[C8mim]Cl对HepG2细胞凋亡和内质网应激通路的影响

为研究离子液体氯化1-辛基-3-甲基咪唑（[C₈mim]Cl）是否通过内质网应激（ERS）通路诱导细胞凋亡,在MTT法检测细胞活力的基础上,用0,50,100,200μmol/L[C₈mim]Cl处理HepG2细胞24h后,采用流式细胞仪检测细胞凋亡,western blot检测ERS通路相关蛋白表达.结果显示：[C₈mim]Cl处理后HepG2细胞凋亡呈浓度依赖性增高.ERS相关蛋白葡萄糖调节蛋白78（GRP78）、磷酸化RNA依赖的蛋白激酶样内质网激酶（p-PERK）、磷酸化真核起始因子2α（p-eIF2α）、磷酸化肌醇需求酶-1（p-IRE1）、激活转录因子4（ATF4）和ATF6显著上调.[C₈mim]Cl还显著诱导了C/EBP同源蛋白（CHOP）和半胱氨酸天冬氨酸蛋白酶4（caspase 4）蛋白表达,促进了caspase 9和caspase 3活性升高.因此,[C₈mim]Cl可通过ERS通路诱导HepG2细胞凋亡.     

内质网应激在氟暴露致小鼠睾丸损伤中的作用

探讨了内质网应激在亚慢性氟暴露致小鼠睾丸损伤中的作用及分子机制.选用健康初断乳ICR雄性小鼠30只,随机分为对照组（C）、低氟组（LF）和高氟组（HF）,分别饮用自来水、5、30 mg·L^-1氟化钠水溶液90 d.亚慢性氟暴露结束后,以睾丸脏器系数、睾丸组织氧化/抗氧化酶和形态结构、精子质量、睾丸细胞凋亡、葡萄糖调节蛋白78（GRP78）、CCAAT/增强子结合蛋白同源蛋白（CHOP）、半胱氨酸天冬氨酸蛋白酶12（CASPASE-12）、半胱氨酸天冬氨酸蛋白酶3（CASPASE-3）为观测点.结果表明,与对照组比,LF组和HF组LDH、SOD、T-AOC活性下降,MDA含量上升,HF组GSH-PX活性下降,差异有统计学意义（p<0.05或p<0.01）;LF组可见细胞层次减少、间隙变大,成熟精子数量减少,HF组细胞溶解、层次紊乱,空泡化严重,少见成熟精子;LF组和HF组小鼠的精子活力降低,HF组小鼠精子数量下降,畸形率上升,差异有统计学意义（p<0.05或p<0.01）;LF组和HF组睾丸细胞凋亡指数上升,差异有统计学意义（p<0.01）;LF组和HF组Grp78、Caspase-12、Caspase-3基因表达水平上升,差异有统计学意义（p<0.05或p<0.01）.结果提示,除氧化应激以外,Caspase-12和Caspase-3基因表达异常可能是氟暴露致小鼠睾丸细胞凋亡异常的分子机制之一.     

Fas/FasL途径在氟暴露致PC12细胞凋亡中的作用

为了探讨Fas/FasL途径在氟暴露致PC12细胞凋亡中的作用及其机制,采用含20、40、80、160mg/L NaF培养液处理PC12细胞.结果表明,所有剂量NaF处理12、24、36、48h,PC12细胞活性升高;上述不同剂量NaF处理24h后,与对照组比,PC12细胞的活性氧水平、细胞凋亡率、细胞内Fas/FasL信号转导通路Fas和FasL、Caspase8、FADD、Caspase3基因和蛋白表达水平均呈显著上升（P < 0.05）,而Bid基因和蛋白表达水平显著下降（P < 0.05）,且呈氟暴露剂量依赖性.结果提示Fas/FasL途径在氟暴露致PC12细胞凋亡中起重要作用,其中FADD可能是Fas/FasL凋亡途径中的重要靶分子.     

梭鱼和青鳉鱼ERα介导的雌激素活性比较研究

为从物种雌激素受体(ERα)敏感性差异的角度探索辽东湾野生梭鱼雌雄同体高发生率的一个可能原因,从梭鱼肝脏cDNA中扩增出长1113 bp的梭鱼ERα(sERα) DEF区片段,并以此构建pGBT9-sERα DEF 质粒,将其和pGAD424-TIF2质粒依次转入Y190酵母细胞中,建立了sERα物种特异性的酵母双杂交筛选系统.在此系统中测试了4种环境中主要的雌激素雌酮(E1)、17β-雌二醇(E2)、雌三醇(E3)及17α-炔雌醇(EE2)对梭鱼ERα的诱导活性,半数雌激素活性浓度(EC50)为3.7、2.4、1698.7、1.2nmol/L,分别是青鳉鱼ERα活性的4.6、2.3、3.4、3.3倍,说明梭鱼ERα对E1、E2、E3、EE2具有较高的敏感性,这为解释辽东湾梭鱼雌雄同体的高发生现象提供了重要线索.     

Mechanism of Deca-BDE-induced apoptosis in Neuro-2a cells: Role of death-receptor pathway and reactive oxygen species-mediated mitochondrial pathway

Decabromodiphenyl ether (BDE-209) is a prevalent polybrominated diphenyl ether (PBDE) congener known to have neurotoxicity. Effects of BDE-209 on Neuro-2a cells were performed in the present study and the possible apoptotic pathway was discussed. Results indicated that BDE-209 induced Neuro-2a cell apoptosis, increased the protein expression of Fas and Fas-associated death domain-containing protein (FADD) and activated the caspase-8 and -3 activities in a concentration-dependent manner, inferring the death-receptor pathway was involved in the apoptotic process. Meanwhile, BDE-209 exposure increased the Bax/Bcl-2 ratio and decreased the cellular mitochondrial membrane potential (MMP) which led to cytochrome C released to the cytoplasm. The intracellular caspase-9 was elevated simultaneously, which caused downstream caspase cascade and triggered cell apoptosis. Moreover, BDE-209 exposure increased cellular reactive oxygen species (ROS) level in a concentration-dependent manner and the addition of N-acetyl-l-cysteine (NAC), known as ROS scavengers, obviously reduced the apoptotic rate and a positive relationship was observed between the degree of apoptosis blocking and the loss of MMP and ROS production. We thus concluded that BDE-209 induced Neuro-2a cell apoptosis via the combination of the death-receptor signaling pathway and the mitochondrial signaling pathway. The elevated ROS production was considered to magnify the intracellular apoptosis signal and played a crucial role in apoptosis of Neuro-2a cells induced by BDE-209.     

Quantum dots enhance Cu2+-induced hepatic L02 cells toxicity

As a new class of xenogenous nanoparticle,quantum dots (QDs) possess the potential to co-exist with Cu2+ in human liver.The combined toxicity is thus concerned.Considering QDs and Cu2+ are known ROS (reactive oxygen species) inducer,we investigated the combined oxidative stress and corresponding protective strategy using human hepatic L02 cells.The results demonstrated that the presence of a small amount of MPA-CdTe QDs (2 μg/mL) in a Cu2+ solution (2.5-20 μg/mL) resulted in a higher toxicity with up to 8-fold cell viability decrease,which was accompanied by cell morphology changes.The combined toxicity was then confirmed as ROS associated oxidative stress with up to 300% and 35% increase of the intracellular ROS level and glutathione S-transferase (GST) activity,respectively.N-acetylcysteine (NAC) can also provide almost complete protection against the induced toxicity.Therefore,the ROS associated oxidant injury might be responsible for the QDs-Cu2+/Cu2+ induced toxicity and could be balanced through cytoprotective antioxidant enzyme GST.     

慢性氟暴露致小鼠海马损伤及L-型钙拮抗剂的干预作用

探讨了慢性氟暴露致小鼠海马损伤及L-型钙通道拮抗剂的干预作用.将140只初断乳ICR雄性小鼠随机分为7组：对照组（C组）、高氟组（HF组,饮用30 mg·L^-1 NaF溶液）、低氟组（LF组,饮用5 mg·L^-1 NaF溶液）、高/低氟+L-型钙通道激动剂组（FPL64176）（HF/LF+FPL）、高/低氟+L-型钙通道拮抗剂组（Nifedipine）（HF/LF+NIF）.染氟6个月,染氟结束前1周,HF/LF+FPL和HF/LF+NIF组分别每天腹腔注射激动剂或拮抗剂（5 mg·kg^-1·d^-1）.用TUNEL法检测小鼠海马CA₁区细胞凋亡水平,用Western Blot法检测细胞膜L-型钙通道Cav1.2、Ca²⁺信号通路分子和下游凋亡调节相关分子蛋白表达水平等.结果表明,与对照组比,HF/LF组小鼠海马组织抗氧化能力显著降低（p<0.05或p<0.01）,细胞凋亡水平极显著上升（p<0.01）,Cav1.2与Bcl-2蛋白表达水平显著下降（p<0.05或p<0.01）,Ca²⁺信号转导通路CaM、CaMKII和促凋亡Bax、Bax/Bcl-2蛋白表达水平显著上升（p<0.05或p<0.01）.注射FPL64176的小鼠海马细胞和上述分子指标的损伤加剧,而注射NIF对海马细胞和上述分子蛋白表达有一定的逆转作用.提示L-型钙离子通道介导了氟暴露致小鼠海马损伤,氟暴露致海马细胞膜L-型钙离子通道Cav1.2蛋白、细胞内Ca²⁺信号转导通路分子和下游凋亡调节相关蛋白表达异常是其分子机制之一,而L-型钙通道拮抗剂NIF可能是一种新型有效的抗氟药物.     

Inhibition of ROS elevation and damage to mitochondrial function prevents lead-induced neurotoxic effects on structures and functions of AFD neurons in Caenorhabditis elegans

Here we investigated the possible roles of oxidative stress in the formation of decreased thermotaxis to cultivation temperature in lead (Pb)-exposed nematodes Caenorhabditis elagans. Exposure to Pb at the examined concentrations decreased thermotaxis behaviors, and induced severe deficits in the structural properties of AFD sensory neurons. Meanwhile, Pb exposure caused the induction of severe oxidative damage, reactive oxygen species (ROS) production, and mitochondrial dysfunction in young adults. Moreover, pre-treatment with the antioxidants dimethyl sulfoxide (DMSO), ascorbate and N-acetyl-L-cysteine (NAC), used to inhibit both the ROS elevation and the mitochondrial dysfunction caused by Pb exposure, at the L2-larval stage prevented the induction of oxidative damage and the formation of severe deficits in thermotaxis and structural properties of AFD sensory neurons in Pb-exposed young adults. Therefore, the formation of oxidative stress caused by Pb exposure may be due to both the induction of ROS elevation and damage to mitochondrial function, and oxidative stress may play a key role in inducing the neurotoxic effects on the structures and function of AFD sensory neurons in Pb-exposed nematodes.     

大气细颗粒物亚慢性染毒对大鼠肺内质网应激相关因子表达的影响

采集冬、夏季太原市大气细颗粒物(PM2.5),并制备PM2.5生理盐水混悬液.将35只雄性SD大鼠随机分为7组:对照组、3个不同剂量夏季PM2.5染毒组(0.2、0.6、1.5 mg·kg~(-1)体重)及3个不同剂量冬季PM2.5染毒组(0.3、1.5、2.7 mg·kg~(-1)体重),每组5只,气道滴注法染毒,每隔2 d染毒1次,共60 d.采用荧光实时定量PCR、Western blot、ELISA方法检测大鼠肺内质网应激指标——葡萄糖调节蛋白78(GRP78)、活化转录因子6(ATF6)、C/EBP同源蛋白(CHOP)、半胱氨酸天冬氨酸蛋白酶12(Caspase12)及血红素氧合酶-1(HO-1)的mRNA和蛋白表达变化.结果表明,与对照组相比,冬季中、高剂量PM2.5染毒组大鼠肺组织GRP78、ATF6、CHOP、Caspase12、HO-1 mRNA和蛋白表达显著增加,夏季高剂量PM2.5染毒组大鼠肺组织这5个基因mRNA和蛋白表达显著增加.冬季和夏季PM2.5组大鼠肺上述5个基因表达有剂量-效应关系.结果表明,太原市PM2.5亚慢性染毒可诱导大鼠肺内质网应激相关基因GRP78/ATF6/CHOP/HO-1表达,说明肺内质网应激反应加强;而CHOP和Caspase-12上调,提示与细胞凋亡关联的内质网相关性死亡途径被激活.冬季和夏季PM2.5引起内质网应激相关因子表达上调的效应没有显著差别.     

氟化钠与强致突变物联合诱致的高等植物细胞微核效应

氟化钠在与强致突变物的联合实验中均发生较强的颉颃(减毒)作用,例如非常显著地抑制由平阳霉素(染色体断裂剂)或秋水仙素(有丝分裂毒素)诱致的微核效应(F＇相似文献   

Mitochondrial electron transport chain is involved in microcystin-RR induced tobacco BY-2 cells apoptosis

Microcystin-RR （MC-RR） has been suggested to induce apoptosis in tobacco BY-2 cells through mitochondrial dysfunction including the loss of mitochondrial membrane potential . TO further elucidate the mechanisms involved in MC-RR induced apoptosis in tobacco BY-2 cells, we have investigated the role of mitochondrial electron transport chain （ETC） as a potential source for reactive oxygen species （ROS）. Tobacco BY-2 cells after exposure to MC-RR （60 mg/L） displayed apoptotic changes in association with an increased production of ROS and loss of Am. All of these adverse effects were significantly attenuated by ETC inhibitors including Rotenone （2 μmol/L, complex I inhibitor） and antimycin A （0.01 μmol/L, complex III inhibitor）, but not by thenoyltrifluoroacetone （S μmol/L, complex Ⅱinhibitor）. These results suggest that rnitochondrial ETC plays a key role in mediating MC-RR induced apoptosis in tobacco BY-2 cells through an increased mitochondrial production of ROS.     

镉暴露对斑马鱼胚胎发育的毒性效应研究

镉是一种具有强致畸性和致癌性的重金属. 为研究镉暴露对早期胚胎发育的毒性效应,以斑马鱼为模式动物,选取5个镉浓度来处理斑马鱼胚胎4~120 hpf (hours post fertilization, 受精后小时),计算镉的半致死(LC₅₀)浓度,研究7.50 mg/L镉对斑马鱼胚胎8个基因表达的影响. 结果表明:镉暴露导致斑马鱼胚胎产生小头、小眼、躯干弯曲、心脏发育异常以及死亡等异常. 通过原位杂交和定量PCR方法分析镉对抗氧化基因(prdx1和gstp1.2)、转录翻译相关基因(atf3、jdp2b和eif4a1b)、应激反应相关基因(hsp70l和hsp90aa1.1)以及脂肪酸结合蛋白基因(fabp7a)表达的影响,发现镉暴露将改变上述基因在组织和器官的表达及表达水平,这些影响可能与镉导致斑马鱼胚胎嗅球、侧线、神经和心脏的发育异常有关. 研究显示,镉的LC₅₀浓度为15.20 mg/L,7.50 mg/L的镉可影响斑马鱼胚胎的氧化应激、转录翻译和早期神经发育等过程,并通过影响基因表达从而干扰斑马鱼胚胎发育,进而可能造成个体嗅觉、视觉和运动等功能缺陷.      

Regulation of matrix stiffness on the epithelial-mesenchymal transition of breast cancer cells under hypoxia environment

Substrate stiffness and hypoxia are associated with tumor development and progression, respectively. However, the synergy of them on the biological behavior of human breast cancer cell is still largely unknown. This study explored how substrate stiffness regulates the cell phenotype, viability, and epithelial-mesenchymal transition (EMT) of human breast cancer cells MCF-7 under hypoxia (1% O₂). TRITC-phalloidin staining showed that MCF-7 cells transformed from round to irregular polygon with stiffness increase either in normoxia or hypoxia. While being accompanied with the upward tendency from a 0.5- to a 20-kPa substrate, the percentage of cell apoptosis was significantly higher in hypoxia than that in normoxia, especially on the 20-kPa substrate. Additionally, it was hypoxia, but not normoxia, that promoted the EMT of MCF-7 by upregulating hypoxia-inducible factor-1α (HIF-1α), vimentin, Snail 1, and matrix metalloproteinase 2 (MMP 2) and 9 (MMP 9), and downregulating E-cadherin simultaneously regardless of the change of substrate stiffness. In summary, this study discovered that hypoxia and stiffer substrate (20 kPa) could synergistically induce phenotype change, apoptosis, and EMT of MCF-7 cells. Results of this study have an important significance on further exploring the synergistic effect of stiffness and hypoxia on the EMT of breast cancer cells and its molecular mechanism.     

Comparison of hydrofluorosilicic acid and pharmaceutical sodium fluoride as fluoridating agents—A cost–benefit analysis

Water fluoridation programs in the United States and other countries which have them use either sodium fluoride (NaF), hydrofluorosilicic acid (HFSA) or the sodium salt of that acid (NaSF), all technical grade chemicals to adjust the fluoride level in drinking water to about 0.7–1 mg/L. In this paper we estimate the comparative overall cost for U.S. society between using cheaper industrial grade HFSA as the principal fluoridating agent versus using more costly pharmaceutical grade (U.S. Pharmacopeia – USP) NaF. USP NaF is used in toothpaste. HFSA, a liquid, contains significant amounts of arsenic (As). HFSA and NaSF have been shown to leach lead (Pb) from water delivery plumbing, while NaF has been shown not to do so. The U.S. Environmental Protection Agency's (EPA) health-based drinking water standards for As and Pb are zero. Our focus was on comparing the social costs associated with the difference in numbers of cancer cases arising from As during use of HFSA as fluoridating agent versus substitution of USP grade NaF. We calculated the amount of As delivered to fluoridated water systems using each agent, and used EPA Unit Risk values for As to estimate the number of lung and bladder cancer cases associated with each. We used cost of cancer cases published by EPA to estimate cost of treating lung and bladder cancer cases. Commercial prices of HFSA and USP NaF were used to compare costs of using each to fluoridate. We then compared the total cost to our society for the use of HFSA versus USP NaF as fluoridating agent. The U.S. could save $1 billion to more than $5 billion/year by using USP NaF in place of HFSA while simultaneously mitigating the pain and suffering of citizens that result from use of the technical grade fluoridating agents. Other countries, such as Ireland, New Zealand, Canada and Australia that use technical grade fluoridating agents may realize similar benefits by making this change. Policy makers would have to confront the uneven distribution of costs and benefits across societies if this change were made.     

柱孢藻毒素对草鱼淋巴细胞毒效应及氧化损伤机理研究

针对淡水水体拟柱孢藻水华产生的柱孢藻毒素,以我国典型食用鱼种草鱼(Ctenophar yngodon idellus)为实验材料,研究了其对鱼体免疫细胞毒效应及机理.结果表明,随着体外暴露剂量的增加,草鱼淋巴细胞活性逐渐降低,暴露24h后100μg·L-1柱孢藻毒素诱导组细胞活性仅为对照组的20%;对诱导组淋巴细胞的DNA检测发现呈现阶梯状电泳的典型细胞凋亡特征;应用流式细胞仪进一步检测了细胞凋亡率,表明1～100μg·L-1柱孢藻毒素均能够诱导细胞凋亡,并且其凋亡毒效应呈现明显的时间-效应和剂量-效应关系;诱导12h后,氧化应激产物活性氧(ROS)和丙二醛(MDA)含量均明显上升,100μg·L-1柱孢藻毒素诱导组ROS含量为对照组的2.5倍,MDA含量为对照组的2倍,诱导24h后,1、10、50和100μg·L-1实验组氧化应激产物含量仍然明显上升,这说明氧化应激是柱孢藻毒素导致草鱼淋巴细胞DNA损伤的重要原因;RT-PCR技术对重要凋亡基因的检测表明,1～100μg·L-1实验组凋亡促进基因Bax表达显著增强(p<0.05),50和100μg·L-1高剂量组凋亡抑制基因Bcl-2表达显著降低(p<0.01).本研究从细胞水平揭示柱孢藻毒素对草鱼免疫细胞具有明显的毒性,该毒效应通过氧化应激介导的DNA损伤表现,凋亡是柱孢藻毒素对草鱼免疫细胞毒性的主要机制.     

氧化石墨烯对嗜热四膜虫的毒性效应

以嗜热四膜虫（Tetrahymena thermophila）作为受试生物,考察了纳米材料氧化石墨烯（GO）对其细胞生长率、乙酰胆碱酯酶（AchE）和氧化应激酶活性、生物膜损伤及细胞凋亡的影响,以探究GO的毒性效应.结果表明,GO浓度高于32mg/L时显著抑制嗜热四膜虫的细胞增殖（P<0.05）,细胞存活率低于50%;在0~64mg/L实验范围内,随GO暴露浓度增加,细胞内活性氧自由基（ROS）和超氧化物歧化酶（SOD）水平呈先升后降的趋势,AchE活性受抑;GO抑制位于线粒体内膜的琥珀酸脱氢酶（SDH）活性,促进细胞质中乳酸脱氢酶（LDH）的释放;64mg/L GO导致四膜虫细胞出现明显凋亡现象.以上结果显示,中低浓度GO（0~8mg/L）暴露下,氧化应激机制对细胞毒性起主要贡献作用;高浓度GO（32和64mg/L）作用下,四膜虫凋亡现象的产生可能是GO抑制其生长作用导致的.     

MEHP对胚胎期海水青鳉(Oryzias melastigma)的内分泌干扰效应

为探讨邻苯二甲酸二（2-乙基己基）酯（DEHP）的代谢产物邻苯二甲酸单-2-乙基己酯（MEHP）对海水青鳉胚胎的内分泌干扰效应,本研究调查了海水青鳉胚胎受精后暴露于MEHP（0.01,0.1,和1 mg/L）直至胚胎发育晚期-受精后10 d（10 dpf）,采用实时定量反转录聚合酶链反应（qRT-PCR）分析MEHP对内分泌干扰标志通路雌激素受体（ER）、过氧化物增殖激活受体（PPAR）通路和芳香化酶（CYP19）基因的影响。结果显示:MEHP对海水青鳉胚胎存活和孵化没有显著影响,而各MEHP处理组显著诱导了编码雌激素受体（ERα）和PPAR受体（PPARα和PPARγ）的基因表达水平,0.01和1 mg/L MEHP显著诱导了雌激素受体（ERγ）基因表达水平。MEHP暴露显著增加卵黄蛋白原（VTG）两个亚型-VTG1、VTG2,卵壳前体蛋白（Choriogenin,Chg）两个亚型-ChgH、ChgL,芳香化酶（CYP19）-CYP19a、CYP19b的基因表达水平。然而,MEHP暴露对海水青鳉胚胎编码雄激素受体的基因雄激素受体α亚型（androgen receptor α,ARα）的表达水平无显著影响。说明MEHP可通过上调芳香化酶CYP19的表达增加雄激素向雌激素的转化,增加的雌激素通过血液循环扩散进入靶组织和细胞结合雌激素受体ERs,导致ERs的上调（ERα和ERγ）,使得雌激素受体激活、二聚化并结合大多数雌激素响应基因如VTG和Chg的雌激素响应元素（EREs）,增加雌激素响应基因VTG和Chg的表达,增加VTG和Chg的合成从而产生内分泌干扰效应。     

Suppression of male reproduction in rats after exposure to sodium fluoride during early stages of development

Sodium fluoride (NaF), a widespread natural pollutant was given to sperm-positive female rats throughout gestation and lactation at a dose of 4.5 and 9.0 ppm via drinking water. The neonates were allowed to grow up to 90 days on tap water, and then sperm parameters, testicular steroidogenic marker enzyme activity levels, and circulatory hormone levels were studied. The sperm count, sperm motility, sperm coiling (hypoosmotic swelling test), and sperm viability were decreased in experimental rats when compared with controls. The activity levels of testicular steroidogenic marker enzymes (3β hydroxysteroid dehydrogenase and 17β hydroxysteroid dehydrogenase) were significantly decreased in experimental animals indicating decreased steroidogenesis. The serum testosterone, follicle stimulating hormone and luteinizing hormone levels were also significantly altered in experimental animals. Our data indicate that exposure to NaF during gestation and lactation affects male reproduction in adult rats by decreasing spermatogenesis and steroidogenesis.     

离子选择性电极法对氟离子吸附反应动力学的研究

尝试建立了一种利用双离子选择性电极法测定土壤对氟离子吸附动力学的新方法.     

蓝藻水华粗提物对小鼠肝脏HSP70,GRP78表达的影响

为研究在活体条件下自然水环境中蓝藻水华对生物体的毒性效应,将小鼠连续7d经灌胃暴露于不同浓度的蓝藻水华粗提物,通过western-blotting法测定小鼠肝组织中热应激蛋白HSP70、与内质网应激相关的GRP78、CHOP以及caspaser-12蛋白表达水平.结果显示,随着暴露浓度的提高,在最高浓度组,HSP70,GRP78的表达水平显著提高,但未见CHOP和caspaser-12表达的明显改变.研究结果表明,蓝藻水华粗提物使小鼠肝组织处于内质网应激状态.