Phthalates are widely used chemicals with ubiquitous human exposure. Evidence indicated that phthalate exposure was associated with an increased risk of aging-related diseases. Klotho is a transmembrane protein with anti-aging functions, and its association with phthalates remains unknown. To find the association between phthalate exposure and serum α-Klotho, a cross-sectional study was performed in 4482 adults (40–79 years old) who completed the National Health and Nutrition Examination Survey (NHANES) (2007–2016). As shown in the results of multivariable linear regression analyses, mono(carboxynonyl) phthalate (MCNP) and mono-n-butyl phthalate (MBP) were inversely associated with α-Klotho, and the regression coefficients of MCNP and MBP were −1.14 (95% confidence interval (CI): −2.00, −0.27) and −0.08 (95% CI: −0.14, −0.02). Subgroup analyses based on the quartiles of each phthalate metabolite showed that both MCNP and MBP were only inversely associated with α-Klotho in the subgroups of the highest levels. For mono-isobutyl phthalate (MIBP), the inverse association with α-Klotho was only statistically significant in the subgroup of the lowest level, and the regression coefficient was −26.87 (95% CI: −52.53, −1.21). Our findings suggest that α-Klotho might be involved in the association of phthalate exposure with aging-related diseases. Future research investigating the causality between phthalates and α-Klotho and its underlying mechanisms is encouraged.

Chronic arsenic exposure is considered to increase the risk of breast cancer. p62 is a multifunctional adaptor protein that controls myriad cellular processes and is overexpressed in breast cancer tissues. Although previous studies have indicated the involvement of p62 accumulation in arsenic tumorigenesis, the underlying mechanism remains obscure. Here, we found that 0.1 µM or 0.5 µM arsenite exposure for 24 weeks induced oncogenic phenotypes in human mammary epithelial cells. Elevated aerobic glycolysis, cell proliferation capacity, and activation of p62-mTOR pathway, as indicated by increased protein levels of p62, phosphorylated-mTOR (p-mTOR) and hypoxia-inducible factor 1α (HIF1α), were observed in chronically arsenite-exposed cells, and of note in advance of the onset of oncogenic phenotypes. Moreover, p62 silencing inhibited acquisition of oncogenic phenotypes in arsenite-exposed cells. The protein levels of p-mTOR and HIF1α, as well as aerobic glycolysis and cell proliferation, were suppressed by p62 knockdown. In addition, re-activation of p‑mTOR reversed the inhibitory effects of p62 knockdown. Collectively, our data suggest that p62 exerts an oncogenic role via mTORC1 activation and acts as a key player in glucose metabolism during arsenite-induced malignant transformation, which provides a new mechanistic clue for the arsenite carcinogenesis.

Chlorophenols are widespread environmental organic pollutants with harmful effects on human beings. Although relationships between chlorophenols and various dysfunctions/diseases have been reported, the contribution of chlorophenols exposure to mortalities is underdetermined. In this cohort study, we included 4 types of urinary chlorophenols, aiming to estimate associations of chlorophenols exposure with all-cause and cause-specific mortalities. Urinary chlorophenols were examined at baseline of National Health and Nutrition Examination Survey (NHANES) 2003-2010, and adjusted for the urinary creatinine level. Associations between chlorophenols and mortalities were estimated using COX regression analyses, results were shown as hazard ratio (HR) and 95% confidence interval (95% CI). By dividing participants into four subgroups based on quartiles of urinary levels of chlorophenols, associations between mortalities and categorical variables of chlorophenols were estimated. Furthermore, the quantile g-computation analysis was used to estimate the joint effects of 4 chlorophenols on mortalities. Among 5817 adults (2863 men), 1034 were deceased during the follow-up. After adjusted for confounders, 2,4,5-trichlorophenol (2,4,5-TCP) was found to be positively associated with both all-cause (HR = 1.46; 95% CI: 1.16, 1.84) and cardiovascular disease (CVD) mortalities (HR = 1.60; 95% CI: 1.00, 2.55). Compared to the subgroup of the lowest level of chlorophenols, participants in subgroups of higher 2,4,5-TCP levels showed higher risk of all-cause mortality (P-value for trend = 0.003). For CVD mortality, HRs in subgroups of higher levels of 2,4-dichlorophenol (2,4-DCP) and 2,4,6-trichlorophenol (2,4,6-TCP) were statistically significant (P-values for trend were 0.017 for 2,4-DCP and 0.049 for 2,4,6-TCP). The HRs (95% CI) of joint effects of 4 chlorophenols were 1.11 (1.01, 1.21) and 1.32 (1.10, 1.57) for all-cause and CVD-specific mortalities, and 2,4,5-TCP showed the highest weight in joint effects. All of these findings implied that among 4 urinary chlorophenols we included, 2,4,5-TCP might be a sensitive one in associations with mortalities among general populations.

Hypertension was inversely associated with MUFA17, MUFA18 and MUFA20 and positively associated with MUFA15. Mutual interactions existed among these MUFAs, and fat accumulation might potentially underlie their associations with hypertension.

BACKGROUND:Published studies have shown positive associations of branched chain and aromatic amino acids with type 2 diabetes mellitus (T2DM), and the findings remain consistent. However, the associations of other essential and semi-essential amino acids, i.e., methionine (Met), threonine (Thr), lysine (Lys), arginine (Arg) and histidine (His), with T2DM remain unknown. Obesity is an important independent risk factor for T2DM, and excessive amino acids can convert into glucose and lipids, which might underlie the associations of amino acids with obesity. Therefore, we aimed to estimate the associations between dietary intakes of these 5 amino acids and T2DM risk, as well as the mediation effects of obesity on these associations, in a Chinese population.METHODS:A total of 10,920 participants (57,293 person-years) were included, and dietary intakes of 5 amino acids were investigated using 24-h dietary recalls. Anthropometric obesity indices were measured at both baseline and the follow-up endpoints. Associations of amino acids with T2DM were estimated using COX regression models, hazard ratios (HRs) and 95% confidence intervals (95% CIs) were shown. The mediation effects of obesity indices were analyzed, and the proportion of the mediation effect was estimated.RESULTS:Higher intakes of the 5 amino acids were associated with increasing T2DM risk, while significant HRs were only shown in men after adjustments. No interaction by gender was found. Regression analyses using quintiles of amino acids intakes showed that T2DM risk was positively associated with amino acids intakes only when comparing participants with the highest intake levels of amino acids to those with the lowest intake levels. Adjusted correlation coefficients between amino acid intakes and obesity indices measured at follow-up endpoints were significantly positive. Mediation analyses showed that mediation effects of obesity indices existed on associations between amino acids intakes and T2DM risk, and the mediation effect of waist circumference remained strongest for each amino acid.CONCLUSIONS:We found positive associations of dietary intakes of Met, Thr, Lys, Arg and His with increasing T2DM risk in general Chinese residents, on which the mediation effect of obesity existed. These findings could be helpful for developing more constructive guidance in the primary prevention of T2DM based on dietary interventions.

The dietary intake of branched-chain amino acids (BCAAs) has been reported to be associated with both elevated blood pressure (BP) and hypertension risk, while published findings were inconsistent, and the causality has never been well disclosed. We performed this prospective study aiming to find out the relationship between dietary BCAAs intake and hypertension risk in the Chinese population. A total of 8491 participants (40,285 person-years) were selected. The levels of dietary BCAAs intake were estimated using the 24-h Food Frequency Questionnaire. Associations of both BP values and hypertension risk with per standard deviation increase of BCAAs were estimated using linear and COX regression analysis, respectively. The hazard ratios and 95% confidence interval were given. Restricted cubic spline analysis (RCS) was used to estimate the nonlinearity. Both systolic and diastolic BP values at the end points of follow-up were positively associated with dietary BCAAs intake. Positive associations between BCAAs intake and hypertension risk were shown in both men and women. By performing a RCS analysis, the nonlinear relationship between BCAAs intake and hypertension was shown. As the intake levels of Ile, Leu, and Val, respectively, exceeded 2.49 g/day, 4.91 g/day, and 2.88 g/day in men (2.16 g/day, 3.84 g/day, and 2.56 g/day in women), the hypertension risk increased. Our findings could provide some concrete evidence in the primary prevention of hypertension based on dietary interventions.

Chronic exposure to arsenic has been associated with a variety of cancers with the mechanisms undefined. Arsenic exposure causes alterations in metabolites in bio-samples. Recent research progress on cancer biology suggests that metabolic reprogramming contributes to tumorigenesis. Therefore, metabolic reprogramming provides a new clue for the mechanisms of arsenic carcinogenesis. In the present manuscript, we review the latest findings in reprogramming of glucose, lipids, and amino acids in response to arsenic exposure. Most studies focused on glucose reprogramming and found that arsenic exposure enhanced glycolysis. However, in vivo studies observed "reverse Warburg effect" in some cases due to the complexity of the disease evolution and microenvironment. Arsenic exposure has been reported to disturb lipid deposition by inhibiting lipolysis, and induce serine-glycine one-carbon pathway. As a dominant mechanism for arsenic toxicity, oxidative stress is considered to link with metabolism reprogramming. Few studies analyzed the causal relationship between metabolic reprogramming and arsenic-induced cancers. Metabolic alterations may vary with exposure doses and periods. Identifying metabolic alterations common among humans and experiment models with human-relevant exposure characteristics may guide future investigations.

Abstract The associations of lean body mass (LBM) with elevated blood pressure (BP) and hypertension were controversial, and the causalities have never been shown. Mid‐upper arm muscle circumference (MAMC), an easily obtained anthropometric measurement, could provide an accurate estimate for LBM. Therefore, a prospective cohort study in general Chinese residents aiming to find out the relationship between LBM estimated using MAMC and hypertension risk was performed. Eight thousand one hundred eighty‐five eligible participants were included in the baseline analysis, among whom 3442 were subsequently selected into cohort analysis. MAMC was calculated using mid‐upper arm circumference (MUAC) and triceps skinfold thickness (TST). Associations of MAMC with BP values and hypertension prevalence were estimated by linear and logistic regression models. Associations with hypertension incidence were estimated by COX regression models, hazard ratio (HR) and 95% confidence interval (CI) were given. Nonlinear relationship between MAMC and hypertension risk was estimated using restricted cubic spline method. Standardized coefficients of MUAC and TST were compared to estimate their strengths of associations with hypertension. Baseline analysis showed that after adjusted for confounders, the increase of systolic BP per standard deviation (SD) of MAMC were 1.97 mmHg (95%CI: 1.46, 2.48) and 1.63 mmHg (95%CI: 1.10, 2.16) respectively in men and women, and the increases of diastolic BP per SD were 1.58 mmHg (95%CI: 1.23, 1.92) and 1.08 mmHg (95%CI: 0.74, 1.42). Additionally, the association of MAMC with the prevalence of hypertension were also found in both men and women (OR = 1.36, 95%CI: 1.26, 1.47 in men; OR = 1.33, 95%CI: 1.22, 1.44 in women). Cohort analysis showed that MAMC increased the risk of hypertension (HR = 1.10, 95%CI: 1.01, 1.19 for men; HR = 1.15, 95%CI: 1.06, 1.26 for women), and a trend of J‐shaped relationship was found. Additionally, the stronger associations of MUAC with both BP values and hypertension than that of TST were found in both baseline and cohort analyses. Findings in our study implied that we cannot neglect the capacity of LBM in predicting hypertension risk, and LBM estimates should be recommended in general health surveys or examinations.

Chronic arsenic exposure is associated with the increased risk of several types of cancer, among which, lung cancer is the most deadly one. Nuclear factor erythroid 2 like 1 (NFE2L1), a transcription factor belonging to CNC-bZIP family, regulates multiple important cellular functions in response to acute arsenite exposure. However, the role of NFE2L1 in lung cancer induced by chronic arsenite exposure is unknown. In this study, we firstly showed that chronic arsenite exposure (36 weeks) led to epithelial-mesenchymal transition (EMT) and malignant transformation in human bronchial epithelial cells (BEAS-2B). During the process of malignant transformation, the expression of long isoforms of NFE2L1 (NFE2L1-L) was elevated. Thereafter, BEAS-2B cells with NFE2L1-L stable knockdown (NFE2L1-L-KD) was chronically exposed to arsenite. As expected, silencing of NFE2L1-L gene strikingly inhibited the arsenite-induced EMT and the subsequent malignant transformation. Additionally, NFE2L1-L silencing suppressed the transcription of EMT-inducer SNAIL1 and increased the expression of E-cadherin. Conversely, NFE2L1-L overexpression increased SNAIL1 transcription but decreased E-cadherin expression. Collectively, our data suggest that NFE2L1-L promotes EMT by positively regulating SNAIL1 transcription, and is involved in malignant transformation induced by arsenite.

Exposure to arsenic (As), an environmental toxicant, causes damages to the central nervous system (CNS) structure and function. Emerging epidemiological studies support that exposure to As, especially during the critical periods of the CNS development, may act as an environmental risk factor of autism spectrum disorders (ASD), which is characterized by behavioral changes, including abnormal social behaviors, restricted interests and repetitive behaviors. However, direct evidence supporting the cause-effect relationship between As exposure and the risk of ASD is still missing. Thus, we aimed to investigate whether As exposure during pregnancy and lactation led to autism-like behaviors in offspring mice in the present study. We established a mice model of exposure to As via drinking water during pregnancy and lactation and conducted a battery of behavioral tests to evaluate social behaviors, repetitive behaviors, anxiety behaviors and learning and memory ability in offspring mice. We found that perinatal exposure to As caused autism-like behaviors in male offspring, which demonstrated by abnormal social behaviors and repetitive behaviors. Anxiety-like behaviors, and learning and memory impairments, known as concomitant behavioral phenotypes in mice with autism-like behaviors, were also observed. Decreases of synaptic density, especially in cortex, hippocampus and cerebellum, are extensively observed in both ASD patients and animal models of ASD. Thus, immunofluorescence staining and western blotting were used to observe the expression of PSD-95 and SYP, well-known markers for presynaptic and postsynaptic membranes, to assess the synaptic density in offspring cortex, hippocampus and cerebellum. We found perinatal exposure to As decreased the expression of PSD-95 and SYP in these brain regions. This indicated that perinatal exposure to As caused decreases of synaptic density, a typical autism-like cellular alteration in brains, which may contribute to autism-like behaviors in offspring.

背景我国北方人群代谢综合征(MS)患病率较高,而身体肥胖指数(BAI)是一个衡量脂肪组织堆积程度的新指标,正常体重肥胖(NWO)已被证实与MS及其危险因素相关,但目前关于BAI、NWO与我国北方人群MS关系的研究报道较少.目的 基于沈阳市沈河区社区居民分析BAI、NWO与MS及其组分的关系.方法 2015年4—6月,采用整群随机抽样方法抽取参与当地健康调查的社区居民2338例,分析其人体测量学指标、代谢指标及生活行为因素;BAI与MS及其组分的关系分析采用多因素Logistic回归分析.结果 校正年龄、吸烟状况、饮酒状况后进行的多因素Logistic回归分析结果显示:男性社区居民BAI与MS及中心性肥胖、三酰甘油(TG)升高有关(P<0.001);女性社区居民BAI与MS及中心性肥胖、血压升高、空腹血糖(FBG)升高、TG升高有关(P<0.05);在男性社区居民中,以正常体质量但BAI≥26.1者为参照,正常体质量且BAI<26.1者MS、中心性肥胖、TG升高发生风险降低,超重且BAI≥26.1者中心性肥胖发生风险升高,肥胖但BAI<26.1者血压升高发生风险升高,肥胖且BAI≥26.1者MS发生风险升高(P<0.05);在女性社区居民中,以正常体质量但BAI≥29.2者为参照,正常体质量且BAI<29.2者MS、中心性肥胖、TG升高发生风险降低,超重但BAI<29.2者血压升高、高密度脂蛋白胆固醇(HDL-C)降低风险升高,超重且BAI≥29.2者MS、中心性肥胖、血压升高发生风险升高,肥胖但BAI<29.2者HDL-C降低发生风险升高,肥胖且BAI≥29.2者MS、中心性肥胖、血压升高、FBG升高、TG升高发生风险升高(P<0.05).结论 沈阳市沈河区社区居民MS患病率较高〔男性、女性分别为50.4％(386/766)、46.6％(733/1572)〕,BAI与其MS发生风险升高有关,且根据体质指数(BMI)和BAI评价的NWO者MS发生风险较非NWO者升高,但根据BMI和BAI评价的肥胖或超重者MS发生风险趋于接近,而BAI的常规测量可能成为监测肥胖及预防MS的好方法.

Chronic arsenic exposure has been associated with various toxic effects, especially to the organs of liver and kidney. As a plant polyphenol, curcumin is the most vital bioactive ingredient of turmeric and has a wide range of pharmacological activities. In the present study, we investigated the potential roles of curcumin against arsenic-induced liver and kidney dysfunctions in mice. Curcumin treatment (200 mg/kg) not only decreased the deposition of arsenic in liver and kidney, but also relieved the hepatic and nephritic biochemical indexes (Glutamic oxaloacetic transaminase [AST], Alanine aminotransferase [ALT], albumin, and creatinine) altered by arsenic at doses of 10 and 25 mg/L via drinking water. What's more, curcumin exerted influences on the activities of myeloperoxidase and on the secretion of inflammatory cytokines in liver and kidney tissues. In addition, the levels of mitogen-activated protein kinases (MAPKs) and nuclear factor kappa B (NF-κB) phosphorylation were declining while NRF2-signaling targets were increasing in mice liver and kidney by curcumin administration. In conclusion, our results here suggest that curcumin could exert both anti-inflammatory and antioxidant functions on arsenic-induced hepatic and kidney injury by inhibiting MAPKs/NF-κB and activating Nrf2 pathways cooperatively.

Objective:To investigate the effects of drinking water-borne arsenic exposure on mammary gland development of female mice in early life.Methods:Healthy and sexually mature C57BL/6J mice were paired according to the female to male ratio of 2∶1. After confirmation of pregnancy, female mice were randomly divided into control (drinking double distilled water), low- (0.5 mg/L) and high- (5.0 mg/L) dose arsenic exposure groups, 10 mice in each group. The exposure time of arsenic in drinking water ranged from day 0 of pregnancy to day 28 after birth. At the end of arsenic exposure, female offspring (10 mice in each group) were sacrificed and mammary glands were dissected for whole tissue staining to evaluate the development of mammary glands and quantitative analysis of mammary gland development indexes. The expression of proliferating cell associated antigen Ki67 was detected by immunohistochemistry.Results:There were no significant differences in body weight and organ coefficients of liver, kidney and mammary glands between female offspring in low- and high-dose arsenic exposure groups and control group ( F=1.018, 1.033, 1.764, 0.199, P > 0.05). Compared with control group, low- and high- dose arsenic exposure groups showed more terminal end buds (TEB) and ductal branches as well as stronger longitudinal growth ability in mammary gland morphological analysis. Quantitative analysis results showed that the numbers of TEB in the low- and high-dose arsenic exposure groups (11.83 ± 4.40, 11.00 ± 3.74) were significantly higher than that in the control group (4.00 ± 1.83, P < 0.05). The ductal lengths in the low- and high-dose arsenic exposure groups [(6.43 ± 1.08), (6.08 ± 1.74) mm] were also significantly longer than that in the control group [(3.71 ± 0.61) mm, P < 0.05]. The distance of leading edge of ducts to the midpoint of lymph nodes in the low- and high-dose arsenic exposure groups [(0.58 ± 1.12), (- 0.02 ± 1.57) mm] was significantly shorter than that in the control group [(- 2.67 ± 0.87) mm, P < 0.05]. The mean maximum area of TEB in the low-dose arsenic exposure group [(0.04 ± 0.01) mm 2] was significantly larger than that in the control group [(0.02 ± 0.01) mm 2, P < 0.05]. Immunohistochemistry staining indicated strong staining of Ki67 within TEB in the low- and high-dose arsenic exposure groups. Conclusion:Early life inorganic arsenic exposure promotes the development of TEB, ductal extension and cell proliferation within TEB in female mice, indicating that early life arsenic exposure alters mammary gland development.

The interaction between arsenic metabolism and potential modifiers on the risk of diabetes is unclear. This research aimed to investigate arsenic metabolism and diabetes prevalence and to identify the interactive effects of arsenic metabolism with some risk factors on diabetes in a Chinese population. A baseline cross-sectional survey was performed in two areas with groundwater arsenic contamination in China. Arsenic levels in water and arsenic metabolites in urine were analyzed. The proportions of each arsenic metabolite (inorganic arsenic [iAs%], monomethylarsonic acid [MMA%], and dimethylarsinic acid [DMA%]) were computed to evaluate arsenic metabolism. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the association between arsenic and diabetes. Interaction on the additive scale between arsenic methylation index and effect modifier was evaluated by calculating the relative excess risk due to interaction (RERI). Compared with participants in the lower tertile of MMA%, participants in the middle and upper tertiles of MMA% were less prone to diabetes (OR: 0.47 and 0.31, respectively). However, participants in the upper tertiles of urinary DMA% (OR: 3.18) were more likely to have diabetes than those participants in the lower tertiles. The stratified analyses revealed that a one-unit increase in DMA% was associated with higher odds of diabetes in females (OR: 1.06, 95% CI: 1.01, 1.11), older people (OR: 1.05, 95% CI: 1.00, 1.10), and subjects with body mass index (BMI) under 25 kg/m2 (OR: 1.07, 95% CI: 1.01, 1.14). The additive interactions between DMA% and female gender (RERI: 0.40, 95% CI: 0.01, 11.88), DMA% and age (RERI: 0.02, 95% CI: 0.01, 8.85), as well as DMA% and BMI (RERI: 0.49, 95% CI: 0.01, 9.62), were statistically significant. In conclusion, efficient arsenic metabolism is associated with higher odds of diabetes. Urinary DMA% and individual factors interact to synergistically influence diabetes occurrence in the Chinese population.

目的 探讨人口服含雄黄中成药(牛黄解毒片)后尿砷含量及砷甲基化能力的变化情况.方法 选取10名健康志愿者(男女各5人,24～26岁),按照说明书口服一日剂量的牛黄解毒片,并于服药前和服药后3、6、9、12、24、48、96和144 h收集尿液,利用氢化物发生-超低温捕集-原子吸收分光光度仪测定尿中各形态砷含量,计算总砷(tAs)浓度、各种形态砷百分比以及甲基化率.结果 与服药前相比,男性和女性志愿者尿液中无机砷(iAs)含量分别在服药后6和3h达到峰值(P＜0.05),一甲基胂(MMA)含量均在服药后6h达到峰值(P＜0.05),二甲基胂(DMA)含量分别在服药后24和9h达到峰值(P＜0.05),尿tAs含量均在服药后6h达到峰值(P＜0.05).服药后,男性和女性志愿者尿无机砷百分比(iAs％)均在服药后6h达到峰值(P＜0.05),一甲基胂百分比(MMA％)分别在3和9h达到峰值(P＜0.05),二甲基胂百分比(DMA％)和一甲基化率(FMR)均在服药后6h达到最低值(P＜0.05),二甲基化率(SMR)分别在服药后3和6h达到最低值(P＜0.05).在同一时间点,与男性志愿者相比,女性志愿者尿液中DMA和tAs含量较高(P＜0.05),iAs％及MMA％较低(P＜0.05),DMA％,FMR及SMR较高(P＜0.05).结论 志愿者服用含雄黄中成药后尿砷浓度显著升高,砷甲基化能力显著下降;女性砷排泄速度较快,砷甲基化能力较强.

Acute exposure to arsenic is known to cause bone marrow depression and result in anemia, in which the dusfunction of cells in the bone marrow niche such as mesenchymal stem cells (MSCs) is vital. However, the mechanism underlying response of MSCs to arsenic challange is not fully understood. In the present study, we investigated the role of nuclear factor erythroid 2-related factor (NRF) 1 (NRF1), a sister member of the well-known master regulator in antioxidative response NRF2, in arsenite-induced cytotoxicity in mouse bone marrow-derived MSCs (mBM-MSCs). We found that arsenite exposure induced significant increase in the protein level of long-isoform NRF1 (L-NRF1). Though short-isoform NRF1 (S-NRF1) was induced by arsenite at mRNA level, its protein level was not obviously altered. Silencing L-Nrf1 sensitized the cells to arsenite-induced cytotoxicity. L-Nrf1-silenced mBM-MSCs showed decreased arsenic efflux with reduced expression of arsenic transporter ATP-binding cassette subfamily C member 4 (ABCC4), as well as compromised NRF2-mediated antioxidative defense with elevated level of mitochondrial reactive oxygen species (mtROS) under arsenite-exposed conditions. A specific mtROS scavenger (Mito-quinone) alleviated cell apoptosis induced by arsenite in L-Nrf1-silenced mBM-MSCs. Taken together, these findings suggest that L-NRF1 protects mBM-MSCs from arsenite-induced cytotoxicity via suppressing mtROS in addition to facilitating cellular arsenic efflux.

Background Wrist circumference (WrC) is an easily obtained measure in estimating the body frame and regional fat distribution, and has increasingly used as an obesity index. The aim of our study is to estimate the association of WrC with elevated blood pressure (BP) among northeastern Chinese community-dwelling residents, and compare the strength of this association to other anthropometric obesity indices. Methods A total of 2,331 adult participants (761 male participants, and 1,570 female participants) were included. WrC and other five generally used obesity indices, including body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), waist-to-height ratio (WHtR) and neck circumference (NC) were measured. Hypertension was defined as systolic blood pressure (SBP)/diastolic blood pressure (DBP) ≥140/90 mmHg or anti-hypertensive medication use. Multivariable linear and logistic regression models were performed to identify associations of BP and hypertension with per standard deviation (SD) increase of obesity indices. Areas under receiver operative characteristic curves (AUC) were calculated to compare the predicting capacity of WrC and other obesity indices on hypertension. Results All of the six obesity indices were positively associated with both SBP and DBP after adjustment for age and gender (P-values of associations of SBP with obesity indices were 0.043 for WrC, and <0.001 for other five indices; P-values of associations of DBP with obesity indices were 0.011 for WrC, 0.031 for WHR, and <0.001 for other four indices), while the association between SBP and WrC showed no statistically significant after further adjusted for life-style and metabolic risk factors (P-value was 0.062). The increases of both SBP and DBP per SD increase of BMI were the largest. The positive associations of five obesity indices but WHR with hypertension were observed after adjustment for all risk factors (P-values were 0.024 for WrC, 0.064 for WHR and <0.001 for other four indices). However, the odd ratios (OR) of WrC was the smallest, while BMI was the largest. Consistently, the AUC of BMI was the largest and statistically larger than that observed for WrC (P-value <0.001). Conclusions WrC was associated with hypertension among northeastern Chinese populations. However, the association was not stronger than the other generally used indices, particularly BMI.

Objective Through determination of selenium content in liver and urine of selenium-induced mice, direct sampling atomic fluorescence spectrometry was established to provide a more accurate and convenient determination method for detection of selenium-related biological samples. Methods Selenium in the sample was released by the electrically heated quartz tube,the selenium in the atomic state was captured by the quartz tube,and the selenium released by the heating quartz tube was carried by the argon-hydrogen mixed gas into the argon-argon flame atomic fluorescence detector for determination; standard curve was established based on selenium content and fluorescence area, and then the content of selenium in the sample was calculated. Results The detection limit of selenium in samples by direct sampling atomic fluorescence spectrometry was 0.28 μg/kg, the correlation coefficient of standard curve was 0.999 3, and the relative standard deviation range was 1.82% - 4.19%. The adding standard recovery of the liver in mice was 87.30%- 100.20%; meanwhile the adding standard recovery of the urine in mice was 93.10% - 96.60%. Conclusions Direct sampling atomic fluorescence method is simple and easy to operate, accuracy and precision are better, the linear range is wide. The samples need not be processed by complex pretreatment,such as acid,etc.,elements loss is avoided and efficiency of detection is improved.The method can be used in a variety of samples for rapid detection of trace selenium.

Objective To compare detection results of inorganic arsenic (iAs) in the water samples with low-pressure high performance liquid chromatography-hydride generation-atomic fluorescence spectrometry (HPLC-HG-AFS) and hydride generation-cold trap-atomic absorption spectrometry (HG-cold trap-AAS) and to analyze the applicability of atomic fluorescence spectrometry in iAs detection in water samples.Methods The accuracy,precision,detection limit,linear range,and other indicators of the two detection methods were analyzed statistically using SPSS 19.0.Results The linear correlation coefficients of the AFS and AAS were all greater than 0.99.The linear range of AFS detection was much wider than that of AAS;while no significant difference was observed in detection limit between the two methods.The precision of the two detection methods was less than 10 ％.The recovery rates of the two detection methods for same samples were not significantly different (t =-1.034,P =0.336).Conclusion Low-pressure HPLC-HG-AFS could be used in effective detection of iAs of various valences due to its wider detection linear range compared to HG-cold trap-AAS;no other significant differences between the two methods exist for the detection ofiAs in water samples.

目的 探讨给与谷胱甘肽(GSH)及其拮抗剂——丁硫氨酸亚砜胺(BSO)对慢性砷暴露小鼠体内砷代谢及氧化应激的影响.方法 将SPF级雌性昆明小鼠随机分为对照组(蒸馏水)、单纯染砷组(50 m//L亚砷酸钠)、GSH干预组(50 mg/L亚砷酸钠+400 mg/kg GSH)和BSO(50 mg/L亚砷酸钠+600mg/kg BSO)干预组,除对照组小鼠饮用蒸馏水外,其余各组均饮用含50 mg/L亚砷酸钠的水溶液连续染毒30周,然后给予400 mg/kg GSH或600 mg/kg BSO,用蒸馏水配制GSH和BSO水溶液,每天两次腹腔注射,连续2d,用氢化物发生-超低温捕集-原子吸收分光光度法测定尿液各形态砷水平,用DTNB及试剂盒法分别测定全血及肝脏中GSH和总抗氧化能力(T-AOC)水平.结果 GSH干预组小鼠尿中二甲基胂(DMA)、DMA含量构成比、二甲基化率(SMR)及总砷含量高于单纯染砷组(P＜0.05),而BSO干预组各形态砷、DMA含量构成比、一甲基化率(FMR)、SMR及总砷含量均低于单纯染砷组(P＜0.05);单纯染砷组小鼠肝脏和血液GSH和T-AOC的水平均低于对照组(P＜0.05).给予GSH干预后,肝脏和血液GSH和T-AOC水平均高于单纯染砷组(P＜0.05)且与对照组差异无统计学意义(P＞0.05).BSO干预组小鼠肝脏和血液GSH和T-AOC的水平均低于其他各组(P＜0.05).结论 外源性GSH干预可以增强砷暴露小鼠的砷甲基化能力,增加砷从尿液中的排出,拮抗砷所致的GSH和T-AOC水平下降,从而减少了砷对机体造成的氧化损伤.