期刊：
Ecotoxicology and Environmental Safety,2019年174:75-82 ISSN：0147-6513
通讯作者：
Yuan, Junlin;Chen, Mingqing
作者机构：
[Yuan, JL; Chen, Mingqing; Yuan, Junlin; Duan, Jiufei; Deng, Ting; Xie, Xiaoman; Ding, Shumao] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
通讯机构：
[Yuan, JL; Chen, MQ] C;Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
关键词：
DBP;DEHP;Estradiol;Hypertension;RAAS
摘要：
Epidemiological studies have shown that high molecular weight phthalates (HMW) such as diethylhexyl phthalate (DEHP), are associated with hypertension in humans, while low molecular weight phthalates (LMW) such as dibutyl phthalate (DBP), have hardly any impact on the elevation of blood pressure. However, the molecular mechanisms responsible for this difference are not completely understood. In this experiment, mice were exposed to 0.1/1/10mg/kg/day DEHP and 0.1/1/10mg/kg/day DBP for 6 weeks, and their blood pressure was monitored using the tail pressure method. The results showed that exposure to DEHP dosages of 1 or 10mg/kg/day resulted in a sharp increase in blood pressure, while exposure to DBP did not induce any significant changes in blood pressure. Investigating the renin-angiotensin-aldosterone system (RAAS) and NO pathway in mice exposed to DEHP, we found that levels of angiotensin-converting enzyme (ACE) and angiotensin II (AngII) increased with increasing exposure to DEHP, and the expression of nitric oxide synthase (eNOS) and the level of NO decreased. Treatment with ACE inhibitor (ACEI) to block the ACE pathway inhibited the enhancement of RAAS expression, inhibited the increase in blood pressure, and inhibited the decrease in NO levels induced by DEHP. However, the expression of ACE, AngII, AT1R, and eNOS in the DBP treatment groups showed no significant changes. When examining estradiol in vivo, we found that exposure to DBP resulted in a significant increase in the level of estradiol, while exposure to DEHP did not lead to a significant change. When ICI182780 was used to block the estradiol receptors, any increase in the level of NO induced by DBP exposure, was inhibited. These results indicate that exposure to DEHP induces an increase in mouse blood pressure through RAAS, and the different effects of DEHP and DBP on blood pressure are partly due to the different estradiol levels induced by DEHP and DBP.
摘要：
Formaldehyde (FA), a ubiquitous indoor environmental pollutant, has been classified as a carcinogen. There are many studies showed that low levels of FA could promote cell proliferation, however, little is known about the signal pathways. To determine the potential molecular mechanisms, human chronic myeloid leukemia cells (K562cells) and human bronchial epithelial cells (16HBE cells) were exposed to different concentrations of FA. The data showed that FA at 0-125muM or 0-60muM promoted the proliferation of K562cells or 16HBE cells respectively, indicating that FA did have the Hormesis effect. FA at 75muM (K562cells) and 40muM (16HBE cells) significantly promoted cell proliferation, increased intracellular reactive oxygen species (ROS) levels, and decreased glutathione (GSH) content. At the same time, FA treatment induced a marked increase in the key molecules of cell division like CyclinD-cdk4 and E2F1. In addition, pyruvate kinase isozyme M2 (PKM2), glucose, glucose transporter 1 (GLUT1), lactic acid and lactate dehydrogenase A (LDHA) content in the Warburg effect were increased. Administering Vitamin E (VE), significantly disrupted cell division and disturbed the Warburg effect, effectively indicating the decrease of cell activity. Conclusively, these findings suggested that low concentrations of FA could promote cell proliferation by accelerating cell division process or enhancing the Warburg effect to embody the Hormesis effect.
摘要：
Formaldehyde (FA), a well-known toxic gas molecule similar to nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S), is widely produced endogenously via numerous biochemical pathways, and has a number of physiological roles in the biosystem. We attempted to investigate the vasorelaxant effects of FA and their underlying mechanisms. We found that FA induced vasorelaxant effects on rat aortic rings in a concentration-dependent manner. The NO/cyclic guanosine 5' monophosphate (cGMP) pathway was up-regulated when the rat aortas were treated with FA. The expression of large-conductance Ca(2+)-activated K(+) (BKCa) channel subunits alpha and beta of the rat aortas was increased by FA. Similarly, the levels of ATP-sensitive K(+) (KATP) channel subunits Kir6.1 and Kir6.2 were also up-regulated when the rat aortas were incubated with FA. In contrast, levels of the L-type Ca(2+) channel (LTCC) subunits, Cav1.2 and Cav1.3, decreased dramatically with increasing concentrations of FA. We demonstrated that the regulation of FA on vascular contractility may be via the up-regulation of the NO/cGMP pathway and the modulation of ion channels, including the upregulated expression of the KATP and BKCa channels and the inhibited expression of LTCCs. Further study is needed to explore the in-depth mechanisms of FA induced vasorelaxation.
作者：
Li Xiao-Xiao;Ding Shu-Mao;Yang Xu;Yuan Jun-Lin*
期刊：
分析化学,2018年46(1):27-32 ISSN：0253-3820
通讯作者：
Yuan Jun-Lin
作者机构：
[Ding Shu-Mao; Yuan Jun-Lin; Yang Xu; Li Xiao-Xiao] Cent China Normal Univ, Coll Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
通讯机构：
[Yuan Jun-Lin] C;Cent China Normal Univ, Coll Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
作者机构：
[陆林洁; 蔡洁; 安结然; 杜俊停; 丁书茂] Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Science, Central China Normal University, Wuhan;430079, China;[陆林洁; 蔡洁; 安结然; 杜俊停; 丁书茂] 430079, China
通讯机构：
Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Science, Central China Normal University, Wuhan, China
作者机构：
[曹昕伟; 刘潇童; 范宏成; 黄鑫; 郭彦彦; 沈世萍; 丁书茂] School of Life Sciences, Central China Normal University, Wuhan;430079, China;[曹昕伟; 刘潇童; 范宏成; 黄鑫; 郭彦彦; 沈世萍; 丁书茂] 430079, China
通讯机构：
School of Life Sciences, Central China Normal University, Wuhan, China
作者机构：
[朱雨晴; 沈世萍; 杨旭; 赵云; 郭晴; 梅宇飞; 丁书茂; 尤会会; 李金泉; 李潇潇] Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Science, Central China Normal University, Wuhan, China
通讯机构：
Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Science, Central China Normal University, Wuhan, China
关键词：
甲醛;卵清蛋白;小鼠;氧化损伤;炎症反应
摘要：
为探讨在单独染毒和卵清蛋白(OVA)联合致敏的条件下,甲醛灌胃染毒对小鼠造成的毒性效应,将雄性Balb/c小鼠随机分为7组:对照组(蒸馏水组);OVA致敏组;2mg/(kg?d) FA(甲醛)组;20mg/(kg?d) FA组;200mg/(kg?d) FA组;200mg/(kg?d)FA+ OVA组;200mg/(kg?d) FA+ OVA +MT(褪黑素)组,以蒸馏水和不同浓度甲醛溶液灌胃,连续21d. OVA致敏组,200mg/(kg?d) FA+ OVA组,200mg/(kg?d) FA+ OVA +MT组在第6,13,20d进行腹腔注射OVA致敏;此外,200mg/(kg?d) FA+ OVA +MT组,每天用1.0mg/mL褪黑素灌胃小鼠(小鼠灌胃剂量10mg/(kg?d)),连续21d.检测肝,肾和肺组织中活性氧自由基(ROS),丙二醛(MDA)和还原型谷胱甘肽(GSH)的含量,并采用ELISA法检测肝组织中IL-4和IFN -γ的水平.结果表明,与对照组相比,甲醛浓度为200mg/(kg?d),小鼠肝脏ROS含量增加(P<0.05),MDA含量增加以及小鼠肾脏GSH含量降低,均有显著性差异(P<0.05).OVA作为致敏剂,甲醛浓度为200mg/(kg?d)时,肝组织中IL-4(Interleukin-4)含量增加(P<0.01),10mg/(kg?d)褪黑素能够降低200mg/(kg?d)甲醛+OVA染毒小鼠肝脏内ROS含量(P<0.05).综上,200mg/(kg?d)甲醛灌胃染毒能使小鼠产生氧化损伤和炎症反应, ROS, MDA水平上升(P<0.05),GSH水平下降(P<0.05),肝脏中细胞因子IL-4水平上升(P<0.01), IFN -γ水平下降(P<0.05).
期刊：
Data in Brief,2016年6(1):948-952 ISSN：2352-3409
通讯作者：
Zhang, L.
作者机构：
[Yang, Xu; Zhang, Yuchao; Liu, Xudong; Ding, Shumao] Section of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Science, Central China Normal University, Wuhan, China;[Zhang, Luoping; McHale, Cliona M] Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, United States
通讯机构：
[Zhang, L.] D;Division of Environmental Health Sciences, United States
摘要：
Di(2-ethylhexyl) phthalate (DEHP) is a common indoor pollutant in the world, which may cause lots of harmful effects in human including diabetes according to epidemiological studies. To explore the underlying role of DEHP in diabetes-like symptoms, Balb/c mice were chose to be the experimental animals in this paper. They were separated as eight groups as follows: (1) saline+normal diet (vehicle control), (2) 10 mg/kg.day DEHP+normal diet, (3) 50 mg/kg.day DEHP+normal diet, (4) 250 mg/kg.day DEHP+normal diet, (5) streptozotocin (STZ)+high fat diet (diabetes model), (6) 10 mg/kg.day DEHP+ STZ+high fat diet, (7) 50 mg/kg.day DEHP+STZ +high fat diet, (8) 250 mg/kg.day DEHP+STZ+high fat diet. The biomarkers of this experiment include four groups: (1) general indicates: body weight and drinking water, (2) blood biomarkers: serum insulin and fasting glucose, (3) pathological examination: pancreas section and kidney section, and (4) biomarkers of oxidative stress: reactive oxygen species (ROS) and malondialdehyde (MDA) in liver cells. Our study results demonstrate that: (1) at our treatment levels DEHP cannot directly induce diabetes, but reduce serum insulin level in DEHP-exposed non-STZ-treated animals, (2) pathological examination finds that these is a dose-dependent damage in the pancreas in DEHP- exposed STZ-treated groups, and (3) the oxidative mechanism may be involved in this pathological process.
摘要：
Formaldehyde and benzene are the two major indoor air pollutants due to their prevalence and toxicity. This study aimed to explore the toxic effect on the spleen and relevant immune responses of Ball* mice caused by exposure to a combination of formaldehyde and benzene. Balb/c mice were divided randomly into five groups (n = 9/group): blank control group (Ctrl); solvent ([corn] Oil) control; formaldehyde only (FA, 3 mg/m(3)); benzene only (BZ, 150 mg/kg BW); and, formaldehyde +benzene group (FA+ BZ). Exposures were performed for 8 hiday, 5 day/week, for 2 weeks. Tail blood was collected after the final exposure; 24-h later, the mice were euthanized to permit assessment of a variety of immune endpoints. The endpoints' three areas were: (1) in living mice, body weight and delayed-type hypersensitivity (DTH) responses; (2) in blood, immune cell counts and serum antibody levels (serum hemagglutination); and, (3) in spleen samples, reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), caspase-3 (cell apoptosis) levels and lymphocyte proliferation. In this study we fund (1) BZ and FA + BZ exposure can lead to the reduction in the number of some immune cells in peripheral blood; (2) Formaldehyde has certain synergistic effects on benzene-induced cytotoxicity in peripheral blood, (3) FA, BZ and FA+ BZ exposure can lead to ROS and GSH depletion in spleen cells, and spleen cell apoptosis (caspase-3 increased) may be one of the downstream events, decreased splenic lymphocyte proliferation; and (4) the FA+ BZ combined exposure can lead to the decreased body weight, serum antibody level (by serum hemagglutination assay). (C) 2016 Elsevier B.V. All rights reserved.
