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Acrylamide (ACR), a neurotoxin with carcinogenic properties that can affect fertility, is commonly found in fried and baked foods such as potato chips. This study was carried out to predict the ACR content in fried and baked potato chips using near-infrared (NIR) spectroscopy. Effective wavenumbers were identified using competitive adaptive reweighted sampling (CARS) and the successive projections algorithm (SPA). Six wavenumbers (12799 cm -1 , 12007 cm -1 , 10944 cm -1 , 10943 cm -1 , 5801 cm -1 , and 4332 cm -1 ) were selected using the ratio (λ i /λ j ) and difference (λ i -λ j ) of any two wavenumbers from the CARS and SPA results. First, partial least squares (PLS) models were established based on full spectral wavebands (12799-4000 cm -1 ), and the prediction models were subsequently redeveloped based on effective wavenumbers to predict ACR content. Results showed that the full and selected wavenumbers-based PLS models obtained the coefficient of determination (R 2 ) of 0.7707 and 0.6670, respectively, and the root mean square errors of prediction (RMSEP) of 53.0442 μg/kg and 64.3810 μg/kg, respectively, in the prediction sets. The results of this work demonstrate the suitability of NIR spectroscopy as a non-destructive method for predicting ACR content in potato chips., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Acrylamide (ACR) is a potential neurotoxin commonly found in the environment, as well as in food repeatedly exposed heat processing, but the mechanism underpinning ACR-induced neurotoxicity remains unclear. This study investigated the potential association and underlying signal transduction of oxidative stress, apoptosis, and autophagy associated with ACR-triggered neurotoxicity. Therefore, U87-MG cells were treated with varying ACR concentrations, while the cell activity reduction depended on the specific dosage and time parameters. Biochemical analyses showed that ACR significantly increased the reactive oxygen species (ROS), malondialdehyde (MDA), and Ca 2+ levels while decreasing the glutathione (GSH) levels and mitochondrial membrane potential (ΔΨm), finally leading to a higher cell apoptotic rate. Moreover, ACR induced U87-MG cell apoptosis and autophagy via ROS-triggered expression in the mitochondrial apoptosis pathway, NF-κB activation, and autophagosome accumulation. In addition, the autophagosome accumulation induced by ACR could probably be ascribed to blocked autophagic flux, inhibiting the autophagosomes from combining with lysosomes, while the inhibition of autophagy caused by ACR further promoted the initiation of apoptosis. In conclusion, the results indicated that the apoptotic and autophagic pathways responded to ACR-induced neurotoxicity. However, inhibited protective autophagy further promoted apoptotic progression. New insights may be derived from these cellular responses that can help develop diverse pathway strategies for assessing the risk posed by ACR.HIGHLIGHTSACR induced mitochondrial- and caspase-dependent apoptosis in U87-MG cells.ACR regulated the autophagic markers and blocked autophagic flux in U87-MG cells.ACR inhibited protective autophagy and promoted apoptotic initiation in U87-MG cells.

Acrylamide (ACR) is a typical environmental contaminant, presenting potential health hazards that have been attracting increasing attention. Its neurotoxicity is known to cause significant damage to health. However, the mechanisms of ACR-induced neurotoxicity require further clarification. This study uses a mouse model to explore how ACR-induced oxidative stress, neuronal lesions, neurotransmission impairment, and neuroinflammation mutually contribute to neurotoxicity. A distinct increase in the cellular reactive oxygen species (ROS) levels, malondialdehyde (MDA), and 8-hydroxy-2-deoxyguanosine (8-OHdG) content and a significant decrease in the glutathione (GSH) content after ACR exposure were indicative of oxidative stress. Moreover, ACR caused neurological defects associated with gait abnormality and neuronal loss while suppressing the acetylcholine (ACh) and dopamine (DA) levels and increasing the protein expression of α-synuclein (α-syn), further inhibiting cholinergic and dopaminergic neuronal function. Additionally, ACR treatment caused an inflammatory response via nuclear factor-kappa B (NF-κB) activation and increased the protein expression of NOD-like receptor protein-3 (NLRP3), consequently activating the NLRP3 inflammasome constituents, including cysteinyl aspartate specific proteinase 1 (Caspase-1), apoptosis-associated speck-like protein containing CARD (ASC), N domain gasdermin D (N-GSDMD), interleukin-1β (IL-1β), and IL-18. The results revealed the underlying molecular mechanism of ACR-induced neurotoxicity via oxidative stress, neurotransmission impairment, and neuroinflammation-related signal cascade. This information will further improve the development of an alternative pathway strategy for investigating the risk posed by ACR. The hypothetical mechanism of ACR-induced neurotoxicity in vivo., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Acrylamide (AA) is a common food contaminant formed during food heat processing that has neurotoxic effects. We hypothesize that AA induces oxidative stress in astrocytes and microglia, leading to neurotoxicity. Oxidative status, translocation of Nrf2 and NF-κB, and related down-stream targets were measured in primary astrocytes and microglia obtained from BALB/c mice. The results showed that AA increased reactive oxygen species (ROS) formation and reduced glutathione levels, causing successive events associated with oxidative stress, including 4-hydroxynonenal and 8-hydroxy-2-deoxyguanosine adduct formation, in both cell types. Both Nrf2 and NF-κB pathways were activated, but Nrf2 and its downstream antioxidative genes acted at earlier stages in both cell types before NF-κB activation. After NF-κB activation, related cytokines, including IL-6, TNF-α, G-CSF, and IL-1β, were released and cell viability decreased. Greater ROS generation, faster glutathione reduction, and increased oxidative adduct formation were observed in microglia compared with astrocytes. Moreover, Nrf2/NF-κB and its downstream genes were up-regulated much faster and to greater degrees in microglia than astrocytes. These results clarify the roles of the Nrf2 and NF-κB pathways in AA-induced neurotoxicity. These cellular responses may provide new insights for the development of adverse outcome pathway approaches for risk assessments of AA., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Acrylamide (AA), is a common food contaminant generated by heat processing. Astrocytes and microglia are the two major glial cell types in the brain that play pivotal but different roles in maintaining optimal brain function. The objective of this study is to investigate the neurotoxicity of AA, using a primary astrocytes/microglia co-culture model. Co-cultural cells obtained from Balb/c mice were cultured and treated with 0-1.0mM AA for 24-96h. Cell viability, reactive oxygen species (ROS) generation, oxidative end produces formation and glutathione (GSH) levels were measured. The expression of nuclear-E2-related factor 2(Nrf2), and nuclear factor kappa-beta (NF-κB) and selected down-stream genes were measured. Results showed that AA treatment led toa dose-dependent toxicity. Oxidative stress was induced as indicated by an increase of ROS, a decrease of GSH levels, and an increase in the formation of 4-hydroxynonenal-adduct and 8-hydroxy-2-deoxyguanosine-adduct. Both Nrf2 and NF-κB pathway contributed to the initiation of oxidative stress but the timing of two factors was different. Nrf2 and its related downstream genes were activated earlier than that in NF-κB pathway. In conclusion, AA-induced neurotoxicity attribute to oxidative stress via Nrf2 and NF-κB pathway. Moreover, the co-culture cell model was proven to be a viable model to study AA neurotoxicity., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Background: Acrylamide (AA) is a potential carcinogen which widely exists in heat-processed foods. The addition of glycine (Gly) has been shown to reduce the formation of AA. The objective of this work was to investigate the kinetics of the inhibition of AA by Gly in both asparagine (Asn)/glucose (Glc) and Asn/Glc/Gly potato model systems during heating at 160 °C, 180 °C, and 200 °C., Results: The simplified two consecutive first-order kinetic model fitted well to the changes of AA in both systems. No significant difference in rate constant (kF) and apparent activation energy (EaF) was observed for AA formation between the two systems (P > 0.05). Whereas EaE and only kE at 200 °C for AA elimination in the Asn/Glc/Gly system was significantly higher than Asn/Glc system (P < 0.05). The elimination reaction between Gly and AA was confirmed by the identification of their major reaction product 2-((3-amino-3-oxopropyl)amino)acetic acid in the Asn/Glc/(15)  N-Gly system., Conclusion: The reduction of AA by Gly is predominantly attributed to the elimination reaction between Gly and AA., (© 2015 Society of Chemical Industry.)

Berries are dietary plants with high antioxidant activity. The aim of this study is to investigate the protective effect of berries (strawberry, grape, and blueberry) against the acrylamide (AA)-induced general toxicity, genotoxicity, and reproductive toxicity in mice model, respectively. Mice were treated with 50 mg/kg b.w./day AA intraperitoneal injection for 5 d after feeding control diet or diet containing freeze-dried strawberry, grape, and blueberry powder. The results showed that AA induced a significant general toxicity, genotoxicity, and reproductive toxicity in mice. Compared with the control diet, the diets containing berries could reverse the AA-induced alterations in liver antioxidant enzymes activities (P < 0.05). Moreover, the AA-induced genotoxicity could be prevented by the diet containing berries. The DNA damage in the lymphocyte and liver cells and the micronucleus formation in bone marrow cell were significantly alleviated (P < 0.05). Meanwhile, the mice fed with diets containing berries showed a recovery in the sperm count, the sperm activity rate, sperm motility parameters, and the abnormal sperm rate (P < 0.05). Berry powders have remarkable intervention against the AA-induced general toxicity, genotoxicity, reproductive toxicity. Abundant phenolics, especially anthocyanins, may contribute to the intervention., (© 2015 Institute of Food Technologists®)

Acrylamide (AA) occurs in many cooked starchy foods and has caused widespread concern as a possible carcinogen. In the present study, we investigate the intervention of AA toxicity in MDA-MB-231 cells pretreated with cyanidin-3-glucoside (Cy-3-glu). Compared to the cells treated with AA, Cy-3-glu significantly inhibited AA-induced cytotoxicity, reduced reactive oxygen species (ROS) generation, recovered glutathione (GSH) depletion and decreased the activities of glutathione peroxidase (GPx) and glutathione S-transferase (GST). Moreover, the expression of GPx1, GSTP1 and gamma-glutamyl cysteine synthase (γ-GCS) were enhanced, and cytochrome P450 2E1 (CYP2E1) expression was inhibited by the pretreatment of Cy-3-glu. Cy-3-glu presents the protective role against oxidative stress induced by AA in MDA-MB-231 cells., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Neo-formed compounds (NFCs) are commonly found in all kinds of foods due to the complex reaction between components during processing. Acrylamide, benzo(a)pyrene and heterocyclic aromatic amines are the main types of NFCs in foods enriched with carbohydrate, fats and proteins, respectively. They have exhibited diverse toxicity, such as neurotoxicity, genotoxicity, potentially carcinogenic and reproductive toxicity. In recent years, various phytochemicals have been found to be effective in alleviation of their related toxicities both in vitro and in vivo . This review provides evidences on the protection roles of phytochemicals against the diverse toxicity induced by three NFCs. Moreover, the prevention mechanisms of phytochemicals are summarized. Three potential aspects involving excellent antioxidant activity, DNA protection and enzyme induction contribute to the successful protection mechanism. Meanwhile, the limitations from existing knowledge have been illustrated and the possible perspectives for the further study have also been considered. The information from this review would be useful to provide an easier and better way to improve human health when considering the possibility of using foods enriched with phytochemicals for prevention of the toxicity of exogenous pollutants. [ABSTRACT FROM AUTHOR]

[Display omitted] • Hyperspectral imaging effectively predicted acrylamide content in roasted coffee. • The visualization images of the acrylamide content in roasted coffee were obtained. • It is helpful for the large-scale detection of acrylamide content in roasted coffee in industries. Since it is carcinogenic to humans, the acrylamide content in heat-processed foods should be detected and controlled. This study investigated the spatial distribution and visualization of the acrylamide content in roasted coffee. First, hyperspectral images were collected, from which the spectral-pixel features were extracted. Besides partial least square (PLS), five wavelengths (888, 1123, 1456, 1636, and 1734 nm) based on the successive projections algorithm (SPA) were used to establish prediction models (multiple linear regression (MLR), CatBoost, and XgBoost). SPA-MLR presented the optimal outcome, with a prediction coefficient of determination (R p 2) and a root mean square error of prediction (RMSEP) of 0.81 and 35.90 μg/kg, respectively. The acrylamide content values for all pixels in the hyperspectral images were subsequently calculated using the prediction equation, thereby producing the spatial distribution and visualization images. The results demonstrated that hyperspectral imaging can effectively predict and visualize the acrylamide levels in roasted coffee. [ABSTRACT FROM AUTHOR]

Pu-erh ripened tea is produced through a unique microbial fermentation process from the sun-dried leaves of large-leaf tea species ( Camellia sinensis (Linn.) var. assamica (Masters) Kitamura) in Yunnan province of China. In this study, the changes of amino acid profiles during fermentation of Pu-erh tea were investigated, based on the improved HPLC–UV method with PITC pre-column derivatization for the simultaneous determination of twenty free amino acids. Results showed that aspartic acid, glutamic acid, arginine, alanine, theanine and tyrosine were the major amino acids in tea samples. Fermentation significantly influenced on the amino acid profiles. The total free amino acid contents significantly decreased during fermentation ( p < 0.05). Meanwhile, low amount of acrylamide were detected. Its concentration increased after 7-days’ fermentation and then decreased gradually. The results provided the useful information for the manipulation of fermentation process according to the changes of amino acids and acrylamide contents in Pu-erh ripened tea. [ABSTRACT FROM AUTHOR]