Nowadays acrylamide is known not only as synthetic material used in industry, but also as carcinogenic, cyto- and genotoxic compound which forms during heat-induced process (due to Maillard reaction) mostly in foodstuff such as potato, bakery, plant derivatives products and coffee. The International Agency for Research on Cancer in 1994 declared acrylamide as a probable carcinogenic agent in humans. After metabolic process, acrylamide is distributed to all organs and tissues in human body. Acrylamide is classified as human neurotoxin, because this effect was observed in humans occupationally exposed to this compound. Acrylamide was found to cause apoptosis by mitochondrial dysfunction. Methods of acrylamide inactivation by microorganisms and bioactive diet compounds have also been reviewed. Moreover, there is still deficit of the European Union legal regulation concerning acrylamide mitigation strategies in food. Regulation 2017/2158 from 20 November 2017 is a step in the right direction when it comes to ensuring food safety and maximum levels of acrylamide in foodstuffs, however when exceeding those, it should result in elimination of such food from the market.

Acrylamide in human diet, its metabolism, toxicity, inactivation and the associated European Union legal regulations in food industry.

Abstrac There has long been a great concern with growing anthropogenic contaminants and their ecological and toxicological effects on living organisms and the surrounding environment for decades. Metabolomics, a functional readout of cellular activity, can capture organismal responses to various contaminant-related stressors, acquiring direct signatures to illustrate the environmental behaviours of anthropogenic contaminants better. This review entails the application of metabolomics to profile metabolic responses of environmental organisms, e.g. animals (rodents, fish, crustacean and earthworms) and microorganisms (bacteria, yeast and microalgae) to different anthropogenic contaminants, including heavy metals, nanomaterials, pesticides, pharmaceutical and personal products, persistent organic pollutants, and assesses their ecotoxicological impacts with regard to literature published in the recent five years. Contaminant-induced metabolism alteration and up/down-regulation of metabolic pathways are revealed in typical organisms. The obtained insights of variations in global metabolism provide a distinct understanding of how anthropogenic contaminants exert influences on specific metabolic pathways on living organisms. Thus with a novel ecotechnique of environmental metabolomics, risk assessments of anthropogenic contaminants are profoundly demonstrated.

Ecological and toxicological assessments of anthropogenic contaminants based on environmental metabolomics

The increased incidence of non-communicable human diseases may be attributed, at least partially, to exposures to toxic chemicals such as persistent organic pollutants (POPs), air pollutants and heavy metals. Given the high mortality and morbidity of pollutant exposure associated diseases, a better understanding of the related mechanisms of toxicity and impacts on the endogenous host metabolism are needed. The metabolome represents the collection of the intermediates and end products of cellular processes, and is the most proximal reporter of the body's response to environmental exposures and pathological processes. Metabolomics is a powerful tool for studying how organisms interact with their environment and how these interactions shape diseases related to pollutant exposure. This mini review discusses potential biological mechanisms that link pollutant exposure to metabolic disturbances and chronic human diseases, with a focus on recent studies that demonstrate the application of metabolomics as a tool to elucidate biochemical modes of actions of various environmental pollutants. In addition, classes of metabolites that have been shown to be modulated by multiple environmental pollutants will be discussed with an emphasis on their use as potential early biomarkers of disease risks. Taken together, metabolomics is a useful and versatile tool for characterizing the disease risks and mechanisms associated with various environmental pollutants.

Application of metabolomics to characterize environmental pollutant toxicity and disease risks.

Serum metabolomics analysis of mice that received repeated airway exposure to a water-soluble PM2.5 extract

The presented study was performed to verify whether rutin and/or quercetin can inhibit liver injury induced by doxorubicin (DXR) in male Wistar rats. In this study, male Wistar rats were treated via the oral route with rutin and quercetin (50 mg/kg) either alone or in combination every other day for five weeks concomitant with receiving intraperitoneal DXR (2 mg/kg) two times a week for five successive weeks. Quercetin, rutin, and their combination significantly improved the deteriorated serum AST, ALT, and ALP activities and total bilirubin level, as well as albumin, AFP, and CA 19.9 levels in DXR-injected rats. Treatments of the DXR-injected group with quercetin and rutin prevented the elevation in liver lipid peroxidation and the reduction in superoxide dismutase, glutathione-S-transferase and glutathione peroxidase activities, and glutathione content. Treatments with quercetin and rutin significantly repressed the elevated expression of liver p53 and TNF-α and enhanced Nrf2 expression. Furthermore, the treatments significantly reduced DXR-induced liver histological changes. In conclusion, rutin and quercetin either alone or in combination may have potential preventive effects against DXR-induced hepatotoxicity through inhibiting oxidative stress, inflammation, and apoptosis as well as modulating the Nrf2 expression.

/pdf/rutin-and-quercetin-counter-doxorubicin-induced-liver-2d6dloho.pdf

Rutin and Quercetin Counter Doxorubicin-Induced Liver Toxicity in Wistar Rats via Their Modulatory Effects on Inflammation, Oxidative Stress, Apoptosis, and Nrf2

This study aimed to assess the toxic effect of chronic exposure to cadmium through a metabolomic approach based on ultra-performance liquid chromatography/mass spectrometry (UPLC–MS). Forty male Sprague–Dawley rats were randomly assigned to the following groups: control, low-dose cadmium chloride (CdCl2) (0.13 mg/kg body weight (bw)), middle-dose CdCl2 (0.8/kg bw), and high-dose CdCl2 (4.9 mg/kg bw). The rats continuously received CdCl2 via drinking water for 24 weeks. Rat urine samples were then collected at different time points to establish the metabolomic profiles. Multiple statistical analyses with principal component analysis and partial least squares–discriminant analysis were used to investigate the metabolomic profile changes in the urine samples and screen for potential biomarkers. Thirteen metabolites were identified from the metabolomic profiles of rat urine after treatment. Compared with the control group, the treated groups showed significantly increased intensities of phenylacetylglycine, guanidinosuccinic acid, 4-pyridoxic acid, 4-aminohippuric acid, 4-guanidinobutanoic acid, allantoic acid, dopamine, LysoPC(18:2(9Z,12Z)), and L-urobilinogen. By contrast, the intensities of creatinine, L-carnitine, taurine, and pantothenic acid in the treated groups were significantly decreased. These results indicated that Cd disrupts energy and lipid metabolism. Meanwhile, Cd causes liver and kidney damage via induction of oxidative stress; serum biochemical indices (e.g., creatinine and urea nitrogen) also support the aforementioned results.

Metabolomic analysis of the toxic effect of chronic exposure of cadmium on rat urine.

1. This study evaluated the toxicity of chronic exposure to low-level cadmium (Cd) in rats using ultra-performance liquid chromatography–mass spectrometry (UPLC–MS). Forty male Sprague–Dawley rats were randomly assigned to four groups, namely, the control group, low-dose group (0.13 mg/kg·bw), middle-dose group (0.8 mg/kg·bw) and high-dose group (4.89 mg/kg·bw). The rats continuously received CdCl2 via drinking water for 24 weeks. Serum samples were collected for metabonomics analysis. The data generated from the UPLC–MS was analysed using principal components analysis (PCA) and partial least-squares discriminant analysis (PLS-DA). PLS-DA model with satisfactory explanatory and predictive ability is capable of discriminating the treatment groups from the control group.2. Finally, the 10 metabolites were identified and showed significant changes in some treatment groups compared with that in the control group (p < 0.0167 or p < 0.003). Exposure to Cd resulted in increased intensities of lysophospha...

Metabonomics analysis of serum from rats given long-term and low-level cadmium by ultra-performance liquid chromatography–mass spectrometry

This research aimed at analysing the protective effect of quercetin against the nephrotoxicity of acrylamide (AA) using metabonomics technology. Rats were randomly divided into six groups, including the control group, AA-treated group (5 mg per kg bw per d), two dosages of quercetin-treated groups (10 and 50 mg per kg bw per d) and two dosages of quercetin plus AA-treated groups. Quercetin and AA were administered to rats daily via gavage and drinking water, respectively. After a 16 week treatment, the kidneys were collected for metabonomics analysis. A total of 14 metabolites were identified in positive and negative modes via the metabonomics profiles of kidney tissues. Compared with the control group, the intensities of uric acid, 6,8-dihydroxypurine, hypoxanthine, guanosine, L-phenylalanine, succinyladenosine, tryptophan, lysophosphatidylcholines (LPC(16 : 0), LPC(18 : 1(9z)), LPC(18 : 2(9z,12z))) and inosine in the AA-treated group were significantly increased (p < 0.01); and the intensities of L-acetylcarnitine, 2-phenylacetamide and pantothenic acid in the AA-treated group were decreased (p < 0.01). However, the intensities of the previously mentioned metabolites had opposite trends in the high-dose quercetin (50 mg per kg bw per d) plus AA-treated groups (p < 0.01 or p < 0.05). The results showed that quercetin exerted protective effects on AA-induced nephrotoxicity by enhancing the antioxidant defence system of the body and regulating phospholipid, energy and amino acid metabolism.

Metabonomics analysis of quercetin against the nephrotoxicity of acrylamide in rats.

This research aims to determine whether quercetin has protective effects against the toxicity of acrylamide (AA) using metabonomic technology. Randomly, the rats were assigned into a control group, AA treatment group, quercetin treatment group and quercetin plus AA treatment group. Quercetin and AA were administered to rats daily via gavage and drinking water for 16 weeks, respectively. To detect the metabonomic profiles of urine, ultra-performance liquid chromatography/mass spectrometry was used. A total of 15 metabolites, including biomarkers of AA exposure (GAMA, AAMA, and iso-AAMA) and quercetin exposure (quercetin and isorhamnetin), were identified. In comparison with the control group, the intensities of GAMA, AAMA, iso-AAMA, 1-salicylate glucuronide, vinylacetylglycine, PE(20:1(11Z)/14:0), 7-ketodeoxycholic acid, cysteic acid, p-cresol sulfate, and l-cysteine in the AA-treated group were statistically significantly increased (p < 0.01), and the intensities of 2-indolecarboxylic acid, 3-acetamidobutanal, and kynurenic acid in the AA-treated group were statistically significantly decreased (p < 0.01). The above-mentioned metabolites were significantly ameliorated in the quercetin (50 mg per kg bw) plus AA-treated group compared with the AA-treated group (p < 0.01 or p < 0.05). However, the intensities of these metabolites in the quercetin (50 mg per kg bw) plus AA-treated groups were still significantly different from those of the control group (p < 0.01 or p < 0.05). The above results suggest that quercetin has a partial protective effect on AA-induced toxicity. The protective effects include regulation of fatty acid metabolism and amino acid metabolism and enhancing the antioxidant defense system.

Metabonomic analysis of quercetin against the toxicity of acrylamide in rat urine.

This study assessed the effects of long-term, low-dose acrylamide (AA) administration in rats using ultra-performance liquid chromatography-mass spectrometry. Forty male Wistar rats were randomly divided into the following four groups: control, low-dose AA (0.2 mg/kg BW), middle-dose AA (1 mg/kg BW), and high-dose AA (5 mg/kg BW). AA was administered to rats via drinking water ad libitum. After 16-week treatment, rat serum was collected for metabonomic analysis. Biochemical tests were further conducted to verify metabolic alterations. Eleven metabolites were identified with significant changes in intensities (increased or reduced) as a result of treatment. These metabolites included citric acid, pantothenic acid, isobutyryl-l-carnitine, eicosapentaenoic acid, docosahexaenoic acid, sphingosine 1-phosphate, LysoPC(20:4), LysoPC(22:6), LysoPE(20:3), undecanedioic acid, and dodecanedioic acid. Results indicate that chronic exposure to AA at no observed adverse effect level does not exert a toxic effect on rats at the body metabolism level. AA disturbed the metabolism of lipids and energy, affected the nervous system of rats, and induced oxidative stress and liver dysfunction.

Metabonomic analysis of toxic action of long-term low-level exposure to acrylamide in rat serum.

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