Nerve Terminals as the Primary Site of Acrylamide Action: A Hypothesis

LoPachin, Richard M.; Ross, Joseph F.; Lehning, Ellen J.

doi:10.1016/s0161-813x(01)00074-2

Cited by 109 publications

(85 citation statements)

References 114 publications

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“…In a well-described rodent model, ACR exposure at 15-50 mg/kg/d produced several neurological deficits, including hind-limb foot splay, decreased fore-and hind-limb grip strength, ataxia, and skeletal muscle weakness (LoPachin et al, 2002). Moreover, ACR exposure resulted in the central-peripheral neuropathy in humans (LoPachin, 2004) and in laboratory animals, including rats and monkeys (Seale et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

The effect of lipoic acid on acrylamide-induced neuropathy in rats with reference to biochemical, hematological, and behavioral alterations

Lebda¹,

Gad

Rashed

2015

Pharmaceutical Biology

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Context: Acrylamide (ACR) is a well-known neurotoxicant and carcinogenic agent which poses a greater risk for human and animal health. Objective: The present study evaluates the beneficial effects of a-lipoic acid (LA) on ACR-induced neuropathy. Materials and methods: A total of 40 male rats were divided into four groups: a placebo group; LA-treated group, administered orally 1% (w/w) LA mixed with diet; ACR-treated group, given 0.05% (w/v) ACR dissolved in drinking water; and LA + ACR-treated group, given LA 1% 7 d before and along with ACR 0.05% for 21 d. After 28 d, blood samples were collected, the rats were decapitated, and the tissues were excised for the measurement of brain biomarkers, antioxidant status, and hematological analysis. Also, the gait score of rats was evaluated. Results: ACR-exposed rats exhibited abnormal gait deficits with significant (p50.05) decline in acetylcholine esterase (AChE) and creatine kinase in serum and brain tissues, respectively. However, the lactate dehydrogenase activity was increased in serum by 123%, although it decreased in brain tissues by À74%. ACR significantly (p50.05) increased the malondialdehyde level by 273% with subsequent depletion of glutathione S-transferase (GST), glutathione peroxidase (GPx), and glutathione reductase (GR) activities and reduced the glutathione (GSH) level in brain tissue. Interestingly, LA significantly (p50.05) improved brain enzymatic biomarkers, attenuated lipid peroxidation (LPO), and increased antioxidant activities compared with the ACR-treated group. Discussion and conclusion: These results suggested that LA may have a role in the management of ACR-induced oxidative stress in brain tissues through its antioxidant activity, attenuation of LPO, and improvement of brain biomarkers.

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Section: Discussionmentioning

confidence: 99%

The effect of lipoic acid on acrylamide-induced neuropathy in rats with reference to biochemical, hematological, and behavioral alterations

Lebda¹,

Gad

Rashed

2015

Pharmaceutical Biology

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“…The low turnover of axonal proteins, when compared to proteins of other cell types, is likely to contribute to this observation (LoPachin et al, 2002. Allam et al (2011) examined the effects of AA on the development of external features and cerebellum in albino rats (see Section 7.3.5.2).…”

Section: Mode Of Action Of Neurotoxicitymentioning

confidence: 99%

Scientific Opinion on acrylamide in food

Publication¹

2015

EFS2

334

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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“…Group 2 (n = 10): Acrylamide Group (25 mg/kg/day): Acrylamide was dissolved in normal saline, and 1 mL solution was daily administered to each rat with gavage (4,(38)(39)(40).…”

Section: Experimental Designmentioning

confidence: 99%

The protective effect of N-acetylcysteine against acrylamide toxicity in liver and small and large intestine tissues

Altınöz¹,

Türköz²,

Vardı³

2015

BLL

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Abstract:The aim of this study was to investigate the protective effects of N-acetylcysteine against acrylamide toxicity in liver and small and large intestine tissues in rats. The rats were divided into four groups. Acrylamide administration increased MDA levels in all tissues significantly (p < 0.05). But acrylamide+NAC administration decreased MDA levels signifi cantly as compared to the acrylamide group, and lowered it to a level close to the control group values (p < 0.05). GSH levels in liver and small intestine tissues reduced signifi cantly in the acrylamide group (p < 0.05). But acrylamide+NAC administration increased GSH levels signifi cantly in all tissues. Whereas GST activity decreased signifi cantly in the acrylamide group in liver and small intestine tissues as compared to the other groups (p < 0.05), the GST activity increased signifi cantly in the acrylamide+NAC group in all tissues as compared to the acrylamide group (p < 0.05). Liver histopathology showed that the liver epithelial cells were damaged signifi cantly in the acrylamide group. Small intestine histopathology showed that the intestinal villous epithelial cells were damaged signifi cantly in the acrylamide group. Our results indicate that a high level of acrylamide causes oxidative damage in liver and small and large intestine tissues, while N-acetylcysteine administration in a pharmacological dose shows to have an antioxidant effect in preventing this damage (Tab. 2, Fig. 2, Ref. 66). Text in PDF www.elis.sk.

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Nerve Terminals as the Primary Site of Acrylamide Action: A Hypothesis

Cited by 109 publications

References 114 publications

The effect of lipoic acid on acrylamide-induced neuropathy in rats with reference to biochemical, hematological, and behavioral alterations

The effect of lipoic acid on acrylamide-induced neuropathy in rats with reference to biochemical, hematological, and behavioral alterations

Scientific Opinion on acrylamide in food

The protective effect of N-acetylcysteine against acrylamide toxicity in liver and small and large intestine tissues

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