Neurotoxicity of acrylamide in developing rat brain: Changes in the levels of brain biogenic amines and activities of monoamine oxidase and acetylcholine esterase.

Husain, Raushan; Dixit, Rakesh; Das, Mukul; Seth, Prahlad K.

doi:10.2486/indhealth.25.19

Cited by 26 publications

(14 citation statements)

References 17 publications

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“…Acrylamide at a high dose is known to increase the activity of monoamine oxidase and decrease that of acetylcholinesterase in the developing rats and increase the striatal dopamine receptors in adult rats (Agrawal et al, 1981a(Agrawal et al, , 1981bHusain et al, 1987). Opposite effects as reflected by a decrease in the activity of monoamine oxidase and striatal dopamine receptors in our study may probably be due to nutritional influ-LPD LPD+ACR…”

Section: Discussioncontrasting

confidence: 57%

Protein malnourishment: A predisposing factor in acrylamide toxicity in pregnant rats

Khanna

Husain

Seth

1992

Journal of Toxicology and Environmental Health

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Exposure to acrylamide (3-10 mg/kg body weight) was found to be lethal for protein-deficient pregnant rats as evidenced by their increased mortality. It had no such effect on the normal protein diet fed pregnant and nonpregnant rats and the protein-malnourished nonpregnant rats. Protein deficiency during pregnancy caused a significant decrease in the activity of brain monoamine oxidase and acetylcholinesterase and striatal [3H]spiperone binding, known to label dopamine receptors; had no significant effect on the binding of 3H-QNB (quinuclidinyl benzilate) to cerebellar and [3H]diazepam to frontocortical membranes, known to label muscarinic and benzodiazepine receptors, respectively; and had no significant effect on brain glutathione (GSH) levels in comparison with pregnant rats fed normal protein diet. Exposure to acrylamide (2 mg/kg body weight) in protein-malnourished pregnant rats caused a marked decrease in the activity of monoamine oxidase and acetylcholinesterase and also in the binding of [3H]spiperone, [3H]QNB, and [3H]diazepam to striatal, cerebellar, and frontocortical membranes, respectively. Kinetic studies revealed that decreased binding of these ligands in the specific brain regions were due to decreased receptor sites (Bmax). A reduction in the brain glutathione content was also observed in these animals in comparison with those fed a low-protein diet during pregnancy. Pregnant rats fed a normal-protein diet on acrylamide exposure, however, showed no such biochemical changes in comparison with the pregnant rats fed normal protein diet. Also, no effect on any of the parameters studied was observed in the adult nonpregnant rats fed a low-protein diet (for 18 d) and those exposed to the monomer (d 6-17) fed either a normal- or low-protein diet in comparison with respective controls. The results indicate that pregnancy under conditions of malnutrition modifies the susceptibility of pregnant rats toward acrylamide.

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Section: Discussioncontrasting

confidence: 57%

Protein malnourishment: A predisposing factor in acrylamide toxicity in pregnant rats

Khanna

Husain

Seth

1992

Journal of Toxicology and Environmental Health

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“…Exposure to the monomer has also been found to alter the neurotransmitter levels, their receptors and associated enzymes involved in the metabolism of neurotransmitters and cause neurotoxicity (Agarwal et al, 1981;Ali et al, 1983;Husain et al, 1987). Enhanced striatal dopamine receptors and decreased GST activity were reported to be the primary changes in acrylamide neurotoxicity in rats since no toxic effect on these parameters was observed following treatment with N,N'-bis acrylamide, a non-neurotoxic analogue .…”

Section: Discussionmentioning

confidence: 99%

Protective effect of Acorus calamus against acrylamide induced neurotoxicity

Shukla

Khanna

Ali

et al. 2002

Phytotherapy Research

100

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Exposure of rats to acrylamide (ACR) caused hind limb paralysis in 58% of the animals on day 10 and decreased behavioural parameters, namely distance travelled, ambulatory time, stereotypic time and basal stereotypic movements compared with the control group. These rats also had a decrease in the reduced glutathione (GSH) content and glutathione-S-transferase (GST) activity in the corpus striatum and an increase in striatal dopamine receptors, as evident by an increase in the binding of 3H-spiperone to striatal membranes. Treatment with the ethanol:water (1:1) extract of the rhizomes of Acorus calamus (AC-002) increased the GSH content and GST activity in the corpus striatum while insignificant changes were observed in other parameters. Rats treated with ACR and AC-002 in combination had a lower incidence of paralysis (18%) compared with those treated with ACR alone on day 10 of the experiment. The rats also showed a partial recovery in other behavioural parameters. The levels of GSH content and GST activity increased in the corpus striatum, while the dopamine receptors decreased compared with the ACR treated rats. The results suggest that the neurobehavioural changes produced by ACR may be prevented following treatment with Acorus calamus rhizomes.

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“…It has been reviewed by SCF (2002), JECFA (FAO/WHO, 2011) and ATSDR (2012). Husain et al (1987) reported significantly decreased levels of selected catecholamines (noradrenaline, dopamine, 5-hydroxytryptamine) in brains of pups of Wistar albino rat dams administered AA at 25 mg/kg per day during lactation. Levels of brain catecholamines were affected in a similar way in rat pups at 12-21 days of age at the beginning of a 5-day period in which they were administered AA by gavage at 25 mg/kg per day, whereas these effects were not seen in rat pups that were 60 days of age at the initiation of dosing.…”

Section: Developmental Toxicitymentioning

confidence: 97%

Scientific Opinion on acrylamide in food

Publication¹

2015

EFS2

329

170

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EFSA was asked to deliver a scientific opinion on acrylamide (AA) in food. AA has widespread uses as an industrial chemical. It is also formed when certain foods are prepared at temperatures above 120 °C and low moisture, especially in foods containing asparagine and reducing sugars. The CONTAM Panel evaluated 43 419 analytical results from food commodities. AA was found at the highest levels in solid coffee substitutes and coffee, and in potato fried products. Mean and 95th percentile dietary AA exposures across surveys and age groups were estimated at 0.4 to 1.9 µg/kg body weight (b.w.) per day and 0.6 to 3.4 µg/kg b.w. per day, respectively. The main contributor to total dietary exposure was generally the category 'Potato fried products (except potato crisps and snacks)'. Preferences in home-cooking can have a substantial impact on human dietary AA exposure. Upon oral intake, AA is absorbed from the gastrointestinal tract and distributed to all organs. AA is extensively metabolised, mostly by conjugation with glutathione but also by epoxidation to glycidamide (GA). Formation of GA is considered to represent the route underlying the genotoxicity and carcinogenicity of AA. Neurotoxicity, adverse effects on male reproduction, developmental toxicity and carcinogenicity were identified as possible critical endpoints for AA toxicity from experimental animal studies. The data from human studies were inadequate for dose-response assessment. The CONTAM Panel selected BMDL 10 values of 0.43 mg/kg b.w. per day for peripheral neuropathy in rats and of 0.17 mg/kg b.w. per day for neoplastic effects in mice. The Panel concluded that the current levels of dietary exposure to AA are not of concern with respect to non-neoplastic effects. However, although the epidemiological associations have not demonstrated AA to be a human carcinogen, the margins of exposure (MOEs) indicate a concern for neoplastic effects based on animal evidence. © European Food SUMMARYFollowing a request from the European Commission, the Panel on Contaminants in the Food Chain (CONTAM Panel) was asked to deliver a scientific opinion on acrylamide (AA) in food. The Panel developed the draft scientific opinion which underwent a public consultation from 1 July 2014 to 15 September 2014. The comments received and how they were taken into account when finalising the scientific opinion were published in an EFSA Technical Report (EFSA, 2015).AA is a low molecular weight, highly water soluble, organic compound. It is used inter alia as an industrial chemical and in the production of polyacrylamides. Heightened concerns about exposure to AA arose in 2002 when it was discovered that it forms when certain foods are prepared at temperatures usually above 120 °C and low moisture. It forms, at least in part, due to a Maillard reaction between certain amino acids, such as asparagine, and reducing sugars. However, several other pathways and precursors have also been proposed to contribute to AA formation. AA forms in numerous baked or fried carbohydrate-rich f...

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Neurotoxicity of acrylamide in developing rat brain: Changes in the levels of brain biogenic amines and activities of monoamine oxidase and acetylcholine esterase.

Cited by 26 publications

References 17 publications

Protein malnourishment: A predisposing factor in acrylamide toxicity in pregnant rats

Protein malnourishment: A predisposing factor in acrylamide toxicity in pregnant rats

Protective effect of Acorus calamus against acrylamide induced neurotoxicity

Scientific Opinion on acrylamide in food

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