Acrylamide-induced apoptosis in rat primary astrocytes and human astrocytoma cell lines

Lee, Jiann-Gwu; Wang, Yan-Shiu; Chou, Chin-Cheng

doi:10.1016/j.tiv.2014.01.005

Cited by 44 publications

(20 citation statements)

References 32 publications

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“…The administration of Vitamin C in the present study reduced significantly, in a concentration-dependent manner, the formation of reactive oxygen species, indicating that Vitamin C may assume a protective role against glycidamide-induced oxidative stress. In addition, the release of these reactive oxygen species has an oxidizing effect on membrane lipids, disrupting membrane integrity through the formation of lipid peroxidation products (Lee et al 2014). In the present study, glycidamide concentrations of 10 μM and above significantly increased levels of MDAwhich is a final product of lipid peroxidationwhen compared to the control, while groups administered with Vitamin C showed significantly lower MDA levels than the glycidamide-treated groups.…”

Section: Discussionsupporting

confidence: 51%

“…Acrylamide and glycidamide were reported to generally trigger apoptotic signals and cause cell death through an increase in oxidative stress (Orta Yilmaz et al 2017). This effect can be attributed to the increase in lipid peroxidation and mitochondrial membrane depolarization associated with oxidative stress (Lee et al 2014). Acrylamide and glycidamide are known to trigger apoptosis in numerous cell lines and various laboratory animal tissues (Yousef & El-Demerdash 2006, Lee et al 2014, Li et al 2017, Kacar et al 2018, Sun et al 2018.…”

Section: Discussionmentioning

confidence: 99%

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The Effects of Vitamin C on Glycidamide-Induced Cellular Damage and Apoptosis in Mouse Leydig Cells

Yılmaz

2019

Trakya University Journal of Natural Sciences

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The aim of this study was to elucidate the role of vitamin C on glycidamide-induced cytotoxicity, oxidative damage and cell death in Leydig (TM3) cells. Leydig cells were exposed to glycidamide (1, 10, 100 and 1000 μM) and/or vitamin C (50 μM) for 24 h. After completion of the exposure time, cell viability, amount of lactate dehydrogenase enzyme, apoptosisnecrosis rates, levels of oxidative stress parameters such as hydroxyl radical, hydrogen peroxide and lipid peroxidation were determined in Leydig cells. The results showed that glycidamide administration decreased Leydig cell viability and increased cytotoxicity significantly at high concentration (1000 μM). In addition, glycidamide generated oxidative damage by significantly increasing the production of reactive oxygen species and lipid peroxidation. Exposure to glycidamide increased the formation of early apoptosis, apoptosis and necrosis in Leydig cells. Consequently, glycidamide has been shown to cause apoptosis due to lipid peroxidation and formation of reactive oxygen species in Leydig cells, and vitamin C has a therapeutic role against toxicity caused by glycidamide.

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Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 99%

The Effects of Vitamin C on Glycidamide-Induced Cellular Damage and Apoptosis in Mouse Leydig Cells

Yılmaz

2019

Trakya University Journal of Natural Sciences

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“…A study by Lee et al (2014b) analysed the effects of AA on rat primary astrocytes and three human astrocytoma-derived cell lines. Treatment with 1 and 2 mM AA for 24-72 hours resulted in decreased cell viability.…”

Section: Mode Of Action Of Neurotoxicitymentioning

confidence: 99%

Scientific Opinion on acrylamide in food

Publication¹

2015

EFS2

332

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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“…ROS causes cell death through apoptotic pathways. Lee et al [2014] and He et al [2017] reported that ACR-induced apoptosis in rat primary astrocytes and human astrocytoma cell lines occurs via up-regulation of Bax/Bcl2 ratio, excess liberation of cytochrome c and the cleavage of capases 3 and 9. Antioxidant agents including rutin [Motamedshariaty et al, 2014], crocin [Mehri et al, 2015], rosemary [Al-Gholam et al, 2016] and epigallocatechin-3-gallate [He et al, 2017] can mitigate ACR neurotoxicity by increasing antioxidant activity.…”

Section: Introductionmentioning

confidence: 99%

Metformin Protects against Experimental Acrylamide Neuropathy in Rats

Oda

2017

Drug Development Research

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Preclinical Research To investigate the potential neuroprotective effects of metformin against experimental acrylamide neuropathy in rats, 24 rats were distributed into four equal groups (6 each). Group 1 was kept as a control. Group 2 (MET) was orally given metformin (200 mg/kg BW/day). Group 3 (ACR) was injected IP with acrylamide (50 mg/kg BW/day). Animals in group 4 (ACR + MET) were administered both MET and ACR at the same dose and route used in groups 2 and 3. Treatments were administered three times a week for three weeks. ACR induced an increase in lipid peroxidation in brain and spinal cord. This was associated with down regulation of bcl2 and up regulation of caspase3 in cerebrum, cerebellum, spinal cord, and sciatic nerve in the ACR-treated group. ACR-treated rats revealed neuronal degeneration and glial cell reaction in brain and spinal cord with axonal degeneration and myelin sheath irregularities in sciatic nerve. MET restored lipid peroxidation in brain and spinal cord, decreased caspase3 activity and up regulated bcl2 expression in cerebrum and sciatic nerve. Histopathological findings in ACR + MET group were lesser severe than those established in ACR-group indicating that MET ameliorates the neuropathic effects of ACR in rats. Drug Dev Res 78 : 349-359, 2017. © 2017 Wiley Periodicals, Inc.

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Acrylamide-induced apoptosis in rat primary astrocytes and human astrocytoma cell lines

Cited by 44 publications

References 32 publications

The Effects of Vitamin C on Glycidamide-Induced Cellular Damage and Apoptosis in Mouse Leydig Cells

The Effects of Vitamin C on Glycidamide-Induced Cellular Damage and Apoptosis in Mouse Leydig Cells

Scientific Opinion on acrylamide in food

Metformin Protects against Experimental Acrylamide Neuropathy in Rats

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