Acrylamide inhibits cellular differentiation of human neuroblastoma and glioblastoma cells

Chen, Jong-Hang; Chou, Chin-Cheng

doi:10.1016/j.fct.2015.04.030

Cited by 31 publications

(18 citation statements)

References 40 publications

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“…What's more, the crosstalk between MAPK and Jak-STAT signal cascades regulates cellular functional events by stimulation of cytokines and growth factors (Eulenfeld 2012). Chen and Chou (2015) reported that AA could cause a down-regulation of the Jak-STAT signaling pathway in human neuroblastoma and glioblastoma cells and the MAPK pathway was important in the regulation of AA-induced cytotoxicity, which was conformed with our current results.…”

Section: A B Csupporting

confidence: 91%

“…The process that AA reacts with DNA occurs slowly (Solomon 1985), while, in contrast, the metabolite GA is considerably more reactive (Beland et al 2013). The gene expression changed by AA or GA on nervous system, reproductive system or relative cell models were widely studied in recent publications (Camacho 2012;Chen and Chou 2015). Camacho et al revealed that exposure to AA could cause the changes in testicular histopathology, gene expression, and serum hormones in male F344 rats (Camacho 2012).…”

Section: Introductionmentioning

confidence: 99%

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Toxicogenomic evaluation of liver responses induced by acrylamide and glycidamide in male mouse liver

Chen¹,

Liu²,

Wang³

et al. 2018

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In current studies, histopathologic method, Agilent GeneChip hybridization and Western blot were used to investigate the toxicity of acrylamide (AA) and glycidamide (GA) in male mouse livers. The histopathologic results demonstrated that AA and GA could cause oxidative damage to mouse liver. Middle dose of GA and AA (50 mg/kg b.w./day) could significantly up-regulate the expression of cytochrome P450, as well as genes related to oxidative injury, cancer and inflammation, and significantly down-regulate the expression of genes related to anti-apoptosis, antioncogene and fatty acid synthesis. Middle and high dose (75 mg/kg b.w./day) of GA and AA could both down-regulate the expression of hepatic anti-oncogene Bcl2 and up-regulate the expression of cancer-related gene Rad51 and EGFR protein. The expression of anti-oncogene P21 induced by AA and GA was decreased. Our current study demonstrated that the oxidative damage, immune injury and carcinogenicity of mouse liver samples could be induced by AA and GA at histopathological, entire genome and protein levels.

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Section: A B Csupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Toxicogenomic evaluation of liver responses induced by acrylamide and glycidamide in male mouse liver

Chen¹,

Liu²,

Wang³

et al. 2018

gpb

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“…Al-Gholam et al reported that the ACR experimental group has been shown to induce apoptosis and oxidation, degeneration of motor neurons, myelin sheath, and neurofilaments [36]. ACR had shown the inhibitory effects on human neuroblastoma, and glioblastoma cellular differentiation leads to disturbances in the nervous system [37,38].…”

Section: Acr and Biochemical Studiesmentioning

confidence: 99%

Review on Chronic Exposure of Acrylamide Causes a Neurotoxicity Risk

Maddu

Begum

2018

INNOCS Theranos Pharmco Sci

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The exposure and inhalation of acrylamide (ACR) are not safe to the human health leading to the potential neurotoxicity. ACR is widely used in biochemical techniques and highly occurs in processing foods such as potato chips prepared at high temperatures. ACR is formed from reducing sugars and asparagine through the Maillard reaction. It exerts various harmful and toxic effects such as neurotoxicity both in humans and animal studies. The extensive damage of synaptic proteins, the formation of ACR-DNA adducts, degeneration of motor neurons, neurofilament reduction, are the most common neurological symptoms. The main metabolite of ACR metabolism is glycidamide, and it causes harmful effects as same as ACR. The main purpose of this study is to analyze the neurotoxic effects of ACR on various regions of the brain and its different mechanistic pathways that are involved in ACR neurotoxicity. The consumption of ACR-containing foods and its exposure are reduced by the human, leading to the reduction of toxic effects associated with ACR.

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“…For example during the building a railroad tunnel near southwest Sweden workers began to develop signs of impaired nerve function, it was as a result of a special gel called Rhoca-Gel, contained AA, that was used to waterproof leaks in the tunnel wall (26). In another study Chen et al showed that AA disrupted nervous system by inhibiting of human neuroblastoma and gelioblastoma cellular differentiation (27).…”

Section: Neurotoxicity Of Acrylamidementioning

confidence: 99%