Effects per se of Organic Solvents in the Cerebral Acetylcholinesterase of Rats

Obregón, Adriana; Schetinger, Maria Rosa Chitolina; Junior, Marcos Corrêa; Morsch, Vera Maria; Silva, José E.P. da; Martins, Marcos A. P.; Bonacorso, Hélio G.; Zanatta, Nilo

doi:10.1007/s11064-005-2612-5

Cited by 43 publications

(12 citation statements)

References 26 publications

(26 reference statements)

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“…Others morphologic and immunoistochemical studies have proven that 7 days after the injection of EB, complete demyelination is attained, at 15 days the first signs of remyelination can be observed, and that remyelination is completed after around 25-30 days of the injection of EB [25,26]. In this context, the white matter tracts arising from the nucleus basalis and projecting to distant forebrain regions could plausibly be interrupted by demyelinating plaques, creating a presynaptic cholinergic deficit responsive to treatment with cholinesterase inhibitors [40], which would make AChE an important therapeutic target [6,8,[15][16][17]41] for the treatment of neurodegenerative diseases [18][19][20][21][22].…”

Section: Discussionmentioning

confidence: 99%

“…3.1.1.7) is found in the cholinergic terminal where it performs the hydrolysis of the neurotransmitter acetylcholine (ACh) [4][5][6][7][8]. Besides its catalytic property [9], AChE has potent effects on cellular adhesion [10], neurite extension [11], as well as participating in the structural regulation of postsynaptic differentiation [12], and it is present in lymphocytes, where it probably plays a role in the regulation of immune functions [13].…”

Section: Introductionmentioning

confidence: 99%

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Acetylcholinesterase Activity in Rats Experimentally Demyelinated with Ethidium Bromide and Treated with Interferon Beta

et al. 2006

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The ethidium bromide (EB) demyelinating model was associated with interferon beta (IFN-beta) to evaluate acetylcholinesterase (AChE) activity in the striatum (ST), hippocampus (HP), cerebral cortex (CC), cerebellum (CB), hypothalamus (HY), pons (PN) and synaptosomes from the CC. Rats were divided into four groups: I control (saline), II (IFN-beta), III (EB) and IV (EB and IFN-beta). After 7, 15 and 30 days rats (n = 6) were sacrificed, and the brain structures were removed for enzymatic assay. AChE activity was found to vary in all the brain structures in accordance with the day studied (7-15-30 days) (P < 0.05). In the group III, there was an inhibition of the AChE activity in the ST, CB, HY, HP and also in synaptosomes of the CC (P < 0.05). It was observed that IFN-beta per se was capable to significantly inhibit (P < 0.05) AChE activity in the ST, HP, HY and synaptosomes of the CC. Our results suggest that one of the mechanisms of action of IFN-beta is through the inhibition of AChE activity, and EB could be considered an inhibitor of AChE activity by interfering with cholinergic neurotransmission in the different brain regions.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Acetylcholinesterase Activity in Rats Experimentally Demyelinated with Ethidium Bromide and Treated with Interferon Beta

et al. 2006

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“…Obregon et al (59) found that DMSO mixed with different brain region homogenates of male Wistar rats inhibited ChE activity at all tested concentrations. However, in our study DMSO had no effect on the liver and kidney tChE after i.p.…”

Section: Sex-and Duration-specific Effects Of Imi In Rat Liver and Kimentioning

confidence: 95%

Sex-, tissue-, and exposure duration-dependent effects of imidacloprid modulated by piperonyl butoxide and menadione in rats. Part I: oxidative and neurotoxic potentials

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et al. 2014

Archives of Industrial Hygiene and Toxicology

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Earlier research has evidenced the oxidative and neurotoxic potential of imidacloprid, a neonicotinoid insecticide, in different animal species. The primary aim of this study was to determine how metabolic modulators piperonyl butoxide and menadione affect imidacloprid's adverse action in the liver and kidney of Sprague-Dawley rats of both sexes. The animals were exposed to imidacloprid alone (170 mg kg -1 ) or in combination with piperonyl butoxide (100 mg kg -1 ) or menadione (25 mg kg -1 ) for 12 and 24 h. Their liver and kidney homogenates were analysed spectrophotometrically for glutathione peroxidase, glutathione S-transferase, catalase, total cholinesterase specific activities, total glutathione, total protein content, and lipid peroxidation levels. Imidacloprid displayed its prooxidative and neurotoxic effects predominantly in the kidney of male rats after 24 h of exposure. Our findings suggest that the observed differences in prooxidative and neurotoxic potential of imidacloprid could be related to differences in its metabolism between the sexes. Co-exposure (90-min pre-treatment) with piperonyl butoxide or menadione revealed tissue-specific effect of imidacloprid on total cholinesterase activity. Increased cholinesterase activity in the kidney could be an adaptive response to imidacloprid-induced oxidative stress. In the male rat liver, co-exposure with piperonyl butoxide or menadione exacerbated imidacloprid toxicity. In female rats, imidacloprid+menadione co-exposure caused prooxidative effects, while no such effects were observed with imidacloprid alone or menadione alone. In conclusion, sex-, tissue-, and duration-specific effects of imidacloprid are remarkable points in its toxicity.

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“…19 Each animal was subjected to its respective drug through intra-peritoneal injection. Each animal was placed individually in the center of the maze and observed for 5 min.…”

Section: Experimental Protocolmentioning

confidence: 99%