Acrylamide exerts its cytotoxicity in NIH/3T3 fibroblast cells by apoptosis

Şahıntürk, Varol; Kaçar, Sedat; Vejselova, Djanan; Kutlu, Hatice Mehtap

doi:10.1177/0748233718769806

Cited by 31 publications

(23 citation statements)

References 28 publications

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“…ROS causes cell apoptosis through the regulated or non‐physiological apoptotic pathway. AA exposure not only activated the mitochondrial apoptotic pathway in PC12 cells but also triggered the downregulation of the Bcl‐2/Bax ratio, over the release of cleavage of caspase‐9 and caspase‐9 (Pan et al., 2017; Sahinturk, Kacar, Vejselova, & Kutlu, 2018). AA can induce endoplasmic reticulum (ER) stress and subsequent eIF2α‐ATF4‐CHOP signaling cascade in SH‐SY5Y cells (Komoike & Matsuoka, 2016).…”

Section: Introductionmentioning

confidence: 99%

6ʹʺ‐p‐Coumaroylspinosin protects PC12 neuronal cells from acrylamide‐induced oxidative stress and apoptosis

Zhou

Cui

et al. 2020

J Food Biochem

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6ʹʺ‐p‐coumaroylspinosin (P‐CS) is a flavonoid isolated from Ziziphi Spinosae Semen (ZSS), whereas, the antioxidative activity has not been reported. Oxidative stress is believed to be one of the main causes of neurodegenerative disorders. In this study, the antioxidative effect of P‐CS on PC12 cells was determined. The cells were treated with acrylamide (AA) in the absence or presence of P‐CS, and cell apoptosis was analyzed. Interestingly, P‐CS pretreatment of the cells could significantly prevent AA‐induced cell death, glutathione (GSH) contents decrease, and reactive oxygen species (ROS) overproduction. Further investigation of the molecular mechanism underlying the effect of P‐CS on cell apoptosis revealed that P‐CS was able to suppress the expression of Bax and Bim induced by AA and inhibit the JNKs pathway. Our findings support a role of P‐CS in preventing neuronal cell apoptosis induced by AA, suggesting its therapeutic potential for the treatment of neurodegenerative disorders as a medicinal supplement. Practical applications Oxidative stress is believed to cause damage in subcellular organelles, nucleic acids, and alteration in protein aggregation as well as disruption of the signaling cascades associated with aging and apoptosis. A small molecule, non‐poisonous natural antioxidant is needed to protect the brain from oxidative stress. Compared with western medicine, natural products carry less risk of adverse effects and are not too expensive, especially for the third‐world countries. Furthermore, ZSS could be used to produce or prepare antioxidants, such as P‐CS, which has been reported significant anti‐oxidative activity in this study.

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Section: Introductionmentioning

confidence: 99%

6ʹʺ‐p‐Coumaroylspinosin protects PC12 neuronal cells from acrylamide‐induced oxidative stress and apoptosis

Zhou

Cui

et al. 2020

J Food Biochem

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“…Similarly, NIH/3T3 cell line was another choice representing the mesenchyme‐derived cells forming the most basic unit of the connective tissues. Previously, Sahinturk, Kacar, Vejselova, and Kutlu () have used NIH/3T3 cell line for evaluating cytotoxicity of acrylamide. All the hits ( 2 , 5e , 5i , and 5m ) along with doxorubicin, representing cytotoxic drugs as positive control and vehicle as negative control, were evaluated in MTT assay using hPBMCs and NIH/3T3 cell line.…”

Section: Resultsmentioning

confidence: 99%

Substituted chloroacetamides as potential cancer stem cell inhibitors: Synthesis and biological evaluation

Padhariya

Srivastava²,

Kharkar

2019

Drug Development Research

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Cancer kills, irrespective of geographical and cultural origin. Novel modalities for treating cancer are desperately needed. Cancer stem cells (CSCs), main culprits behind chemoresistance and tumor relapse, are one of the few logical choices. Herein, we report the synthesis and biological evaluation of small molecules with chloroacetamide war-head. These molecules were screened for viability against various breast, prostate, and oral cancer cell lines using MTT and soft-agar assays. Further, promising hits were screened in sphere-forming assay with the aim of discovering potential anti-CSC agents. Our optimism yielded four hits inhibiting self-renewal of cancer cells with stem-like characters in vitro. Finally, the hits were evaluated for in vitro toxicity against human peripheral blood mononuclear cells and mouse embryonic fibroblast cell line.Overall, these preliminary investigations yielded three hits exhibiting promising anti-CSC potential with little or no toxicity against normal cells. K E Y W O R D Sbreast cancer, cancer stem cells, chloroacetamides, CSCs, oral cancer, prostate cancer, softagar assay, sphere-forming assay

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“…In this study AA, increased the OH˙ levels concentration‐dependently, however, H 2 O 2 levels increased only at 1000 μM AA concentration (Figure D and E). Several reports indicated that oxidative stress‐related AA toxicity results in overproduction of intracellular ROS, lipid peroxidation and mitochondrial dysfunction . MDA, which is a biomarker of the degraded oxidant status and final product of lipid peroxidation in cells, has increased depending on the concentration of AA (Figure C).…”

Section: Discussionmentioning

confidence: 99%

Therapeutic effect of curcumin on acrylamide‐induced apoptosis mediated by MAPK signaling pathway in Leydig cells

Yildizbayrak¹,

Erkan

2019

J Biochem & Molecular Tox

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Acrylamide exerts its cytotoxicity in NIH/3T3 fibroblast cells by apoptosis

Abstract: In conclusion, our results suggested that the IC of acrylamide against NIH/3T3 cells for 24 h was 6.73 mM and that acrylamide exerted its cytotoxic and anti-proliferative effects on these cells mainly via apoptosis.

Cited by 31 publications

References 28 publications

6ʹʺ‐p‐Coumaroylspinosin protects PC12 neuronal cells from acrylamide‐induced oxidative stress and apoptosis

6ʹʺ‐p‐Coumaroylspinosin protects PC12 neuronal cells from acrylamide‐induced oxidative stress and apoptosis

Substituted chloroacetamides as potential cancer stem cell inhibitors: Synthesis and biological evaluation

Therapeutic effect of curcumin on acrylamide‐induced apoptosis mediated by MAPK signaling pathway in Leydig cells

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