目的 了解湘江河底泥中3种内分泌干扰物壬基酚(NP)、辛基酚(OP)和双酚A(BPA)的分布特征,并进行环境风险评估.方法 子2017年7月,在湘江河上、中、下游7个采样点进行底泥采样,检测底泥中NP、OP和BPA的含量,采用风险熵(RQ)对底泥中NP、OP和BPA的环境风险进行初步评估..结果采样点底泥中均可检测出NP、OP、BPA,含量分 别为(589.8±352.4)、(528.5±404.5)和(377.5±228.0)μg/kg.下游河段底泥中NP、OP、BPA的含量均的高于上游,差异有统计学意义(P＜0.05).底泥中NP、OP、BPA的含量两两间均呈正相关(P＜0.05).各采样点底泥中NP、OP和BPA的风险熵值均大于1,其中,BPA的风险熵值远高于NP、OP.结论 湘江河河底泥中存在较严重的NP、OP和BPA污染,且这三种污染物对环境的威胁较大,应加强管理.

OBJECTIVES:Although it has been shown that exposure to environmental endocrine disruptors (EDCs) has been implicated as a potential risk factor for metabolic disease, information on adverse effect of chronic low-dose exposure to nonylphenol (NP), on the development and progress of type 2 diabetes mellitus (T2DM) is scarce. NP, as an EDC, is a ubiquitous degradation product of nonylphenol polyethoxylate (NPE) that is primarily used in cleaning and industrial processes. METHOD:Eighty Sprague-Dawley rats were assigned into 8 groups (n = 10 per group): rats fed a normal-diet (ND) as the control (C-ND); rats fed a normal diet and were gavaged with NP at a dose level of 0.02 μg/kg/day (NP-L-ND), 0.2 μg/kg/day (NP-M-ND) or 2 μg/kg/day (NP-H-ND), respectively; rats fed a high-sucrose/high-fat diet (HSHFD) as the HSHFD control (C-HSHFD); rats fed a HSHFD and were gavaged with NP at a dose level of 0.02 μg/kg/day (NP-L-HSHFD), 0.2 μg/kg/day (NP-M-HSHFD) or 2 μg/kg/day (NP-H-HSHFD), respectively. RESULT:On day 180, the rats in the groups treated with NP-M-HSHFD and NP-H-HSHFD showed significant increases in body weight (p < 0.05) in comparison with the C-ND group. Fast blood glucose (FBG) level in the NP-M-HSHFD and NP-H-HSHFD groups was higher than that in the C-ND group (F = 96.17, p < 0.001). The fast serum insulin (FINS) level of rats was lower in both the NP-M-HSHFD and NP-H-HSHFD groups compared with the C-ND group (F = 145.56, p < 0.001). Serum leptin (LEP) level in both the NP-M-HSHFD and NP-H-HSHFD groups was lower when compared with the C-ND group (F = 34.62, p < 0.001). The effect of NP at the dose level of 0.2 μg/kg/day on FBG, serum FINS and LEP levels in rats was greatest among the treatment groups (p < 0.05). Oral glucose tolerance test showed increased area under the curve (AUC) in treatment groups at week 12 (p < 0.05). A decrease of pancreatic islet numbers and size was exhibited in the pancreatic tissue of NP-M-HSHFD and NP-H-HSHFD treated rats compared with C-ND treated rats. Co-exposure to NP and HSHFD causes inflammatory changes histologically. CONCLUSION:Chronic low-dose exposure to NP might induce impaired glucose tolerance, which further lead to insulin resistance, and pancreatic β cell insulin secretion deficiency, ultimately increase the risk of T2DM. Moreover, additive toxic effects of NP and HSHFD on pancreatic beta-cell function and glucose metabolism have been identified in rats as well.

OBJECTIVES:To investigate the effects of Nonylphenol (NP) in pups from dams exposed during gestational and lactational periods on immediate early genes (c-jun, c-fos) in hippocampus and the learning and memory of F1 rats. MATERIALS AND METHODS:Twenty eight pregnant dams, stratified by pregnancy date, were randomly assigned into 4 groups, which were gavaged with NP at the doses of 50 mg/kg/day, 100 mg/kg/day, 200 mg/kg/day and groundnut oil, respectively. Step-down avoidance test, and learning and memory effects of NP were evaluated on 8-weeks-old pups. The expressions of c-jun and c-fos and the activities of choline acetyltransferase (ChAT) and acetylcholinesterase (AchE) were evaluated in hippocampus of pups. RESULTS:Compared to the control, reaction time (RT) that pups spent to jump to the platform was longer (P=0.02), the number of errors were higher (P=0.01), and the step-down latency was shorter in the 200 mg/kg/day NP-treated group (P=0.04). Exposure to NP induced a significant reduction in ChAT activity in hippocampus in the 100 (P=0.005) and 200 mg/kg/day NP-treated groups (P=0.002), whereas exposure to 200 mg/kg/day caused a significant increase in AchE activity (P=0.004); a dose-response relationship was revealed between ChAT and AchE activities and NP exposure in the hippocampus of pups (r=-0.821, P=0.01; r=0.757, P=0.04). Exposure to NP in the 100 and 200 mg/kg/day NP-treated groups exhibited an increase in number of c-fos and c-jun positive cells. CONCLUSION:Exposure to NP might negatively affect learning and memory ability in F1 rats, possibly due to the alterations in the expression of c-jun and c-fos, and ChAT, AchE activities in hippocampus of pups.

Endocrine-disrupting chemical (EDC) has been thought to play a role in non-alcoholic fatty liver disease (NAFLD). However, the toxic effects of Nonylphenol (NP), an EDC, on non-alcoholic fatty liver disease have never been elaborated. This study aimed to investigate whether exposure to NP could induce NAFDL, a promoting effect of high-sucrose-high-fat diet (HSHFD) on the adverse effects caused by NP was evaluated. Fourth eight male rats were assigned to four groups and each group was treated with a specific testing sample: normal-diet (ND) control group (C-ND); normal diet plus NP (180mg/kg/day) group (NP-ND); high-sucrose-high-fat-diet control group (C-HSHFD); HSHFD plus NP (180mg/kg/day) group (NP-HSHFD). At the age of 80 day, sonogram presents diffusely increased hepatic echogenicity in the NP-HSHFD group. The oblique diameter of liver in the NP-HSHFD group was significantly bigger than that in both the C-ND and NP-ND groups. At the age of 90 day, exposure to NP-HSHFD and NP-ND caused a significant increase in NP concentration in liver as compared to the C-ND group. The rats in the groups treated with NP+ND, HSHFD and NP+HSHFD produced significant increases in the body weight, fat weight and FMI, respectively, when compared to the C-ND group. The liver weight and hepatosomatic indexes (HIS) of rats in the NP-HSHFD group are higher than those in the C-HSHFD group. Exposure to NP-HSHFD induced the increases in plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL) as compared to the C-ND group. Morphological examination of liver tissue from rats exposed to NP+HSHFD shown steatosis with marked accumulation of lipid droplets, hepatocellular ballooning degeneration and inflammatory cell infiltration. Chronic exposure to NP might induce NAFLD in male rats. The high-sucrose-high-fat diet accelerates and exacerbates the development of NAFLD caused by NP exposure.

Objective To survey the nonylphenol(NP) concentration of tap water in two districts (A district and B district)of one south-west city and to provide data support for the prevention and control of NP pollution.Methods (Sampling point:on July 16,2016,according to the water quality testing sampling points requirements,set a sampling point in the water source and the factory outlet of each city,and set 3 sampling points in different sections in the tip water by a certain distance gradient.In two urban areas(A and B)a total of 10 sampling points were set.(Sample size:repeatedly collected three times at each point,and 30 samples were collected in all.(Samples handing:used high-performance liquid chromatograph.Results NP were detected in the tap water of A district and B district,and the rate of detection was 100％,with the concentration range of source water being 0.195 ～ 1.174μg/L,the water outlet of waterworks being 0.269 ～ 1.042μg/L,tip water being 0.32 ～ 5.434μg/L.The concentration of tip water of A district was six times higher than B district (t =-4.348,P ＜ 0.05).Conclusion The survey results show that tap water in both cities was detected in NP,and the NP average concentration of sources water at a moderate level compared to the rest cites of China.The NP average concentration of tip water in A was higher than that in B,lower than the US fresh water reference standard 6.6pg/L.It is necessary to treat residents living sewage and industrial wastewater.

Backgroundsystemic arterial hypertension is the most prevalent cardiovascular disease; physical activity for hypertensive patients is related to several beneficial cardiovascular adaptations. This paper evaluated the effect of water- and land-ergometry exercise sessions on post-exercise hypotension (PEH) of healthy normotensive subjects versus treated or untreated hypertensive patients.MethodsForty-five older women composed three experimental groups: normotensive (N, n = 10), treated hypertensive (TH, n = 15) and untreated hypertensive (UH, n = 20). The physical exercise acute session protocol was performed at 75% of maximum oxygen consumption (VO2max) for 45 minutes; systolic (SBP), diastolic (DBP) and mean (MBP) blood pressure were evaluated at rest, peak and at 15, 30, 45, 60, 75 and 90 minutes after exercise cessation. Additionally, the heart rate variability (HRV) was analyzed by R-R intervals in the frequency domain for the assessment of cardiac autonomic function.ResultsIn both exercise modalities, equivalent increases in SBP were observed from rest to peak exercise for all groups, and during recovery, significant PEH was noted. At 90 minutes after the exercise session, the prevalence of hypotension was significantly higher in water-than in the land-based protocol. Moreover, more pronounced reductions in SBP and DBP were observed in the UH patients compared to TH and N subjects. Finally, exercise in the water was more effective in restoring HRV during recovery, with greater effects in the untreated hypertensive group.ConclusionOur data demonstrated that water-ergometry exercise was able to induce expressive PEH and improve cardiac autonomic modulation in older normotensive, hypertensive treated or hypertensive untreated subjects when compared to conventional land-ergometry.

目的：观察壬基酚（NP）围产期暴露对子代大鼠的肝毒性，并探讨其可能的机制。方法将成功交配的32只孕鼠随机分为4组，每组8只，NP 低、中、高剂量组分别予以 NP 50、100、200 mg／kg 加玉米油灌胃，对照组予以等容量玉米油灌胃；单笼饲养，空腹灌胃自受孕第6天起至生产后第21天止。仔鼠出生第60天麻醉后内眦取血，剖取肝脏；电镜观察肝细胞超微结构，免疫组化法检测肝组织肿瘤坏死因子α（TNF-α），高效液相法色谱法检测血清 NP。结果 NP 低、中、高剂量组仔鼠肝细胞核内染色质聚集，核膜深染，胞质中有大量的脂滴，且大部分脂滴与溶酶结合，染色较深，且剂量越高表现越明显。仔鼠肝组织 TNF-α阳性表达的积分光密度、血清 NP 水平对照组＜NP 低剂量组＜NP 中剂量组＜NP 高剂量组，P 均＜0．01；相关分析显示，仔鼠肝脏组织 TNF-α阳性表达的积分光密度与血清 NP 水平呈正相关（r ＝0．92，P ＜0．01）。结论围产期接触 NP 可对子代大鼠造成肝脏损伤，可能与 NP上调肝组织 TNF-α表达有关。