The impact of acrylamide (AA) on microorganisms is still not clearly understood as AA has not induced mutations in bacteria, but its epoxide analog has been reported to be mutagenic in Salmonella strains. The aim of the study was to evaluate whether AA could influence the growth and viability of beneficial intestinal bacteria. The impact of AA at concentrations of 0-100 µg/mL on lactic acid bacteria (LAB) was examined. Bacterial growth was evaluated by the culture method, while the percentage of alive, injured, and dead bacteria was assessed by flow cytometry after 24 h and 48 h of incubation. We demonstrated that acrylamide could influence the viability of the LAB, but its impact depended on both the AA concentration and the bacterial species. The viability of probiotic strain Lactobacillus acidophilus LA-5 increased while that of Lactobacillus plantarum decreased; Lactobacillus brevis was less sensitive. Moreover, AA influenced the morphology of L. plantarum, probably by blocking cell separation during division. We concluded that acrylamide present in food could modulate the viability of LAB and, therefore, could influence their activity in food products or, after colonization, in the human intestine.

The aims of this study are to investigate the effect of acrylamide on the level of proinflammatory cytokines in the blood of acrylamide-treated rats and to find the modulatory impact of probiotics on those cytokines. Thirty-two rats were divided into four groups: rats which received 20 mg acrylamide, acrylamide with 20 mg probiotics, acrylamide with 200 mg probiotics, and standard water and food (groups 1-4, respectively). The serum levels of cytokines were measured on days 0, 15, and 30. Group 1 showed an increased serum level of IL-1β, IL-6, and TNF-α after 15 days, and they decreased in day 30. Serum IL-6 level was significantly decreased on days 15 and 30 in rats in group 2 compared to the controls. TNF-α and IL-1β levels were not statistically different after treated with probiotics. The exposure of rats to acrylamide led to increased systemic inflammation as evidenced by higher levels of proinflammatory cytokines, and probiotics can modulate this inflammation.

A dataset of manufacturers' measurements of acrylamide levels in 40,455 samples of fresh sliced potato crisps from 20 European countries for years 2002 to 2011 was compiled. This dataset is by far the largest ever compiled relating to acrylamide levels in potato crisps. Analysis of variance was applied to the data and showed a clear, significant downward trend for mean levels of acrylamide, from 763 ± 91.1 ng g⁻¹ (parts per billion) in 2002 to 358 ± 2.5 ng g⁻¹ in 2011; this was a decrease of 53% ± 13.5%. The yearly 95th quantile values were also subject to a clear downward trend. The effect of seasonality arising from the influence of potato storage on acrylamide levels was evident, with acrylamide in the first 6 months of the year being significantly higher than in the second 6 months. The proportion of samples containing acrylamide at a level above the indicative value of 1000 ng g⁻¹ for potato crisps introduced by the European Commission in 2011 fell from 23.8% in 2002 to 3.2% in 2011. Nevertheless, even in 2011, a small proportion of samples still contained high levels of acrylamide, with 0.2% exceeding 2000 ng g⁻¹.

Branched poly(N-isopropylacrylamide) was functionalized with Amphotericin B (AmB) at the chain ends to produce an antifungal material. The polymer showed antifungal properties against AmB-sensitive strains of Candida albicans, Fusarium keratoplasticum and Aspergillus flavus (minimal inhibitory concentration ranged from 5 to 500 µg ml-1) but was not effective against an AmB resistant strain of C. albicans nor against Candida tropicalis. The polymer end groups bound to the AmB target, ergosterol, and the fluorescence spectrum of a dye used as a solvatochromic probe, Nile red, was blue shifted indicating that segments of the polymer became desolvated on binding. The polymer was less toxic to corneal and renal epithelial cells and explanted corneal tissue than the free drug. Also, the polymer did not induce reactive oxygen species release from peripheral blood mononuclear cells, nor did it cause a substantial release of the proinflammatory cytokines, tumour necrosis factor-α and interleukin-1β (at 0.5 mg ml-1).

Thermal processes induce the formation of undesired toxic components, such as acrylamide (AA), which has been shown to induce brain toxicity in humans and classified as Group 2A by the International Agency of Research in Cancer (IARC), as well as some mycotoxins. AA and mycotoxins' toxicity is studied in several in vitro models, including the neuroblastoma cell line model SH-SY5Y cells. Both AA and mycotoxins occur together in the same food matrix cereal base (bread, pasta, potatoes, coffee roasting, etc.). Therefore, the goal of this review is to deepen the knowledge about the neurological effects that AA and mycotoxins can induce on the in vitro model SH-SY5Y and its mechanism of action (MoA) focusing on the experimental assays reported in publications of the last 10 years. The analysis of the latest publications shows that most of them are focused on cytotoxicity, apoptosis, and alteration in protein expression, while others are interested in oxidative stress, axonopathy, and the disruption of neurite outgrowth. While both AA and mycotoxins have been studied in SH-SY5Y cells separately, the mixture of them is starting to draw the interest of the scientific community. This highlights a new and interesting field to explore due to the findings reported in several publications that can be compared and the implications in human health that both could cause. In relation to the assays used, the most employed were the MTT, axonopathy, and qPCR assays. The concentration dose range studied was 0.1-10 mM for AA and 2 fM to 200 µM depending on the toxicity and time of exposure for mycotoxins. A healthy and varied diet allows the incorporation of a large family of bioactive compounds that can mitigate the toxic effects associated with contaminants present in food. Although this has been reported in some publications for mycotoxins, there is still a big gap for AA which evidences that more investigations are needed to better explore the risks for human health when exposed to AA and mycotoxins.

Acrylamide, a potential carcinogen, exists in carbohydrate-rich foods cooked at a high temperature. It has been reported that acrylamide can cause DNA damage and cytotoxicity. The present study aimed to investigate the potential mechanism of human hepatocarcinoma HepG2 cell proliferation induced by acrylamide and to explore the antagonistic effects of a natural polyphenol curcumin against acrylamide via miR-21. The results indicated that acrylamide (≤100 μmol/L) significantly increased HepG2 cell proliferation and miR-21 expression. In addition, acrylamide reduced the PTEN expression in protein level, while induced the expressions of p-AKT, EGFR and cyclin D1. The PI3K/AKT inhibitor decreased p-AKT protein expression and inhibited the proliferation of HepG2 cells. In addition, curcumin effectively reduced acrylamide-induced HepG2 cell proliferation and induced apoptosis through the expression of miR-21. In conclusion, the results showed that acrylamide increased HepG2 cell proliferation via upregulating miR-21 expression, which may be a new target for the treatment and prevention of cancer.

Acrylamide (ACR), a recognized neurotoxicant in humans and experimental animals, is widely used in industry and in food generated through Maillard reaction. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator of the cellular defense system and activates antioxidants and cytoprotective genes. The exact roles of Nrf2 in environmental electrophile-induced neurotoxicity is poorly understood. The aim of this study was to determine the roles of Nrf2 in ACR-induced neurotoxicity including degeneration of monoaminergic axons and sensorimotor dysfunction. Male 10-week-old C57BL/6JJcl Nrf2-knockout mice and wild type (WT) counterparts were each divided into four groups of 12 and provided with drinking water containing acrylamide at 0, 67, 110 or 200 ppm for four weeks. The effects of acrylamide were examined by landing foot spread test, immunohistochemistry for noradrenaline (NA) and serotonin (5-HT)-containing axons and Iba1-positive microglia in the prefrontal cortex as well as quantitative real-time polymerase chain reaction (qRT-PCR) on antioxidant, proinflammatory and anti-inflammatory genes in the prefrontal cortex. Relative to the wild type, exposure of Nrf2-knockout mice to acrylamide increased hindlimb splay length, microglial area and process length as well as decreasing the density of NA and 5-HT-immunoreactive axons to a greater extent. Moreover, deletion of Nrf2 gene suppressed acrylamide-induced mRNA upregulation of Nrf2-antioxidants, NAD(P): quinone oxidoreductase 1 (NQO1), superoxide dismutase-1 (SOD-1) and heme oxygenase-1 (HO-1) as well as anti-inflammatory markers such as, arginase-1 (Arg1), found in the inflammatory zone-1 (Fizz1), chitinase-like 3 (Chi3l3), interleukin-4 receptor alpha (IL-4Rα), cluster of differentiation  206 (CD206) and transforming growth factor beta-1 (TGFβ1) while enhancing acrylamide-induced upregulation of pro-inflammatory cytokines, interleukin-1 beta (IL-1β), tumor necrosis-alpha (TNF-α) and inducible nitric oxide synthase (iNOS) in the prefrontal cortex. The results demonstrate susceptibility of mice lacking the Nrf2 gene to acrylamide-induced neurotoxicity and neuroinflammation with the activation of microglia. Moreover, the results suggest the role of Nrf2 not only in induction of antioxidant gene expression, but also in suppression of proinflammatory cytokine gene expression.

Drying and roasting are conventional processes in the nut industry. However, roasting as an important procedure in nuts manufacturing may cause some physicochemical changes in nuts. Acrylamide is one of these chemical compounds that is formed due to the roasting process. Acrylamide is known as a neurotoxicant, carcinogen, and reproductive toxicant. In this study, raw and salted pistachios were roasted under three conditions including hot-air, infrared (IR), and microwave methods. Then, 80 pistachio kernels were analyzed by ultra-high-performance liquid chromatography. The results showed that all samples contained different ranges of acrylamide between 57 ± 0.86 and 851 ± 2.8 μg/kg. Besides, raw pistachios and sun-dried pistachios also contained acrylamide, with the amount of 57 ± 0.86 and 93 ± 1.07 μg/kg, respectively. The highest acrylamide amount was found in raw pistachio (unsalted) roasted by IR method, while lower acrylamide amount observed in the microwave method. The amount of acrylamide in salted and roasted pistachios was less than just roasted pistachios under the same conditions. Finally, in all the treatments, increasing temperature, time, voltage, and power lead to an increase in acrylamide levels. The results showed that acrylamide in the roasted pistachios may cause health problems. This study presents a novel investigation in the effects of roasting conditions (temperature, power, voltage, and time) on acrylamide content in pistachios.

The aim of this study was to investigate the effects of acrylamide (AA) on fracture healing histologically, biochemically, and radiologically in a rat femur fracture model.

Two series of olmutinib derivatives containing an acrylamide moiety were designed and synthesized, and their IC50 values against cancer cell lines (A549, H1975, NCI-H460, LO2, and MCF-7) were evaluated. Most of the compounds exhibited moderate cytotoxic activity against the five cancer cell lines. The most promising compound, H10, showed not only excellent activity against EGFR kinase but also positive biological activity against PI3K kinase. The structure-activity relationship (SAR) suggested that the introduction of dimethylamine scaffolds with smaller spatial structures was more favorable for antitumor activity. Additionally, the substitution of different acrylamide side chains had different effects on the activity of compounds. Generally, compounds H7 and H10 were confirmed as promising antitumor agents.

Acrylamide is an industrial chemical which has toxic effects on reproduction. In this study, we investigated whether acrylamide administered prenatally can induce follicular atresia in the newborn guinea pig ovary. Another aim was to describe the localization of vimentin filaments and determine their participation in atresia. After prenatal acrylamide treatment, the pool of primordial and primary follicles was significantly reduced. The number of caspase 3 and TUNEL positive oocytes increased compared to the control group. There were no differences in Lamp1 (autophagy marker) staining. A vimentin immunosignal was present in the granulosa cells of primordial, primary and secondary follicles. Interestingly, in contrast to the control group, the oocytes from all follicles in the ACR-treated females were negative for vimentin. These data suggest that prenatal exposure to acrylamide reduced the number of ovarian follicles by inducing follicular atresia mediated by oocyte apoptosis. Acrylamide-induced apoptosis may be associated with destruction of vimentin filaments.

Acrylamide (AA) is a carcinogenic compound that causes severe reproductive impairments and represents a high environmental risk factor. Thymoquinone (TQ) has a unique antioxidant activity and has been widely used as a protective agent against various types of toxicity.

Acrylamide (ACR) is a toxic chemical agent that can induce hepatotoxicity through different mechanisms including oxidative stress and apoptosis. Amifostine is an important hepatoprotective and anti-oxidant compound. In this research, the hepatoprotective effect of amifostine on ACR-induced hepatotoxicity in rats has been investigated.

In this work, poly(N-isopropyl acrylamide-co-acrylamide) [P(NIPAAm-co-AAm)] nanogels were modified by hydrolysis above the lower critical solution temperature (LCST) to localize carboxylic acid functional groups at the surface (surface hydrolysis). PNIPAAm copolymerized with 15% and 20% nominal AAm in the feed were prepared and compared to equivalent hydrogels with acrylic acid. The effect and extent of surface hydrolysis was confirmed by potentiometric titration and zeta potential. These surface modified nanogels were then modified with primary amine functionalized PEG chains. Surface hydrolysis-mediated PEGylation had little effect on the swelling response of the nanogels, while also preventing adsorption of model proteins in physiological relevant conditions. While both 15% and 20% AAm gels both decreased protein adsorption, only the 20% AAm gels resulted in fully preventing protein adsorption. The results presented here point to surface hydrolysis as a new route to passivate nanogels for use in vivo.

Male wistar rats (weighting 160-180 g) were divided into six groups of six animals per group. Groups A and F served as control. Groups B, C, D, and E received acrylamide at 20 mg/kg body weight for 28 days and groups C and E received additionally vitamin E (50 IU/kg body weight) for 1 to 28 days and 29 to 42 days of experiment, respectively. The animals from groups A, B, and C were sacrificed on day 28 of experiment and from groups D, E, and F on day 42 of experiment, respectively. The FOB (Functional Observational Battery) and histopathological changes were investigated at the end of 4(th) week and 6(th) week. FOB at the end of 4(th) week, of rats given acrylamide alone, or in combination with vitamin E, revealed a significant change in CNS, neuromuscular, and autonomic domains. A marked decrease in grip strength was recorded. A significant increase in foot splay, reduction in width and angle of sequential stride was noticed. Degenerative changes, necrosis, congestion, and kupffer cell proliferation in liver while vacuolar degenerative changes in tubular epithelium, coagulative necrosis, and hemorrhages in kidney were constant findings in acrylamide intoxicated rats. Neuronal degeneration, severe gliosis, congestion were found in brain. Spinal cord revealed demyelination. Acute microscopic softening of lumbar cord, bilateral necrosis with malacia and liquefaction of white matter, and loss of myelin from grey matter were seen. In the recovery period, vitamin E-treated rats revealed improvement in remyelination of spinal cord. In brain mild gliosis was seen. Thus, it appears that vitamin E is not able to protect them from acrylamide toxicity during active feeding, but after cessation of acrylamide feeding treatment with vitamin E revealed faster recovery as compared to the non-treated group.

The current study aimed to evaluate the neuroprotective effect of exogenous melatonin against acrylamide (ACR)-induced oxidative stress and inflammatory and apoptotic responses in the brain tissues in pinealectomized rats (PINX). ACR is a toxic chemical carcinogen that occurs owing to the preparation of carbohydrate-rich foods at high temperatures or other thermal processes. The rats who underwent pinealectomy and sham pinealectomy were exposed to ACR (25 mg/kg b.w., orally) alone or with exogenous melatonin (10 mg/kg b.w., i.p.) for 21 consecutive days. Alterations of brain oxidant/antioxidant status, dopamine (DA), Brain-Derived Neurotropic Factor (BDNF) inflammatory mediator and apoptosis during exposure to ACR in pinealectomized rats were more than without pinealectomized rats. Histopathological changes were more in brain tissue of pinealectomized rats after ACR administration. Exogenous melatonin treatment in ACR -exposed rats following pinealectomy increased the activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT) and improved brain total antioxidant status (TAS) compared to PINX+ACR. Moreover, melatonin suppressed lipid peroxidation, inflammatory pathways and apoptosis in ACR-intoxicated brain tissues. In addition, after exposure to ACR on pinealectomized rats, melatonin treatment ameliorated BDNF and DA levels in brain tissues. Furthermore, exogenous melatonin intervention in ACR-intoxicated rats significantly rescued the architecture of neuronal tissues. In summary, the present study, for the first time, suggested that exogenous melatonin treatment could reduce oxidative damage by increasing the activities of antioxidant enzymes, inhibiting lipid peroxidation and inflammation, and improving histopathological alterations in the brain tissue of pinealectomized rats after ACR administration.

Acrylamide (ACR), which is formed during the Maillard reaction, is used in various industrial processes. ACR accumulation in humans and laboratory animals results in genotoxicity, carcinogenicity, neurotoxicity, and reproductive toxicity. In this study, we investigated the mechanisms by which ACR may induce vasorelaxation and neuromuscular toxicity. Vasorelaxation was studied using an isolated rat aortic ring model. The aortic rings were divided into the following groups: with or without endothelium, with nitric oxide synthase (NOS) inhibition, with acetylcholine receptor inhibition, and with extracellular calcium inhibition. Changes in tension were used to indicate vasorelaxation. Neuromuscular toxicity was assessed using a phrenic nerve-diaphragm model. Changes in muscle contraction stimulated by the phrenic nerve were used to indicate neuromuscular toxicity. ACR induced the vasorelaxation of phenylephrine-precontracted aortic rings, which could be significantly attenuated by NOS inhibitors. The results of the phrenic nerve-diaphragm experiments revealed that ACR reduced muscle stimulation and contraction through nicotinic acetylcholine receptor (AChR). ACR-induced vasotoxicity was regulated by NOS through the aortic endothelium. Nicotinic AChR regulated ACR-induced neuromuscular blockage.

Acrylamide (AA) is a food contaminant in thermally processed products that is object of tight control. A simple and easy-to-apply methodology for routine monitoring of AA levels in food products could allow producers to be players in the control of their own products. In this work, a simple methodology for AA quantification without derivatization was developed for biscuits, for which the benchmark levels recommended by EFSA are 350 µg/kg, and 150 µg/kg for biscuits for infants and young children. Headspace-solid phase microextraction (HS-SPME) was used in 120 mL screwed-cap vials with a carboxen/polydimetylsiloxane fiber, 4 g of biscuits, and 10 mL of water during 15 min at room temperature under stirring. The addition of 30 mL of propanol under stirring during 15 min at room temperature and 15 min at 60 °C was used to promote AA transfer to the headspace. The fiber exposure was 45 min. A gas chromatography-mass spectrometry analysis allowed to obtain an external calibration curve at m/z 71, with linearity R2 > 0.99 and precision RSD < 9%. The detection and quantification limits were 27.4 µg/kg and 91.5 µg/kg, respectively. The methodology was successfully used in biscuits with lower AA amount, where mitigation strategies (asparaginase or pectate) were applied.

We show the use of 5'-Acrydite oligonucleotides to copolymerize single-cell DNA or RNA into balls of acrylamide gel (BAGs). Combining this step with split-and-pool techniques for creating barcodes yields a method with advantages in cost and scalability, depth of coverage, ease of operation, minimal cross-contamination, and efficient use of samples. We perform DNA copy number profiling on mixtures of cell lines, nuclei from frozen prostate tumors, and biopsy washes. As applied to RNA, the method has high capture efficiency of transcripts and sufficient consistency to clearly distinguish the expression patterns of cell lines and individual nuclei from neurons dissected from the mouse brain. By using varietal tags (UMIs) to achieve sequence error correction, we show extremely low levels of cross-contamination by tracking source-specific SNVs. The method is readily modifiable, and we will discuss its adaptability and diverse applications.

Acrylamide (ACR) has been classified as a neurotoxic agent in animals and humans. Melatonin (MT) has been shown to be potentially effective in preventing oxidative stress related neurodegenerative disorders. In this study, whether MT exerted a protective effect against ACR-induced oxidative damage was investigated. Results in cells showed that reactive oxygen species (ROS) and malondialdehyde (MDA) significantly increased after ACR treatment for 24 h. MT preconditioning or cotreatment with ACR reduced ROS and MDA products, whereas the inhibitory effect of MT on oxidant generation was attenuated by blocking the MT receptor. Increased DNA fragmentation caused by ACR was significantly decreased by MT coadministration. In vivo, rats at 40 mg/kg/day ACR by gavage for 12 days showed weight loss and gait abnormality, Purkinje cell nuclear condensation, and DNA damage in rat cerebellum. MT (i.p) cotreatment with ACR not only recovered weight and gait of rats, but also decreased nuclear condensation and DNA damage in rat cerebellum. Using MDA generation, glutathione (GSH) level, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities in rat cerebellum as indicators, MT alleviated ACR-induced lipid peroxidation and depressed antioxidant capacity. Our results suggest that MT effectively prevents oxidative damage induced by ACR.