A systematic review: on the mercaptoacid metabolites of acrylamide, N-acetyl-S-(2-carbamoylethyl)-L-cysteine.

Acrylamide is widely found in a variety of fried foods and cigarettes and is not only neurotoxic and carcinogenic, but also has many potential toxic effects. The current assessment of acrylamide intake through dietary questionnaires is confounded by a variety of factors, which poses limitations to safety assessment. In this review, we focus on the levels of AAMA, the urinary metabolite of acrylamide in humans, and its association with other diseases, and discuss the current research gaps in AAMA and the future needs. We reviewed a total of 25 studies from eight countries. In the general population, urinary AAMA levels were higher in smokers than in non-smokers, and higher in children than in adults; the highest levels of AAMA were found in the population from Spain, compared with the general population from other countries. In addition, AAMA is associated with several diseases, especially cardiovascular system diseases. Therefore, AAMA, as a biomarker of internal human exposure, can reflect acrylamide intake in the short term, which is of great significance for tracing acrylamide-containing foods and setting the allowable intake of acrylamide in foods.

Stimulating the expression of sphingosine kinase 1 (SphK1) is beneficial to reduce acrylamide-induced nerve cell damage.

Sphingosine kinase 1 (SphK1) is an important signaling molecule for cell proliferation and survival. However, the role of SphK1 in acrylamide (ACR)-induced nerve injury remains unclear. The purpose of this study was to investigate the role and potential mechanism of SphK1 in ACR-induced nerve injury. Liquid chromatography triple quadrupole tandem mass spectrometry (LC-MS/MS) and reverse transcription-quantitative PCR (RT-qPCR) were used to detect sphingosine 1-phosphate (S1P) content in serum and SphK1 content in whole blood from an occupational work group exposed to ACR compared to a non-exposed group. For in vitro experiments, SphK1 in human SH-SY5Y neuroblastoma cells was activated using SphK1-specific activator phorbol 12-myristate 13-acetate (PMA). Our research also utilized cell viability assays, flow cytometry, western blots, RT-qPCR and related protein detection to assess activity of the mitogen activated protein kinase (MAPK) signaling pathway. The results of the population study showed that the contents of SphK1 and S1P in the ACR-exposed occupational contact group were lower than in the non-exposed group. The results of in vitro experiments showed that expression of SphK1 decreased with the increase in ACR concentration. Activating SphK1 improved the survival rate of SH-SY5Y cells and decreased the apoptosis rate. Activating SphK1 in SH-SY5Y cells also regulated MAPK signaling, including enhancing the phosphorylation of extracellular signal-regulated protein kinases (ERK) and inhibiting the phosphorylation of c-Jun N-terminal kinase (JNK) and p38. These results suggest that activating SphK1 can protect against nerve cell damage caused by ACR.

Assessing the impacts of differential depositional settings and/or anthropogenic perturbations on sulfur and iron diagenesis in sediments of the Bohai Sea and North Yellow Sea.

Natural processes and human activities exert important impacts on elemental cycling in coastal sediments, which has not been well documented. Sediments in the Bohai Sea and North Yellow Sea were investigated to assess the impacts of the Yellow River inputs and/or anthropogenic perturbations on diagenesis of iron and sulfur. Labile iron (0.5 M HCl-extractable iron) in the sediments is low due to iron-poor nature of source materials. Dynamic regimes and low availability of labile organic carbon (OC) result in relatively low sulfide contents in deltaic sediments. However, low but continuous supply of labile OC exported from an anthropogenically impacted bay could substantially elevate sulfide burial in sediments near the bay. Neither offshore oil exploitations nor frequent algal blooms in the seas have detectable influences on iron and sulfur diagenesis in the sediments. The sediments are capable of quickly consuming porewater sulfide by reaction with reactive iron under the current conditions.

Platelet-rich plasma regulating the repair of ultraviolet B-induced acute tissue inflammation: adjusting macrophage polarization through the activin receptor-follistatin system.

Ultraviolet B (UVB) is one of the most common exogenous factors in skin aging, especially photoaging. Once a large amount of UVB accumulates within a short period of time, skin tissue can become inflamed. It has also been found in clinics that platelet-rich plasma (PRP) can promote wound repair; therefore, the aim of this study was to identify the mechanism by which PRP repairs UVB-induced skin photodamage. We used PRP of Sprague-Dawley rats with the two-spin technique in the established acute UVB radiation photodamage model and harvested the corresponding skin after 1, 7, and 28 d. Hematoxylin and eosin staining was used to observe tissue inflammation. We found that PRP reduces inflammation in the early stages of UVB-induced acute skin damage, and then promotes the proliferation of collagen in the middle and late stages. Moreover, PRP can stimulate Act A and M1 polarization in the early stage, while inhibiting activin A (Act A) and inducing M2 polarization in the middle and late stages. In conclusion, this study demonstrates that PRP plays an important regulatory role in helping reduce UVB-induced acute skin tissue inflammation by adjusting macrophage polarization, which alleviates skin inflammation and stimulates collagen regeneration.

The association of blood non-esterified fatty acid, saturated fatty acids, and polyunsaturated fatty acids levels with mild cognitive impairment in Chinese population aged 35-64 years: a cross-sectional study.

OBJECTIVES: The aim of this study was to explore the correlation between blood profiles and cognitive functions or mild cognitive impairment (MCI) in the Chinese population aged 35-64 years old. METHODS: A cross-sectional study was performed, which recruited 675 Chinese adults aged 35-64 years old from Beijing, China. Their cognitive performance was assessed with Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA), the serum lipids levels were measured by hexokinase method and colorimetric assay, and the plasma fatty acids profiles were analyzed by fast gas chromatography. RESULTS: Among the 675 participants, 84 (12.4%) had MCI. Age, years of education, saturated fatty acids (SFAs) and monounsaturated fatty acids (MUFAs) were associated with MMSE scores (all P < 0.05). Age, years of education, smoking, drinking, non-esterified fatty acids (NEFAs), SFAs, MUFAs, n-3 polyunsaturated fatty acids (n-3 PUFAs) and n-6/n-3 PUFAs were associated with MoCA scores (all P < 0.05). Increased age (P = 0.002) and smoking (P = 0.028) were positively associated with the prevalence of MCI, while educational level (P = 0.005) and alcohol drinking (P = 0.003) both were negatively correlated to the prevalence of MCI. Elevated serum NEFAs (P = 0.032), high plasma SFAs (P = 0.023), and excessive polyunsaturated fatty acids (PUFAs) levels (P = 0.033) were significantly associated with increased frequency of MCI. CONCLUSION: In the Chinese population aged 35-64 years, advanced age and cigarette smoking were risk factors of MCI, whereas higher educational level and alcohol drinking were protective factors for MCI. Excessive serum or plasma levels of NEFAs, SFAs and PUFAs were associated with an increased risk of MCI.

A urinary metabolomic study from subjects after long-term occupational exposure to low concentration acrylamide using UPLC-QTOF/MS.

Because long-term occupational exposure to low concentrations of acrylamide (ACR) has the potential to cause neurological damage, it is important to identify biomarkers that can be used to evaluate this risk. In the present study, urine metabolomics of the ACR-exposed and non-exposed groups to identify potential metabolites was carried out using ultra high performance liquid chromatography coupled with quadrupole time of flight mass spectrometry. Serum biochemical indexes of the exposed and non-exposed groups were also determined. Principal component analysis showed a differential separation between exposed group and non-exposed group and a total of 7 metabolites were identified in positive and negative ionization modes; Area under curve of anthranilic acid, ß-guanidinopropionic acid and mesobilirubinogen were 0.980, 0.843 and 0.801 respectively and these metabolites showed high sensitivity and specificity. The 13 biochemical indexes were divided into three classes based on physiological functions. Only biomarkers of dysregulated liver function including alanine aminotransferase, aspartic transaminase, total bilirubin, direct bilirubin and triglyceride were significantly higher in the exposed group than in the non-exposed group. This study identifies important related metabolic changes in the bodies of workers after long-term occupational exposure to low concentration ACR and suggests new biomarkers of nervous system injury caused by ACR. The study also provides a sound basis for exploring the biochemical mechanisms and metabolic pathways of nervous system toxicity caused by ACR.

Inflammation and Cognitive Function in Overweight and Obese Chinese Individuals.

BACKGROUND: The role(s) of inflammation in obesity-associated cognitive decline in overweight or obese populations is not completely understood. OBJECTIVE: To investigate the profile of plasma inflammatory cytokines in overweight and obese Chinese individuals and to assess the relationship between inflammation and cognitive function. METHODS: We evaluated the cognitive domains of 282 Chinese adults, aged 35 to 64 years, using the Mini-Mental State Examination (MMSE) and the Montreal Cognitive Assessment (MoCA). The participants were classified into three groups according to their body mass index. Inflammatory cytokines were determined by immune turbidimetric analysis and enzyme-linked immunosorbent assay. Data were analyzed using covariance and partial correlation analyses after adjusting for gender, age, education level, hypertension, and hyperlipemia. RESULTS: The total MoCA scores of the overweight and obese groups were significantly lower than that of the control group. The obese group displayed a significantly higher level of tumor necrosis factor-α than the overweight and control groups and a significantly higher level of transforming growth factor-ß than the control group. The overweight group displayed a significantly higher interleukin-4 level than the control and obese groups. After adjusting for confounding factors, however, we found no significant correlation between the level of plasma inflammatory cytokines and MMSE or MoCA total score. CONCLUSIONS: Compared to normal-weight Chinese participants, overweight and obese Chinese participants revealed significant differences in their inflammatory cytokines profile; however, the inflammatory cytokine levels did not correlate with the significantly lower cognitive scores observed in the overweight and obese groups.

5-aminolaevulinic acid-based photodynamic therapy inhibits ultraviolet B-induced skin photodamage.

To evaluate the photoprotective effect of 5-aminolaevulinic acid-based photodynamic therapy (ALA-PDT) on ultraviolet B (UVB)-induced skin photodamage. In vivo experiments, the dorsal skin of hairless mice were treated with ALA-PDT or saline-PDT, and then exposed to 180 mJ/m2 UVB. Results showed that the number of sunburn cells and apoptotic cells in the epidermis of ALA-PDT-treated groups at 24 h after UVB irradiation were significantly decreased compared with those in the UVB groups. And the removal rate of CPDs was obviously higher in ALA-PDT-treated groups. At 48 h, the number of Ki67 positive nuclei in ALA-PDT-UVB group was significantly fewer than that in UVB group. Further in vitro experiments, human keratinocyte cell line (HaCaT) cells of two groups (one treated with ALA-PDT, the other untreated), were exposed to 60 mJ/m2 UVB irradiation. We found 0.5 mmol/L of ALA and 3 J/cm2 of red light did not affect the vitality of cells, and could reduce UVB induced apoptosis, accelerate the clearance of CPDs, inhibit proliferation and activate p53. Thus, our data demonstrate that ALA-PDT pretreatment can induce a protective DNA damage response that protects skin cells from UVB-induced photodamages.

Acute myeloid leukemia with adult atopic dermatitis as first manifestation: A case report.

RATIONALE: Atopic dermatitis (AD) is a chronic recurrent dermatitis with profound itching, which could be the first manifestation of acute myeloid leukemia (AML). PATIENT CONCERNS: A 53-year-old Chinese man suffered a 6-month history of systemic symmetrical dermatitis, accompanied with profound itching. The patient was diagnosed as "eczema" in several hospitals, and the effects of antihistamine and topical steroid creams were poor. Nocturnal sleep was seriously affected by aggravating pruritus. Laboratorial examination was compatible with AML-M4. DIAGNOSES: AML-M4 with AD as first manifestation. INTERVENTIONS: IA regimen (ayninen and cytarabine) were used in induction chemotherapy. However, the patient did not achieve complete remission, and although his rash had improved, he still experienced severely general body itching. On the seventh day of chemotherapy, the patient entered the period of granulocyte deficiency with infection. OUTCOMES: The patient died due to septic shock after chemotherapy. LESSONS: The case strengthens the awareness of AML with AD as first manifestation and raises oncological vigilance in patients with AD refractory.

Diagenesis of sulfur, iron and phosphorus in sediments of an urban bay impacted by multiple anthropogenic perturbations.

Solid-phase speciation and porewater chemistry measured by the diffusive gradients in thin films (DGT) technique were used to understand the diagenesis of sulfur (S), iron (Fe), and phosphorus (P) in sediments of Jiaozhou Bay (China), which has been impacted by multiple anthropogenic perturbations. Despite water eutrophication, sediments of the bay are low in organic carbon and sulfide, but high in unsulfidized Fe(II). Dissimilatory iron reduction (DIR) prevails in sediments of the bay, and there is no evidence for responses of S and Fe diagenesis to the water eutrophication, which is largely attributable to unique depositional and diagenetic regimes in association with multiple anthropogenic perturbations. Good coupling of porewater Fe2+ and P in the porewaters suggests that P mobilization is driven mainly by DIR. Low Fe2+/P ratios in porewaters imply that oxidative regeneration of Fe oxides within the upper sediments is incapable of efficiently scavenging upward diffusing P.

NF-κB-mediated inflammatory damage is differentially affected in SH-SY5Y and C6 cells treated with 27-hydroxycholesterol.

Previous studies have demonstrated that 27-hydroxycholesterol (27-OHC), a cholesterol metabolite, was involved in the inflammatory process of Alzheimer's disease (AD). The present study aimed to investigate the 27-OHC-induced inflammatory damage to neurons and astrocytes and the underlying mechanism(s) accounting for this damage. Human neuroblastoma cells (SH-SY5Y cells) and rat glioma cells (C6 cells) were treated with vehicle or 27-OHC (5, 10, or 20 µM) for 24 hr. The levels of secreted interleukin-1ß (IL-1ß), interleukin-10 (IL-10), tumor necrosis factor alpha (TNF-α), and inducible nitric oxide synthase (iNOS) were determined by using an enzyme-linked immunosorbent assay (ELISA). Immunofluorescence staining was used to determine the cellular expression of toll-like receptor 4 (TLR4) and transforming growth factor-ß (TGF-ß). The mRNA and protein expression levels of nuclear factor-κB p65 (NF-κB p65), nuclear factor-κB p50 (NF-κB p50) and cyclooxygenase-2 (COX-2) in both SH-SY5Y and C6 cells were also detected by real-time PCR and Western blot, respectively. The results of this study showed that 27-OHC treatment increased secretion of TNF-α and iNOS and decreased secretion of IL-10, upregulated expression of TGF-ß, NF-κB p65 and p50, and downregulated expression of COX-2 in SH-SY5Y cells. In C6 cells, treatment with 27-OHC resulted in decreased secretion of IL-1ß, IL-10, TNF-α, and iNOS, and increased expression of TLR4 and TGF-ß. These results suggest that 27-OHC may cause inflammatory damage to neurons by activating the TGF-ß/NF-κB signaling pathway and to astrocytes by activating the TLR4/TGF-ß signaling, which results in the subsequent release of inflammatory cytokines.

A Near-Infrared Ratiometric Fluorescent Probe for Highly Selective Recognition and Bioimaging of Cysteine.

A benzothiazole-based near-infrared (NIR) ratiometric fluorescent probe (HBT-Cys) was developed for discriminating cysteine (Cys) from homocysteine (Hcy) and glutathione (GSH). The probe was designed by masking phenol group in the conjugated benzothiazole derivative with methacrylate group that could be selectively removed by Cys, and therefore an intramolecular charge transfer (ICT) fluorescence was switched on in the NIR region. In the absence of Cys, the probe exhibited a strong blue fluorescence emission at 431 nm, whereas a NIR fluorescence emission at 710 nm was significantly enhanced accompanied by a decrease of emission at 431 nm in the presence of Cys, allowing a ratiometric fluorescence detection of Cys. The fluorescence intensity ratio (I710nm/I431nm) showed a good linear relationship with Cys concentration of 1-40 µM with the detection limit of 0.5 µM. The sensing mechanism was explored based on MS experimental analysis and DFT theoretical calculation. Moreover, the fluorescent probe was successfully used for fluorescence bioimaging of Cys in living cells.

Sulfur, iron, and phosphorus geochemistry in an intertidal mudflat impacted by shellfish aquaculture.

Dissolved sulfide, iron (Fe), and phosphorus (P) in a mudflat (Jiaozhou Bay, China) impacted by shellfish aquaculture were measured in situ by the diffusive gradients in thin films (DGT) technique. A combination of porewater and solid-phase chemistry was used to characterize the interplays of Fe and S, and their control on P mobilization. Below the subsurface layer, two times higher fluxes (FDGT) of dissolved Fe2+ from porewater to the DGT device than those of dissolved sulfide indicate that dissimilatory iron reduction (DIR) dominates over sulfate reduction (SR). Spatial coupling of dissolved Fe2+ and P points to P release driven mainly by reductive dissolution of Fe. Much higher FDGT values of dissolved Fe2+ relative to dissolved P imply that oxidative regeneration of Fe oxides at the sediment-water interfaces (SWIs) of the transitional mudflat serves as an effective "iron curtain" of upward diffusing P. In the mudflat sediments of DIR prevalence, the accumulation of total reduced inorganic sulfur (TRIS) is dampened, which can largely ascribed to enhanced oxidative loss of sulfide and/or limited availability of degradable organic carbon in the dynamic regimes. Low dissolved sulfide concentrations in the sediments leave the majority of reactive Fe unsulfidized and thus abundantly available to buffer newly produced sulfide.

Application of cryoablation to treat peritoneal carcinomatosis from gastric cancer in a rabbit model.

OBJECTIVES: Peritoneal carcinomatosis is one of the causes of death in patients with advanced gastric cancer. We assumed that cryoablation could be applied as adjuvant therapy to control peritoneal carcinomatosis from gastric cancer. METHODS: We investigated the feasibility of cryoablation technique in rabbit model using a novel cryoablation balloon probe. The cryozones were harvested 7 days after cryoablation for histological evaluation. The levels of cytokines in the peripheral blood of rabbits were also detected. RESULTS: The results demonstrated that cryoablation could be applied in a rabbit model of peritoneal carcinomatosis from gastric cancer. Seven days after cryoablation, necrotic tumor cells could be seen the cryozones. Higher level of IFN-γ was observed. The level of IL-10 was decreased after treatment. CONCLUSIONS: The findings provided the experimental basis for the future application of cryoablation in patients.

Elaidic acid induces cell apoptosis through induction of ROS accumulation and endoplasmic reticulum stress in SH­SY5Y cells.

Elaidic acid, which is a major trans fatty acid, has been reported to be involved in neurotoxicity; however, the underlying molecular mechanisms underlying its neurotoxic effects remain largely unknown. Therefore, the present study aimed to investigate the potential mechanisms underlying elaidic acid­induced neuronal damage in vitro. The SH­SY5Y neuroblastoma cell line was used as a model in the present study. Following treatment of cells with various concentrations of elaidic acid or with vehicle for 24 h, cell viability was measured using the MTT assay. Mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) release were measured using flow cytometry. Cell apoptosis was measured by Annexin V­fluorescein isothiocyanate/propidium iodide double staining, and cellular redox status was determined using ELISA analysis. Furthermore, western blotting was used to detect the protein expression levels of factors associated with oxidative damage and components of the endoplasmic reticulum (ER) stress/unfolded protein response (UPR) signaling pathways. The results demonstrated that elaidic acid treatment inhibited cell viability, elevated cell apoptosis and resulted in a loss of MMP. In addition, elaidic acid induced marked alterations in cellular redox status. Treatment with high doses of elaidic acid treatment also enhanced the release of ROS, and upregulated lipid peroxide and malondialdehyde levels; however, it reduced superoxide dismutase and glutathione peroxidase activities. Furthermore, elaidic acid resulted in upregulation of nuclear factor erythroid 2­related factor 2 and downregulation of heme oxygenase 1, which are two key antioxidative factors. Elaidic acid treatment also induced or inhibited the expression of numerous ER stress/UPR­associated molecules. It induced glucose­regulated protein 78 (GRP78) expression, whereas the expression levels of activating transcription factor 4 (ATF4) and CCAAT/enhancer­binding protein homologous protein (CHOP) were upregulated and then downregulated following treatment with various doses of elaidic acid. These results indicated that elaidic acid inhibited SH­SY5Y cell growth and induced apoptosis by enhancing oxidative stress and activating the ER stress/UPR signaling pathway and the GRP78/ATF4/CHOP pathway.

In situ, high-resolution DGT measurements of dissolved sulfide, iron and phosphorus in sediments of the East China Sea: Insights into phosphorus mobilization and microbial iron reduction.

Dissolved sulfide, iron (Fe), and phosphorus (P) concentrations in sediments of the East China Sea were simultaneously measured in situ by diffusive gradients in thin films (DGT) technique. The results, by combination with solid-phase Fe speciation, were used to characterize the interplays of Fe, S and P. Diverse distributions of dissolved sulfide among the sites are attributable to highly dynamic diagenetic regimes and varying availability of labile organic carbon (OC). The DGT technique provided high-resolution evidence for coexistence of microbial iron reduction (MIR) and sulfate reduction in localized zones, and for Fe-coupled P mobilization. Measured Fe2+/P ratios suggest that Fe2+ reoxidatiion at the oxic zones can serve as an efficient scavenger of P. Empirical estimation indicates that MIR plays an important role in anaerobic OC mineralization in the sediments, which is a combined result of low availability of labile OC, high reactive Fe content, and unsteady diagenetic regimes.

Ethaselen: a novel organoselenium anticancer agent targeting thioredoxin reductase 1 reverses cisplatin resistance in drug-resistant K562 cells by inducing apoptosis.

It has been reported that Ethaselen shows inhibitory effects on thioredoxin reductase (TrxR) activity and human tumor cell growth. In order to find an efficient way to reverse cisplatin resistance, we investigated the reversal effects of Ethaselen on cisplatin resistance in K562/cisplatin (CDDP) cells that were established by pulse-inducing human erythrocyte leukemic cell line K562, which are fivefold more resistant to cisplatin compared to K562 cells. The morphology and growth showed that the adhesion of K562/CDDP further decreased while the cell volume increased. The proliferation of K562/CDDP is strengthened. The antitumor activities in vitro were assessed by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and combination index (CI), showing the significant synergic effects of cisplatin and Ethaselen. Focusing on apoptosis, a series of comparisons was made between K562 and K562/CDDP. Cisplatin induced higher reactive oxygen species (ROS) generation in K562 and subsequently induced the formation of mitochondrial permeability transition pores (PTPs). In addition, cisplatin increased the ratio of Bax to Bcl-2 in K562, which can influence the mitochondrial membrane permeability. PTP formation and mitochondrial membrane permeabilization eventually resulted in the release of cytochrome c and activation of the Caspase pathway. However, these effects were not clearly seen in K562/CDDP, which may be the reason for the acquired CDDP resistance. However, Ethaselen can induce a high level of ROS in K562/CDDP by TrxR activity inhibition and increased ratio of Bax to Bcl-2 in K562/CDDP by nuclear factor κB (NF-κB) suppression, which subsequently induces the release of cytochrome c in K562/CDDP. This response is partly responsible for the reversal of the cisplatin resistance in K562/CDDP cells.

27-Hydroxycholesterol regulates cholesterol synthesis and transport in C6 glioma cells.

The oxysterol 27-Hydroxycholesterol (27-OHC) is a major cholesterol metabolite that can cross the blood brain barrier (BBB) from peripheral circulation to the brain. Currently, the role of 27-OHC on cholesterol homeostasis in astrocytes and the underlying mechanisms are not defined. Since all brain cholesterol is essentially synthesized in brain itself and astrocytes as net producers of cholesterol are essential for normal brain function, here we investigated the effects of 27-OHC on cholesterol synthesis and transport in C6 glioma cells. C6 cells were treated with 5, 10 and 20µM 27-OHC for 24h and the cell viability and apoptosis, the cholesterol levels and metabolism-related mediators, genes and proteins were subsequently assessed using cell-counting kit (CCK)-8, Amplex red, ELISA, real-time PCR and Western blot, respectively. We found that 27-OHC decreased cholesterol levels by down-regulating the expression of sterol-regulated element binding protein-1 (SREBP-1a), 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CR) and low density lipoprotein receptor (LDLR) and promoted cholesterol transport by up-regulating the expression of peroxisome proliferator-activated receptors-γ (PPAR-γ), liver X receptor-α (LXR-α), ATP-binding cassette transporter protein family member A1 (ABCA1) and apolipoprotein E (ApoE)genes. Our results suggested that 27-OHC may represent a sensitive modulator of cholesterol metabolism disorder by suppressing cholesterol synthesis and stimulating cholesterol transport in astrocytes.

Metabolomics analysis of serum from subjects after occupational exposure to acrylamide using UPLC-MS.

Since occupational exposure to acrylamide (ACR) may cause nerve damage, sensitive biomarkers to evaluate the early effects of ACR on human health are needed. In the present study, we have compared a group of individuals with occupational exposure to ACR (contact group, n = 65) with a group of individuals with no exposure (non-contact group, n = 60). Serum metabolomics analysis of the contact and non-contact groups was carried out using ultra performance liquid chromatograph/time of flight mass spectrometry, combined with multivariate analysis, to identify potential metabolites. Serum biochemical indexes of the contact and non-contact groups were also determined using an automatic biochemistry analyzer. There was a clear separation between the contact group and the non-contact group; receiver operator characteristic curve analysis suggested that phytosphingosine, 4E,15Z-bilirubin IXa and tryptophan were the best metabolites to use as biomarkers. Liver function was also found to be abnormal in the contact group. Important, ACR-related, metabolic changes were seen in the contact group and new biomarkers for assessing the toxicity of ACR on the central nervous system have been proposed. This study will provide a sound basis for exploring the toxic mechanisms and metabolic pathways of ACR.