Effective Suppression of Acrylamide Neurotoxicity by Lithium in Mouse

Song, Lingzhen; Wang, Jiutao; Zhang, Wei; Ren, Yan; Xiu, Hu; Chen, Shulin; Zhao, Shanting

doi:10.1007/s11064-014-1418-8

Cited by 6 publications

(5 citation statements)

References 38 publications

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“…Previous studies have reported that ACR inhibits neurogenesis through the activation of the GSK3β signaling pathway. 40 By comparison, taurine has been shown to exert an antidepressant-like effect, influencing depression-related signaling cascades in the hippocampus by altering the levels of phosphorylated GSK3β. 41 In addition, taurine has an impact on various signaling pathways and the gene expression of many proteins, including those involved in the Akt/PKB and PI3K/Akt signaling pathways, especially GSK3β phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have reported that ACR inhibits neurogenesis through the activation of the GSK3β signaling pathway. 40 By In (a), a P < 0.05, compared with the control group; b P < 0.05, compared with the ACR group; c P < 0.05, compared with the ACR + TAU group. In (b), a P < 0.05, compared with the control group; b P < 0.05, compared with the TAU group; c P < 0.05, compared with the TAU + MK-2206 group; d P < 0.05, compared with the ACR group; e P < 0.05, compared with the ACR + MK-2206 group; f P < 0.05, compared with the ACR + TAU group.…”

Section: Discussionmentioning

confidence: 99%

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Taurine attenuates acrylamide-induced axonal and myelinated damage through the Akt/GSK3β-dependent pathway

Sun

Wang

et al. 2018

Int J Immunopathol Pharmacol

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Acrylamide (ACR), formed during the Maillard reaction induced by high temperature in food processing, is one of the main causes of neurodegenerative diseases. Taurine, a free intracellular β-amino acid, is characterized by many functions, including antioxidation, anti-inflammatory, and neuroprotective properties. This promotes its application in the treatment of neurodegenerative diseases. In this study, the neuroprotective effects of taurine against ACR-induced neurotoxicity and the potential underlying mechanisms were explored. Rats were intoxicated with ACR and injected with taurine in different groups for totally 2 weeks between January and July 2017. Electron microscopic analysis was used to observe the changes in tissues of the rats. Meanwhile, the levels of proteins including p-Akt, p-GSK3β, SIM312, and MBP were detected by Western blot. Furthermore, the GSK3β phosphorylation in taurine-treated dorsal root ganglion (DRG) with ACR was examined in the presence of the Akt inhibitor, MK-2206. The analysis of behavioral performances and electron micrographs indicated that taurine treatment significantly attenuated the toxic manifestations induced by ACR and stimulated the growth of axons and the medullary sheath, which was associated with the activation of the Akt/GSK3β signaling pathway. Mechanistically, it was found that taurine activated GSK3β, leading to significant recovery of the damage in ACR-induced sciatic nerves. Furthermore, MK-2206, an inhibitor of Akt, was applied in DRG cells, suggesting that taurine-induced GSK3β phosphorylation was Akt dependent. Our findings demonstrated that taurine attenuated ACR-induced neuropathy in vivo, in an Akt/GSK3β-dependent manner. This confirmed the treatment with taurine to be a novel strategy against ACR-induced neurotoxicity.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Taurine attenuates acrylamide-induced axonal and myelinated damage through the Akt/GSK3β-dependent pathway

Sun

Wang

et al. 2018

Int J Immunopathol Pharmacol

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“…The authors concluded that 'green tea extract is a potent antioxidant antidote for the AA toxic effects upon testicular function'. Song et al (2014) Effective suppression of AA neurotoxicity by lithium in mouse.…”

Section: Yassa Et Al (2014)mentioning

confidence: 99%

Scientific Opinion on acrylamide in food

Publication¹

2015

EFS2

342

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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“…Similar findings have been reported in Drosophila melanogaster (fruit fly) studies (Prasad and Muralidhara, , ). Glycogen synthase kinase 3 beta (GSK‐3β) is activated by ACR treatment, causing a lack of neurogenesis in the hippocampus (Song et al ., ), and curcumin was shown to inhibit this enzyme (Aggarwal and Sung, ; Bustanji et al ., ). Although no study has looked into both ACR toxicity and GSK‐3β inhibition by curcumin, it seems reasonable to assume that this mechanism of action contributes to the protective effect of curcumin, especially when considering that lithium, another GSK‐3β inhibitor, also protects against ACR (Song et al ., ).…”

Section: Introductionmentioning

confidence: 99%

The Potential for Plant Derivatives against Acrylamide Neurotoxicity

Adewale

Brimson

Odunola

et al. 2015

Phytotherapy Research

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Certain industrial chemicals and food contaminants have been demonstrated to possess neurotoxic activity and have been suspected to cause brain-related disorders in humans. Acrylamide (ACR), a confirmed neurotoxicant, can be found in trace amount in commonly consumed human aliments as a result of food processing or cooking. This discovery aroused a great concern in the public, and increasing efforts are continuously geared towards the resolution of this serious threat. The broad chemical diversity of plants may offer the resources for novel antidotes against neurotoxicants. With the goal of attenuating neurotoxicity of ACR, several plants extracts or derivatives have been employed. This review presents the plants and their derivatives that have been shown most active against ACR-induced neurotoxicity, with a focus on their origin, pharmacological activity, and antidote effects.

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Effective Suppression of Acrylamide Neurotoxicity by Lithium in Mouse

Cited by 6 publications

References 38 publications

Taurine attenuates acrylamide-induced axonal and myelinated damage through the Akt/GSK3β-dependent pathway

Taurine attenuates acrylamide-induced axonal and myelinated damage through the Akt/GSK3β-dependent pathway

Scientific Opinion on acrylamide in food

The Potential for Plant Derivatives against Acrylamide Neurotoxicity

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