Protective effects of (-)-epigallocatechin gallate and curcumin against acrylamide toxicity

Wang, Shanshan; Wang, Hufei; Chen, Yanqiu; Liu, Jilai; He, Xiaozhen; Huang, Da; Wu, Yuanzi; Chen, Yonghai; Weng, Zuquan

doi:10.1080/02772248.2021.1951731

Cited by 9 publications

(5 citation statements)

References 74 publications

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“…Several cellular studies in animals or fish proved the potential protective role of herbs or their extracts against ACR hazards for natural phytochemical compounds such as eugenol, iso-eugenol, turmeric, polyphenol, flavonoids, N-acetylcysteine, gallate, and carnosic acid (Albalawi et al 2018;Faria et al 2019a;Krishnan and Kang 2019;Ning et al 2021;Singh et al 2019;Wang et al 2021). Table 4 displays a collection of references that demonstrate the possible ameliorative effect of certain phytochemical substances against ACR toxicity.…”

Section: Phytochemicalsmentioning

confidence: 99%

Acrylamide toxicity in aquatic animals and its mitigation approaches: an updated overview

Naiel,

Negm,

Ghazanfar

et al. 2023

Environ Sci Pollut Res

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Acrylamide (ACR) is widely applied in various industrial activities, as well as in the water purification process. Furthermore, ACR is synthesized naturally in some starchy grains exposed to high temperatures for an extended time during the cooking process. Because of its widespread industrial usage, ACR might be released into water stream sources. Also, ACR poses a high risk of contaminated surface and ground-water resources due to its high solubility and mobility in water. Furthermore, animal studies have indicated that ACR exposure may cause cancer (in many organs such as lung, prostate, uterus, and pancreas), genetic damage (in both somatic and germ cells), and severe effects on reproduction and development. Recently, numerous studies have shown that ACR has a mild acute cytotoxic impact on aquatic species, particularly during early life stages. Besides, wide-spectrum usage of ACR in many industrial activities presented higher environmental risks as well as major hazards to consumer health. This literature was designed to include all potential and accessible reports on ACR toxicity related with aquatic species. The Preferred Reporting Items for Systematic Reviews were applied to evaluate the risk effects of ACR on aquatic organisms, the ACR sub-lethal concentration in the ecosystem, and the possible protective benefits of various feed additives against ACR toxicity in fish. The major findings are summarized in Tables 2 and 3. The primary aim of this literature was to specify the hazards of ACR toxicity related with fish welfare and possible suggested strategies to reduce its risks.

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Section: Phytochemicalsmentioning

confidence: 99%

Acrylamide toxicity in aquatic animals and its mitigation approaches: an updated overview

Naiel,

Negm,

Ghazanfar

et al. 2023

Environ Sci Pollut Res

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“…AA induced DNA strand breaks in several human cell lines (THP‐1 monocyte, liver HepaRG, CaCo‐2) (Xiao et al, 2016 ; Mandon et al, 2019 ; Nowak et al, 2020 ), human lymphocytes (Wang et al, 2021 ) and mouse and human spermatozoa (Katen et al, 2017 ). In the case of mouse spermatozoa, increased DNA strand breakage was observed only following exposure to GA, the active AA metabolite.…”

Section: Assessmentmentioning

confidence: 99%

“…Some observations indicate however that at least a fraction of AA‐induced DNA strand breaks might be due to DNA oxidation. These include elevation of ROS levels together with mitochondria depolarisation occurring in parallel with DNA strand breaks in CaCo‐2 cells (Nowak et al, 2020 ) and modulation of these by antioxidants such as curcumin and epigallocatechin in human lymphocytes (Wang et al, 2021 ) (see Section 3.2 ).…”

Section: Assessmentmentioning

confidence: 99%

“…Such evidence comes from an association of AA‐induced DNA strand breaks with oxidative stress, both in vitro and in vivo . Both oxidative stress and DNA strand breaks were reduced by antioxidants (Zhao et al, 2015a , b ; Ansar et al, 2016 ; Nowak et al, 2020 ; Wang et al, 2021 ). The demonstration of enhanced DNA breaks induced by enzymes involved in the repair of oxidative DNA damage (Fpg, EndoIII or OGG1) in the comet assay was shown to implicate DNA oxidation in various studies, however, the interpretation of the studies using Fpg to imply DNA oxidation should be taken with caution since Hansen et al ( 2018 ) provided evidence that DNA damage revealed through the use of Fpg may also be produced by GA directly.…”

Section: Assessmentmentioning

confidence: 99%

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Assessment of the genotoxicity of acrylamide

Benford¹,

Bignami²,

Chipman³

et al. 2022

EFS2

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EFSA was requested to deliver a statement on a recent publication revisiting the evidence for genotoxicity of acrylamide (AA). The statement was prepared by a Working Group and was endorsed by the CONTAM Panel before its final approval. In interpreting the Terms of Reference, the statement considered the modes of action underlying the carcinogenicity of AA including genotoxic and non‐genotoxic effects. Relevant publications since the 2015 CONTAM Panel Opinion on AA in food were reviewed. Several new studies reported positive results on the clastogenic and mutagenic properties of AA and its active metabolite glycidamide (GA). DNA adducts of GA were induced by AA exposure in experimental animals and have also been observed in humans. In addition to the genotoxicity of AA, there is evidence for both secondary DNA oxidation via generation of reactive oxygen species and for non‐genotoxic effects which may contribute to carcinogenesis by AA. These studies extend the information assessed by the CONTAM Panel in its 2015 Opinion, and support its conclusions. That Opinion applied the margin of exposure (MOE) approach, as recommended in the EFSA Guidance for substances that are both genotoxic and carcinogenic, for risk characterisation of the neoplastic effects of AA. Based on the new data evaluated, the MOE approach is still considered appropriate, and an update of the 2015 Opinion is not required at the present time.

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“…Several studies have shown that antioxidants can counteract the effects of ROS and free radicals [18], such that antioxidant-rich substances have emerged as potential agents for preventing and adjuvating oxidative stress and DNA damage [19][20][21]. More precisely, compounds such as polyphenols have been shown to play a direct role as radical scavengers and metal chelators and to exert indirect effects by modulating levels of transcription factors and enzymes [22][23][24]. Therefore, the aim of the present study was to examine the protective effects of resveratrol against Cr(VI)-induced genotoxicity in vivo and the underlying metabolic processes including 8-hydroxydeoxyguanosine (8-OHdG, 7,8-dihydro-8-oxodeoxyguanosine) adduct repair, the endogenous antioxidant component system, and apoptosis, which may be involved in preventing Cr(VI)-induced DNA damage.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Resveratrol against Hexavalent Chromium-Induced Genotoxic Damage in Hsd:ICR Male Mice

et al. 2022

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The aim of this study is to examine the ability of resveratrol to counteract hexavalent chromium [Cr(VI)]-induced genetic damage, as well as the possible pathways associated with this protection. Hsd:ICR male mice are divided into groups of the following five individuals each: (a) control 1, distilled water; (b) control 2, ethanol 30%; (c) resveratrol, 50 mg/kg by gavage; (d) CrO3, 20 mg/kg intraperitoneally; (e) resveratrol + CrO3, resveratrol administered 4 h prior to CrO3. The assessment is performed on peripheral blood. Micronuclei (MN) kinetics are measured from 0 to 72 h, while 8-hydroxydeoxyguanosine (8-OHdG) adduct repair levels, endogenous antioxidant system biomarkers, and apoptosis frequency were quantified after 48 h. Resveratrol reduces the frequency of Cr(VI)-induced MN and shows significant effects on the 8-OHdG adduct levels, suggesting that cell repair could be enhanced by this polyphenol. Concomitant administration of resveratrol and Cr(VI) results in a return of the activities of glutathione peroxidase and catalase to control levels, accompanied by modifications of superoxide dismutase activity and glutathione levels. Thus, antioxidant properties might play an important role in resveratrol-mediated inhibition of Cr(VI)-induced oxidant genotoxicity. The increase in apoptotic cells and the decrease in necrosis further confirmed that resveratrol effectively blocks the actions of Cr(VI).

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Protective effects of (-)-epigallocatechin gallate and curcumin against acrylamide toxicity

Cited by 9 publications

References 74 publications

Acrylamide toxicity in aquatic animals and its mitigation approaches: an updated overview

Acrylamide toxicity in aquatic animals and its mitigation approaches: an updated overview

Assessment of the genotoxicity of acrylamide

Protective Effect of Resveratrol against Hexavalent Chromium-Induced Genotoxic Damage in Hsd:ICR Male Mice

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