Effects of Acrylamide Treatment on Oxidant and Antioxidant Levels in Rats

Yerlikaya, Fatma Hümeyra; Toker, Aysun; Yener, Yeşim

doi:10.9775/kvfd.2012.8518

Cited by 7 publications

(8 citation statements)

References 37 publications

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“…Also, proapoptotic transcription factor FOXO1, down-regulated by miR-27a-3p, contributed to endometrioid endometrial adenocarcinoma (Narasimhan et al, 2012;Yang et al, 2015). These results suggested that miR-27a-3p is related to oxidative stress response, which has been regarded as the main reason of AA toxicity (Alturfan et al, 2012;Yerlikaya, Toker, & Yener, 2013). However, there are few studies on miR-27a-5p which may be involved in several signal pathways including Wnt.…”

Section: Mir-27a-5p Showed High Expression In Sd Rats With Low-dose Long-term Exposure Of Aamentioning

confidence: 96%

Acrylamide alters the miRNA profiles and miR‐27a‐5p plays the key role in multiple tissues of rats

Zhang

Yang

et al. 2020

Food Frontiers

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Acrylamide (AA) is the potential carcinogen, which can induce multiple toxic effects in laboratory animals and humans. So far, increasing attention have been paid to toxical mechanism and intervention measures of AA, however, these details and methods are still obscure. MicroRNAs (miRNAs) have been demonstrated to be involved in toxical functional mechanisms induced by chemicals in vivo or vitro. To explore novel target and mechanism of AA toxicity, a more detailed miRNA expression profiling study is needed. In this study, we established the short‐term high‐dose model of rats with the treatment of 35 mg/kg·b.w./day AA for 17 days, analyzed the miRNAs expression profiling in AA and control groups, and discovered the altered miRNA profiles in 11 tissues with AA treatment. Interestingly enough, the expression of miR‐27a‐5p were significantly up‐regulated in AA group, especially in bladder and hepar. Furthermore, we found miR‐27a‐5p increased in 11 tissues of long‐term low‐dose AA‐treated rats (3.5 mg/kg·b.w./day for 68 days). Therefore, these results revealed that AA changed miRNAs profiles in multiple tissues of SD rats for the first time and suggested that miR‐27a‐5p could be used as the target biomarker for the detection and interference of AA toxicity.

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Section: Mir-27a-5p Showed High Expression In Sd Rats With Low-dose Long-term Exposure Of Aamentioning

confidence: 96%

Acrylamide alters the miRNA profiles and miR‐27a‐5p plays the key role in multiple tissues of rats

Zhang

Yang

et al. 2020

Food Frontiers

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“…The CONTAM Panel noted a number of other studies on AA, that were either confirmative, performed at extremely high dose levels, or of unclear relevance, which are not described in detail (Begum Sheikh and Kedam, 2010;Céspedes-Camacho et al, 2010;Muthukumar et al, 2011;Zhang et al, 2011;Yener and Dikmenli, 2011;Szewczyk et al, 2012;El-Alfy et al, 2013;Tarskikh et al, 2013;Yerlikaya et al, 2013).…”

Section: Modes Of Action Of Carcinogenicitymentioning

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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“…It has been suggested that alteration of the dopamine receptor is responsible for the change in thyroid metabolism [65] . AA also causes oxidative stress in rats [72] and the thyroid has a very high oxidation level [72] , [73] .…”

Section: Introductionmentioning

confidence: 99%

Transcriptomics analysis and hormonal changes of male and female neonatal rats treated chronically with a low dose of acrylamide in their drinking water

Collí-Dulá

Friedman

Hansen³

et al. 2016

Toxicology Reports

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Acrylamide is known to produce follicular cell tumors of the thyroid in rats. RccHan Wistar rats were exposed in utero to a carcinogenic dose of acrylamide (3 mg/Kg bw/day) from gestation day 6 to delivery and then through their drinking water to postnatal day 35. In order to identify potential mechanisms of carcinogenesis in the thyroid glands, we used a transcriptomics approach. Thyroid glands were collected from male pups at 10 PM and female pups at 10 AM or 10 PM in order to establish whether active exposure to acrylamide influenced gene expression patterns or pathways that could be related to carcinogenesis. While all animals exposed to acrylamide showed changes in expected target pathways related to carcinogenesis such as DNA repair, DNA replication, chromosome segregation, among others; animals that were sacrificed while actively drinking acrylamide-laced water during their active period at night showed increased changes in pathways related to oxidative stress, detoxification pathways, metabolism, and activation of checkpoint pathways, among others. In addition, thyroid hormones, triiodothyronine (T3) and thyroxine (T4), were increased in acrylamide-treated rats sampled at night, but not in quiescent animals when compared to controls. The data clearly indicate that time of day for sample collection is critical to identifying molecular pathways that are altered by the exposures. These results suggest that carcinogenesis in the thyroids of acrylamide treated rats may ensue from several different mechanisms such as hormonal changes and oxidative stress and not only from direct genotoxicity, as has been assumed to date.

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Effects of Acrylamide Treatment on Oxidant and Antioxidant Levels in Rats

Cited by 7 publications

References 37 publications

Acrylamide alters the miRNA profiles and miR‐27a‐5p plays the key role in multiple tissues of rats

Acrylamide alters the miRNA profiles and miR‐27a‐5p plays the key role in multiple tissues of rats

Scientific Opinion on acrylamide in food

Transcriptomics analysis and hormonal changes of male and female neonatal rats treated chronically with a low dose of acrylamide in their drinking water

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