypothesis that low oxygen levels increase ammonia toxicity. Moreover, the hypoxic events may increase blood flow by hypoxia increasing NTPDase activity, thus producing adenosine, a potent vasodilator.No presente estudo, avaliou-se o efeito de diferentes níveis de saturação de oxigênio e amônia sobre a atividade das enzimas NTPDase (ecto-nucleosídeo trifosfato difosfohidrolase, E.C. 3.6.1.5) e acetilcolinesterase (AChE, E.C. 3.1.1.7) em encéfalo total de jundiás (Rhamdia quelen). Os peixes foram expostos a diferentes níveis de oxigênio dissolvido e amônia, níveis altos de oxigênio (6,5 mg/L) ou baixos de oxigênio (3,5 mg/L), e níveis altos de amônia (0,1 mg/L) ou baixos de amônia (0,03 mg/L). Os peixes foram divididos em quatro diferentes grupos: (A) controle ou alto nível de oxigênio dissolvido mais baixo nível de NH 3 ; (B) baixo nível de oxigênio dissolvido mais baixo nível de NH 3 ; (C) alto nível de oxigênio dissolvido mais alto nível de amônia; (D) baixo nível de oxigênio dissolvido mais alto nível de NH -3 . As atividades de ambas as enzimas nos grupos C e D somente foram alteradas após 24 horas de exposição. A hidrólise do ATP e ADP em encéfalo total de jundiás foi aumentada após 24h de exposição para 104% e 155% no grupo D quando comparado ao grupo controle, respectivamente. A atividade da AChE apresentou após 24h de exposição um aumento de 37% no grupo C e 27% no grupo D, ambos comparados ao grupo controle. Os resultados obtidos corroboram com a hipótese que baixos níveis de saturação de oxigênio aumentam a toxicidade da amônia. Além disso, os eventos de hipóxia podem aumentar o fluxo sanguíneo, e este evento aumenta a atividade da NTPDase produzindo adenosina, um potente vasodilatador.

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Acetylcholinesterase inhibition and increased food consumption rate in the zebrafish, Danio rerio, after chronic exposure to parathion

Cited by 111 publications

References 29 publications

Methylmercury accumulation, histopathology effects, and cholinesterase activity alterations in medaka (Oryzias latipes) following sublethal exposure to methylmercury chloride

Methylmercury accumulation, histopathology effects, and cholinesterase activity alterations in medaka (Oryzias latipes) following sublethal exposure to methylmercury chloride

Vitamin E as antioxidant in female african catfish (Clarias gariepinus) exposed to chronic toxicity of atrazine

NTPDase and acetylcholinesterase activities in silver catfish, Rhamdia quelen (Quoy & Gaimard, 1824) (Heptapteridae) exposed to interaction of oxygen and ammonia levels

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