Protective effects of a <i>Ganoderma atrum</i> polysaccharide against acrylamide induced oxidative damage <i>via</i> a mitochondria mediated intrinsic apoptotic pathway in IEC-6 cells

Jiang, Guoyong; Zhang, Lulu; Wang, Hui; Chen, Qian; Wu, Xiaolin; Yan, Xiaoli; Chen, Yi; Xie, Mingyong

doi:10.1039/c7fo01619k

Cited by 30 publications

(19 citation statements)

References 25 publications

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“…Numerous studies have implied that mitochondrial apoptosis is involved in neuronal death in ACRinduced neurotoxicity. [34][35][36] In this present study, we proved that NR1 could resist ACR-induced neurotoxicity by regulating the mitochondrial apoptosis pathway. It is also the first time that NR1 has been proved to inhibit ACR-induced neurotoxicity.…”

Section: Discussionsupporting

confidence: 57%

Neuroprotective effects of notoginsenoside R1 by upregulating Trx-1 on acrylamide-induced neurotoxicity in PC12

Wang

Thomas

et al. 2020

Hum Exp Toxicol

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Acrylamide (ACR) is a water-soluble chemical that is commonly used in chemical and cosmetic manufacture. Many studies have been carried out to investigate the neurotoxicity mechanisms of ACR, resulting in oxidative stress and nerve damages. One of the commonly used traditional Chinese medicines is notoginsenoside R1 (NR1). However, its mitochondrial-mediated apoptotic effect caused in ACR-induced neurotoxicity has not been reported. Our results have shown that NR1 resisted the neurotoxicity induced by ACR by upregulating the levels of thioredoxin-1 (Trx-1) in Rat adrenal chromaffin cell tumor (PC12) cells. NR1 inhibited the increase in levels of Bax, caspase-9, and caspase-3, which was instigated by ACR. Moreover, NR1 inhibited the decrease in levels of B-cell lymphoma 2 and Trx-1 induced by ACR. The downregulation of Trx-1 aggravated the mitochondrial-mediated apoptosis and increased the expression of the above molecules, which was induced by ACR. In contrast, overexpression of Trx-1 attenuated the mitochondrial-mediated apoptosis and inhibited the expression of the mentioned molecules induced by ACR. Our results suggested that NR1 protected ACR-induced mitochondrial apoptosis by upregulating Trx-1.

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Section: Discussionsupporting

confidence: 57%

Neuroprotective effects of notoginsenoside R1 by upregulating Trx-1 on acrylamide-induced neurotoxicity in PC12

Wang

Thomas

et al. 2020

Hum Exp Toxicol

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“…Due to definite exposure of humans to acrylamide for various sources, probably detoxification of this compound inside the body can be a suitable approach to reduce its toxicity. It is well confirmed that oxidative stress and mitochondrial dysfunction have a main role in acrylamideinduced toxicity [11]. Therefore, natural compounds with antioxidant and antitumorigenic properties can probably play a promising role in inhibiting the toxicity caused by acrylamide.…”

Section: Introductionmentioning

confidence: 97%

Mitochondrial, lysosomal and DNA damages induced by acrylamide attenuate by ellagic acid in human lymphocyte

et al. 2021

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Acrylamide (AA), is an important contaminant formed during food processing under high temperature. Due to its potential neurotoxicity, reproductive toxicity, hepatotoxicity, immunotoxicity, genotoxicity and carcinogenicity effects, this food contaminant has been recognized as a human health concern. Previous studies showed that acrylamide-induced toxicity is associated with active metabolite of acrylamide by cytochrome P450 enzyme, oxidative stress, mitochondrial dysfunction and DNA damage. In the current study, we investigated the role of oxidative stress in acrylamide’s genotoxicity and therapeutic potential role of ellagic acid (EA) in human lymphocytes. Human lymphocytes were simultaneously treated with different concentrations of EA (10, 25 and 50 μM) and acrylamide (50 μM) for 4 h at 37°C. After 4 hours of incubation, the toxicity parameters such cytotoxicity, ROS formation, oxidized/reduced glutathione (GSH/GSSG) content, malondialdehyde (MDA) level, lysosomal membrane integrity, mitochondria membrane potential (ΔΨm) collapse and 8-hydroxy-2’-deoxyguanosine (8-OHdG) were analyzed using biochemical and flow cytometry evaluations. It has been found that acrylamide (50 μM) significantly increased cytotoxicity, ROS formation, GSH oxidation, lipid peroxidation, MMP collapse, lysosomal and DNA damage in human lymphocytes. On the other hand, cotreatment with EA (25 and 50 μM) inhibited AA-induced oxidative stress which subsequently led to decreasing of the cytotoxicity, GSH oxidation, lipid peroxidation, MMP collapse, lysosomal and DNA damage. Together, these results suggest that probably the co-exposure of EA with foods containing acrylamide could decrease mitochondrial, lysosomal and DNA damages, and oxidative stress induced by acrylamide in human body.

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“…The AA group and two low dose groups showed glomerular atrophy, and enlarged bowman's space (black arrow). There was no obvious pathological damage in the two high dose groups (SOD, CAT) and GSH, and increase the level of LPO in rats [36,37]. Our results showed that no obvious ataxia and hind limb valgus were observed in rats fed high doses of L. plantarum ATCC8014.…”

Section: Discussionmentioning

confidence: 51%

Protective effect of Lactobacillus plantarum ATCC8014 on acrylamide-induced oxidative damage in rats

Zhao

Liu

et al. 2020

Appl Biol Chem

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Acrylamide (AA), which is mainly found in fried foods, causes neurotoxicity, genetic toxicity, carcinogenic effects, and DNA damage. This study confirms that a strain of lactic acid bacteria (Lactobacillus plantarum ATCC8014) could alleviate the toxicity of rats by inhibiting the AA-induced oxidative damage. Forty-eight adult male SD rats were randomly divided into eight groups: control group, AA group (40 mg/kg), three different doses (1 × 10 7 CFU/ml, 1 × 10 8 CFU/ ml, 1 × 10 9 CFU/ml of Lactobacillus plantarum ATCC8014) of prevention groups and therapeutic groups, respectively. At the end of three-week experiment, AA treatment produced a significant reduction in the rate of weight gain along with the symptoms of hind limb splay and ataxia. Histological examinations revealed various degrees of injury in five tissues. Levels of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) in group AA rats were significantly decreased, but the level of lipid peroxidation (LPO) was significantly increased (p < 0.05). Both prevention and therapeutic groups with 1 × 10 9 CFU/ml of Lactobacillus plantarum ATCC8014 could effectively reduce the injury of AA to the body. However, reductions in both groups were not statistically significant.

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Protective effects of a Ganoderma atrum polysaccharide against acrylamide induced oxidative damage via a mitochondria mediated intrinsic apoptotic pathway in IEC-6 cells

Cited by 30 publications

References 25 publications

Neuroprotective effects of notoginsenoside R1 by upregulating Trx-1 on acrylamide-induced neurotoxicity in PC12

Neuroprotective effects of notoginsenoside R1 by upregulating Trx-1 on acrylamide-induced neurotoxicity in PC12

Mitochondrial, lysosomal and DNA damages induced by acrylamide attenuate by ellagic acid in human lymphocyte

Protective effect of Lactobacillus plantarum ATCC8014 on acrylamide-induced oxidative damage in rats

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