Enzyme and behavioral changes in young chicks as a result of carbaryl treatment

Farage-Elawar, Miranda

doi:10.1080/15287398909531237

Cited by 37 publications

(15 citation statements)

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“…Evidence in the literature suggests that there is a functional association between mitochondrial dysfunction and cognitive impairment (Roubertoux et al 2003). Carbamates, like other anticholinesterases, have been shown to interfere with the process of learning and memory (Farage-Elawar 1989). The results suggest that impaired mitochondrial functions might influence neurobehavioral deficits, observed following carbofuran exposure.…”

Section: Results and Disscusionmentioning

confidence: 93%

Mitochondrial Oxidative Stress and Dysfunction in Rat Brain Induced by Carbofuran Exposure

et al. 2008

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Repeated low-dose exposure to carbofuran exerts its neurotoxic effects by non-cholinergic mechanisms. Emerging evidence indicates that oxidative stress plays an important role in carbofuran neurotoxicity after sub-chronic exposure. The purpose of the present study is to evaluate the role of mitochondrial oxidative stress and dysfunction as a primary event responsible for neurotoxic effects observed after sub-chronic carbofuran exposure. Carbofuran was administered to rats at a dose of 1 mg/kg orally for a period of 28 days. There was a significant inhibition in the activity of acetylcholinesterase (66.6%) in brain samples after 28 days of carbofuran exposure. Mitochondrial respiratory chain functions were assessed in terms of MTT (3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide) reduction and activity of succinate dehydrogenase in isolated mitochondria. It was observed that carbofuran exposure significantly inhibited MTT reduction (31%) and succinate dehydrogenase activity (57%). This was accompanied by decrease in low-molecular weight thiols (66.6%) and total thiols (37.4%) and an increase in lipid peroxidation (43.7%) in the mitochondria isolated from carbofuran-exposed rat brain. The changes in mitochondrial oxidative stress and functions were associated with impaired cognitive and motor functions in the animals exposed to carbofuran as compared to the control animals. Based on these results, it is clear that carbofuran exerts its neurotoxicity by impairing mitochondrial functions leading to oxidative stress and neurobehavioral deficits.

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Section: Results and Disscusionmentioning

confidence: 93%

Mitochondrial Oxidative Stress and Dysfunction in Rat Brain Induced by Carbofuran Exposure

et al. 2008

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“…The deficits in learning and memory activity observed after one week of exposure of MCP or DDVP persisted even after 28 days post exposure. Anticholinesterases and oxidative stress have been shown to interfere with the process of learning and memory (Farage-Elawar 1989;Liu et al 2003). It has been suggested that there is a functional association between mitochondrial dysfunction and cognitive impairment (Roubertoux et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Impaired Mitochondrial Functions in Organophosphate Induced Delayed Neuropathy in Rats

2009

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Acute exposure to organophosphates induces a delayed neurodegenerative condition known as organophosphate-induced delayed neuropathy (OPIDN). The mechanism of OPIDN has not been fully understood as it does not involve cholinergic crisis. The present study has been designed to evaluate the role of mitochondrial dysfunctions in the development of OPIDN. OPIDN was induced in rats by administering acute dose of monocrotophos (MCP, 20 mg/kg body weight, orally) or dichlorvos (DDVP, 200 mg/kg body weight, subcutaneously), 15-20 min after treatment with antidotes [atropine (20 mg/kg body weight) and 2-PAM (100 mg/kg body weight) intraperitoneally]. MDA levels were observed to be higher and thiol content was lower in mitochondria from brain regions of OP exposed animals. This was accompanied by decreased activities of the mitochondrial enzymes; NADH dehydrogenase, succinate dehydrogenase, and cytochrome oxidase. In addition, mitochondrial functions assessed by MTT reduction also confirmed mitochondrial dysfunctions following development of OPIDN. The spatial long-term memory evaluated using elevated plus-maze test was observed to be deficit in OPIDN. The results suggest impaired mitochondrial functions as a mechanism involved in the development of organophosphate induced delayed neuropathy.

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“…This decrease in the spontaneous locomotor activity could be due to the inhibition of the neuropathy target esterase as demonstrated in the case of anti-cholinesterase exposure [49]. Farage-Elawar [50] has also reported significantly decreased motor activity and exploration in chicks treated with carbaryl. The decrease in motor conduction velocity following carbofuran exposure could also be responsible for the decrease observed in the locomotor activity [51].…”

Section: Resultsmentioning

confidence: 94%

Perturbed Synaptosomal Calcium Homeostasis and Behavioral Deficits Following Carbofuran Exposure: Neuroprotection by N-Acetylcysteine

Kamboj

Sandhir

2007

Neurochem Res

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The protective effects of N-acetylcysteine (NAC) on carbofuran-induced alterations in calcium homeostasis and neurobehavioral functions were investigated in rats. Rats were exposed to carbofuran at a dose of 1 mg/kg body weight, orally for a period of 28 days. A significant decrease in Ca2+ATPase activity was observed following carbofuran exposure with a concomitant increase in K+ -induced (45)Ca2+ uptake through voltage operated calcium channels. This was accompanied with a marked accumulation of intracellular free calcium in synaptosomes. The increase in intracellular calcium levels were associated with an increased lipid peroxidation and decreased glutathione content in carbofuran exposed animals. NAC administration (200 mg/kg body weight, orally) to the carbofuran exposed animals had a beneficial effect on carbofuran-induced alterations in calcium homeostasis and resulted in repletion in glutathione levels and resulted in lowering the extent of lipid peroxidation. Marked impairment in the motor functions were seen following carbofuran exposure, which were evident by the significant decrease in the locomotor activity and reduction in the retention time of the rats on rotating rods. Cognitive deficits were also seen as indicated by the significant decrease in active and passive avoidance response. NAC treatment, on the other hand, protected the animals against carbofuran-induced neurobehavioral deficits. The results support the hypothesis that carbofuran exerts its toxic effects by disrupting calcium homeostasis, which may have serious consequences on neuronal functioning, and clearly show the potential beneficial effects of N-acetylcysteine on carbofuran induced alterations in synaptosomal calcium homeostasis.

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Enzyme and behavioral changes in young chicks as a result of carbaryl treatment

Cited by 37 publications

References 0 publications

Mitochondrial Oxidative Stress and Dysfunction in Rat Brain Induced by Carbofuran Exposure

Mitochondrial Oxidative Stress and Dysfunction in Rat Brain Induced by Carbofuran Exposure

Impaired Mitochondrial Functions in Organophosphate Induced Delayed Neuropathy in Rats

Perturbed Synaptosomal Calcium Homeostasis and Behavioral Deficits Following Carbofuran Exposure: Neuroprotection by N-Acetylcysteine

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