Acrylamide induces intrinsic apoptosis and inhibits protective autophagy <i>via</i> the ROS mediated mitochondrial dysfunction pathway in U87-MG cells

Deng, Linlin; Zhao, Mengyao; Cui, Yanan; Xia, Quanming; Jiang, Lihua; Yin, Hao; Zhao, Liming

doi:10.1080/01480545.2021.1979030

Cited by 17 publications

(9 citation statements)

References 42 publications

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“…ATF4 and CHOP, as well as PERK-mediated endoplasmic reticulum stress (ERS), participated in AA-induced autophagy [28]. It has also been reported that AA regulates the autophagy signaling pathway in U87-MG cells by increasing the expression of p62 and Beclin-1 and decreasing the protein expression ratio of LC3-I/LC3-II [44]. In vitro study with PC12 cell, it was found that AA promoted the protein expressions of Beclin-1, LC3-II as well as p62.…”

Section: Acrylamide Induces Cell Autophagy In Nervous Systemsmentioning

confidence: 99%

“…AA could also cause the accumulation of cellular reactive oxygen species (ROS) by increasing the mRNA level of ERS-dependent apoptosis factor C/EBP homologous protein (CHOP) and inactivating the NF-κB pathway [34,43]. Research has proved that AA could activate the NF-κB cascade, increase the ratio of Bax/ Bcl-2, and cause the cleavage of caspase-3, caspase-9, and PARP to induce apoptosis [44].…”

Section: Acrylamide Induces Apoptosis In Nervous Related Cellsmentioning

confidence: 99%

“…For example, AA-induced autophagic accumulation may be attributed to the blocking of autophagic fux, preventing the autophagic from binding to the lysosome. Additional information confrming the association between apoptosis and autophagy fux suggests that limiting the protective autophagy induced by AA further promotes apoptosis initiation [44]. However, the level of autophagy changes greatly sometimes, and the relationship between apoptosis and autophagy during the AA-induced damage process has not been fully elucidated.…”

Section: Acrylamide Suppresses Cell Autophagymentioning

confidence: 99%

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Research Progress of Programmed Cell Death Induced by Acrylamide

Wang

et al. 2023

Journal of Food Quality

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Acrylamide exposure through environment pollution and diet is very common in daily life. With the deepening of the study on the toxicity of acrylamide, it has attracted widespread attention for the effects of acrylamide on multiple organs through affecting a variety of programmed cell death. Multiple studies have shown that acrylamide could exert its toxic effect by inducing programmed cell death, but its specific molecular mechanism is still unclear. In this review, the research on the main forms of programmed cell death (apoptosis, autophagy, and programmed necrosis) induced by acrylamide and their possible mechanisms are reviewed. This review may provide basic data for further research of acrylamide and prevention of its toxicity.

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Section: Acrylamide Induces Cell Autophagy In Nervous Systemsmentioning

confidence: 99%

Section: Acrylamide Induces Apoptosis In Nervous Related Cellsmentioning

confidence: 99%

Section: Acrylamide Suppresses Cell Autophagymentioning

confidence: 99%

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Research Progress of Programmed Cell Death Induced by Acrylamide

Wang

et al. 2023

Journal of Food Quality

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“…In case of traumic spinal cord injury (TSCI), allicin can reduce the ROS levels and enhance NADPH levels by regulation of HSP70, Akt and iNOS pathways [ 156 , 157 ]. Toxic effects of acrylamide (ACR) on the peripheral and central nervous system is well established [ 158 , 159 ]. The combined therapy with allicin and melatonin has shown recovery of ACR damaged neurons by regulating DNA damage, increasing the levels of neurotransmitters [ 160 ].…”

Section: Allicin As a Neuroprotective Agent To Fight Against Neurological Diseasesmentioning

confidence: 99%

Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment

et al. 2021

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Allicin (diallylthiosulfinate) is a defense molecule produced by cellular contents of garlic (Allium sativum L.). On tissue damage, the non-proteinogenic amino acid alliin (S-allylcysteine sulfoxide) is converted to allicin in an enzyme-mediated process catalysed by alliinase. Allicin is hydrophobic in nature, can efficiently cross the cellular membranes and behaves as a reactive sulfur species (RSS) inside the cells. It is physiologically active molecule with the ability to oxidise the thiol groups of glutathione and between cysteine residues in proteins. Allicin has shown anticancer, antimicrobial, antioxidant properties and also serves as an efficient therapeutic agent against cardiovascular diseases. In this context, the present review describes allicin as an antioxidant, and neuroprotective molecule that can ameliorate the cognitive abilities in case of neurodegenerative and neuropsychological disorders. As an antioxidant, allicin fights the reactive oxygen species (ROS) by downregulation of NOX (NADPH oxidizing) enzymes, it can directly interact to reduce the cellular levels of different types of ROS produced by a variety of peroxidases. Most of the neuroprotective actions of allicin are mediated via redox-dependent pathways. Allicin inhibits neuroinflammation by suppressing the ROS production, inhibition of TLR4/MyD88/NF-κB, P38 and JNK pathways. As an inhibitor of cholinesterase and (AChE) and butyrylcholinesterase (BuChE) it can be applied to manage the Alzheimer’s disease, helps to maintain the balance of neurotransmitters in case of autism spectrum disorder (ASD) and attention deficit hyperactive syndrome (ADHD). In case of acute traumatic spinal cord injury (SCI) allicin protects neuron damage by regulating inflammation, apoptosis and promoting the expression levels of Nrf2 (nuclear factor erythroid 2-related factor 2). Metal induced neurodegeneration can also be attenuated and cognitive abilities of patients suffering from neurological diseases can be ameliorates by allicin administration.

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“…Acrylamide exerts its harmful effects by increasing the level of reactive oxygen species (ROS) and decreasing the antioxidant capacity via its deleterious effects to the endogenous antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) ( 13 , 14 ). Also, it provokes the production of inflammatory cytokines, including TNF-α and IL-1β ( 12 , 14 ), and induces mitochondrial and caspase-dependent apoptosis ( 15 , 16 ).…”

Section: Introductionmentioning

confidence: 99%

Taify Pomegranate Juice (TPJ) Abrogates Acrylamide-Induced Oxidative Stress Through the Regulation of Antioxidant Activity, Inflammation, and Apoptosis-Associated Genes

et al. 2022

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Acrylamide (ACR) has various effects on biological systems, including oxidative stress and its associated metabolic disorders. Previous research reports that plants growing at high altitude have a different profile of antioxidants. In the current report, the Taify pomegranate juice (TPJ) of the Taify pomegranate growing at the Taif region (high altitude), Saudi Arabia, was investigated for its protective activity from ACR-induced oxidative stress. Rats were treated with ACR, TPJ, or TPJ+ACR, and various assays, including blood chemistry, liver function biomarkers, gene expression of endogenous antioxidant enzymes, oxidative stress regulatory genes, inflammation biomarkers, and apoptosis, were estimated using biochemical, real-time PCR, histopathological, and immunohistochemical analysis. TPJ showed a protective function of ACR-induced alteration of AST, ALT, GGT, urea, total proteins, albumin, MDA, and NO. It also increased the level of the endogenous antioxidative enzymes, including SOD, catalase, and GSH. It showed anti-inflammatory activity by reduction the TNF-α, IL-6 secretion and the enhancing of IL-10 levels. At the gene expression level, TPJ upregulated the expression of endogenous antioxidant genes (SOD and catalase) and of antioxidant-regulating genes Nrf2 and HO-1; downregulated the expression of inflammatory genes TGF-β1, COX2, and the apoptotic gene caspase-3; and upregulated the expression of antiapoptotic gene Bcl2. At the histological level, TPJ showed a protective effect from the ACR-induced hepatic histological damage. Results of this study conclude that TPJ has a protective effect from ACR-induced oxidative stress and its associated metabolic alterations through its antioxidant and anti-inflammatory activities.

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Acrylamide induces intrinsic apoptosis and inhibits protective autophagy via the ROS mediated mitochondrial dysfunction pathway in U87-MG cells

Cited by 17 publications

References 42 publications

Research Progress of Programmed Cell Death Induced by Acrylamide

Research Progress of Programmed Cell Death Induced by Acrylamide

Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment

Taify Pomegranate Juice (TPJ) Abrogates Acrylamide-Induced Oxidative Stress Through the Regulation of Antioxidant Activity, Inflammation, and Apoptosis-Associated Genes

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