3，4－二羟基苯乙酮对老年大鼠血小板膜磷脂成分的影响

ＤＨＡＰ１００ｍｇ·ｋｇ－１·ｄ－１，ｐｏ，持续１０周，可使老龄大鼠血小板膜磷脂（ＰＬ）含量增加，膜磷脂与膜胆固醇比值（ＰＬ／Ｃ）相对增高；血小板磷脂成分——磷脂酰乙醇胺（ＰＥ）和磷脂酰胆碱（ＰＣ）含量也有明显增加（ｐ＜０．０１），但血小板膜总脂及膜胆固醇含量无明显变化（Ｐ＞０．０５）。本实验结果提示：ＤＨＡＰ对血小板功能的影响可能与其抑制血小板膜磷脂降解、改变血小板膜组分有关。     

基于代谢组学技术研究绞股蓝总皂苷抑制tau蛋白过表达诱导的细胞损伤机制

目的 研究绞股蓝总皂苷(GPs)对tau蛋白过表达细胞代谢的影响,探讨GPs治疗阿尔茨海默病(AD)的机制。方法 通过采用CRISPR/Cas9技术构建微管相关蛋白tau (MAPT)过表达N2a细胞系(MAPT细胞);用CCK-8法检测GPs对N2a、MAPT细胞存活率的影响;体外培养N2a (对照组)、MAPT细胞(模型组),向MAPT细胞中加入GPs (50、100 μg·mL^-1)进行干预,共同孵育24 h后收集细胞,采用Western blotting技术检测总tau蛋白量水平;利用代谢组学技术检测GPs对MAPT细胞内源性代谢产物的影响,明确差异代谢产物及通路。结果 50、100、200 μg·mL^-1 GPs对N2a细胞活力无明显影响;5、50、100、200 μg·mL^-1 GPs对MAPT细胞活力无显著性影响;与对照组相比,MAPT细胞内tau蛋白水平明显增加(P<0.001);与模型组比较,50 μg·mL^-1 GPs可明显减少MAPT细胞内总tau蛋白含量(P<0.05);代谢组学结果显示,按照差异代谢产物数量占比从高到底依次为脂质和类脂分子,有机酸及其衍生物,核苷、核苷酸和类似物等。通过京都基因与基因组百科全书(KEGG)通路分析,差异代谢产物主要富集在核苷酸代谢、氨基酸合成、甘油磷脂代谢等通路。与模型组比较,给药后参与甘油磷脂代谢通路的胞磷胆碱和磷脂酰胆碱水平显著增加(P<0.001),甘油磷酰胆碱、甘油-3-磷乙醇胺水平显著降低(P<0.001)。结论 GPs可以减少细胞内tau蛋白的异常过表达,通过增加胞磷胆碱和磷脂酰胆碱水平、减少甘油磷酰胆碱和甘油-3-磷乙醇胺水平调控甘油磷脂代谢通路。     

药用辅料中不同来源溶血磷脂酰胆碱含量限值的合理性分析

目的：通过比较蛋黄来源及大豆来源溶血磷脂酰胆碱对红细胞影响的差异来评价目前药用辅料中不同来源溶血磷脂酰胆碱含量限值的合理性。方法：采用体外红细胞溶血试验及红细胞渗透脆性试验考察两种不同来源溶血磷脂酰胆碱对红细胞的影响。结果：蛋黄来源及大豆来源溶血磷脂酰胆碱红细胞溶血IC₅₀分别为0.0427mg·mL^-1、0.0801mg·mL^-1;二者在0.65%、0.60%、0.55% NaCl低渗盐溶液中引起的溶血率亦具有显著性差异,蛋黄来源溶血磷脂酰胆碱的溶血率明显高于大豆来源溶血磷脂酰胆碱。但红细胞凝聚试验结果表明,二者均未见引起红细胞凝聚。结论：两种不同来源的溶血磷脂酰胆碱致溶血能力具有显著性差异,建议应分别制定不同来源磷脂类产品中溶血磷脂酰胆碱的含量限值,以保证临床用药安全。     

半枝莲粗多糖对S180荷瘤小鼠红细胞膜脂类成分的影响

目的 探讨半枝莲粗多糖对S₁₈₀荷瘤小鼠红细胞膜脂类含量的影响。方法 48只小鼠,♂,随机分为正常对照组、模型对照组、阳性对照(黄芪多糖)组、半枝莲粗多糖低、中、高剂量(50,100,200 mg·kg^-1)组,除正常对照组外其他组小鼠右前腋皮下接种肿瘤。采用紫外分光光度计检测红细胞膜胆固醇、磷脂含量,采用GC-MS检测红细胞膜磷脂脂肪酸的百分含量。结果 与模型对照组比较,半枝莲粗多糖显著提高S₁₈₀荷瘤小鼠红细胞膜磷脂含量、降低胆固醇含量及二者比值,棕榈一烯酸(C_16∶1)、油酸(C_18∶1)、亚油酸(C_18∶2)、不饱和脂肪酸/总脂肪酸的比例均有不同程度的升高。结论 半枝莲粗多糖可增加S₁₈₀荷瘤小鼠红细胞膜磷脂含量,降低胆固醇及其比值,并且增加不饱和脂肪酸在总脂肪酸中的比例,可能通过这些指标共同作用提高红细胞膜的流动性,从而增加红细胞的免疫功能,实现抗肿瘤作用。     

何首乌水溶性成分2,3,5,4′-四羟基二苯乙烯-2-O-β-D葡糖苷(ST I)对内皮细胞表达VEGF的影响何首乌水溶性成分2,3,5,4′-四羟基二苯乙烯-2-O-β-D葡糖苷(ST I)对内皮细胞表达VEGF的影响

目的研究何首乌水溶性成分2,3,5,4′-四羟基二苯乙烯-2-O-β-D葡糖苷(ST I)对溶血磷脂酰胆碱(LPC)诱导人脐静脉内皮细胞株ECV304细胞中血管内皮生长因子(VEGF)表达的影响。方法在ECV304细胞培养基中加入LPC(2.5 mg·L^-1)或LPC与ST I共孵24 h，收集各组条件培养基，用基础酶联免疫吸附试验(ELISA)检测各组条件培养基中VEGF蛋白含量；用原位杂交法、RT-PCR及Realtime RT-PCR法检测LPC对内皮细胞VEGF mRNA的表达及ST I的影响。结果ECV304细胞暴露于LPC后，VEGF蛋白分泌明显增加；加入ST I后VEGF蛋白含量明显降低; LPC可以使ECV304中VEGF mRNA的表达明显升高, 并使VEGF165 mRNA的表达升高；ST I可剂量依赖性地抑制VEGF165 mRNA的高表达。结论LPC能诱导ECV304细胞表达高水平的VEGF蛋白及VEGF mRNA，1×10^-5 mol·L^-1 ST I可抑制LPC的作用，降低VEGF的高表达。     

手性溶液萃取分离氧氟沙星对映体

目的研究氧氟沙星对映体在手性环境中的萃取分配行为,为外消旋体膜萃取拆分提供理论和设计依据。方法以0.25 mol·L^-1 L-二苯甲酰酒石酸醇溶液为有机相,含0.14 g·L^-1氧氟沙星的0.1 mol·L^-1磷酸氢二钠/磷酸缓冲液为水相,考察了pH对氧氟沙星对映体在水-有机相分配系数(K)和分离因子(α)的影响,研究了不同碳数醇的溶剂化效应,同时运用中空纤维膜对氧氟沙星外消旋体进行初步分离。结果以癸醇为溶剂,pH 6.86时,L-二苯甲酰酒石酸对氧氟沙星外消旋体萃取分配系数大于4.7,α达1.18;用中空纤维支载液膜双有机相逆流分级萃取技术,11个22 cm长膜器串联,产品光学纯度达90%以上。结论L-二苯甲酰酒石酸在醇溶剂中对磷酸氢二钠缓冲液中的RS-氧氟沙星对映体有较强的立体选择性,其中癸醇的效果最好,pH对K和α有较大影响,综合K和α值,取pH 6.86时,手性萃取效果最佳;利用高效中空纤维膜,可使RS氧氟沙星对映体得到不同程度的分离。     

磷脂对甘草酸二铵小肠吸收的影响

研究磷脂对甘草酸二铵及甘草次酸小肠吸收的影响。建立大鼠原位单向肠灌流及伴有肠系膜插管的肠灌流模型，采用高效液相色谱法检测灌流液及血浆中的药物浓度，计算表观通透系数P_app和吸收速率常数K_a。建立大鼠灌胃后肝门静脉取血模型，测定门静脉血浆中药物浓度，以对灌流结果进一步验证。甘草酸二铵和甘草次酸均能跨肠壁吸收，其P_app分别为0.36和5.73 cm·min^-1，加入磷脂后，P_app分别提高到0.68和7.98 cm·min^-1。磷脂使甘草酸二铵本身的吸收略有增加，但统计学检验差异不显著，但对其肠道菌群代谢物甘草次酸的吸收有显著促进作用。     

油酰乙醇胺对东莨菪碱诱导小鼠认知功能损伤的保护作用

目的 探讨油酰乙醇胺对东莨菪碱诱导小鼠认知功能损伤的保护作用。方法 将小鼠随机分为6组：对照组、模型组、多奈哌奇组（阳性药,3 mg·kg^-1）和油酰乙醇胺低、中、高剂量（50、100、200 mg·kg^-1）组,每组6只。在ig给药4周后,除对照组外,各组ip 3 mg·kg^-1的东莨菪碱建立阿尔茨海默病（AD）模型。避暗、跳台行为学实验检测小鼠记忆功能; ELISA法检测小鼠海马和大脑皮层中乙酰胆碱（Ach）和乙酰胆碱酯酶（AChE）水平;HE染色观察小鼠大脑皮层及海马损伤。结果 与对照组比较,模型组的避暗潜伏期显著缩短、避暗错误次数显著增加（P<0.001）;大脑皮层、海马的Ach水平显著减少（P<0.01、0.001）,AChE活性显著升高（P<0.001）;模型组的小鼠脑组织形态结构不均匀,组织细胞呈弥散状,提示组织存在病变。与模型组比较,各给药组的避暗潜伏期显著升高、避暗错误次数显著减少（P<0.01）;油酰乙醇胺给药组的小鼠大脑皮层、海马组织Ach水平显著升高（P<0.05、0.01）,AChE活性显著降低（P<0.01、0.001）;小鼠脑组织形态结构病理改变减轻。结论 油酰乙醇胺对东莨菪碱诱导学习记忆障碍模型小鼠的认知功能具有改善作用,其作用机制可能与调节胆碱能系统功能、促进神经细胞存活有关。     

多烯磷脂酰胆碱联合复方丹参滴丸对非酒精性脂肪肝的临床研究

目的 研究多烯磷脂酰胆碱联合复方丹参滴丸对非酒精性脂肪肝患者的临床治疗效果。方法 选择2012年1月-2015年12月在西安医学院附属宝鸡医院进行诊治的非酒精性脂肪肝患者116例,随机分为观察组与对照组,每组58例。对照组采用复方丹参滴丸治疗,观察组采用多烯磷脂酰胆碱联合复方丹参滴丸治疗,均治疗3个月。比较两组的临床有效率;分别于治疗前后检测肝功能指标：天氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）、γ-谷氨酰转肽酶（γ-GT）、总胆汁酸（TBIL）;血脂指标：总胆固醇（TC）、三酰甘油（TG）;肝纤维化指标：层粘连蛋白（LN）、透明质酸（HA）、Ⅲ型前胶原（PCⅢ）、IV型胶原（IV-C）;并进行上腹部CT平扫,计算肝/脾CT比值。结果 观察组的有效率为91.4%（53/58）,明显高于对照组的72.4%（42/58）（P<0.05）;与同组治疗前比较,治疗后两组的AST、ALT、γ-GT、TBIL、TC、TG水平均明显降低,肝/脾CT比值明显升高（P<0.05）,且观察组的改善程度明显优于对照组（P<0.05）;与治疗前比较,两组治疗后的LN、PCⅢ、IV-C和HA水平均明显降低（P<0.05）,且观察组的降低程度明显优于对照组（P<0.05）。结论 多烯磷脂酰胆碱联合复方丹参滴丸可以明显改善非酒精性脂肪肝患者的肝功能和肝纤维化,降低血脂。     

Cationic amphiphilic drugs as a potential tool for modifying phospholipids of tumor cells. An in vitro study of chlorpromazine effects on Krebs II ascites cells

[³²P]orthophosphate and [U-¹⁴C]glycerol incorporation into Krebs ascites cell lipids was studied in vitro in the presence of chlorpromazine (CPZ)¹. At concentrations not exceeding 0.1 mM, the drug produced no cell damage within 3 hr incubation. Under these conditions, CPZ inhibited the incorporation of [³²P]orthophosphate into phosphatidylcholine and phosphatidylethanolamine and of [U-¹⁴C]glycerol into phosphatidylcholine and triglycerides, in a dose-dependent manner. On the other hand, synthesis of phosphatidic acid and phosphatidylglycerol was greatly enhanced, whereas phosphatidylinositol showed no major change. These results are compatible with an inhibition of phosphatidate phosphohydrolase, redirecting phospholipid biosynthesis towards the anionic classes. In vitro treatment of cells for 3 hr induced profound changes of phospholipid composition, which displayed a relative increase of phosphatidylglycerol and phosphatidic acid at the expense of phosphatidylcholine and phosphatidylethanolamine. The use of amphipathic cationic drugs can thus offer an interesting model for studying the relationship between cell proliferation and membrane phospholipid biosynthesis.     

Effect of polychlorinated biphenyls (PCBs) administration on phospholipid biosynthesis in rat liver

The effect of PCBs or phenobarbital on the biosynthesis of phospholipids in hepatic endoplasmic reticulum of rats was studied by the intraperitoneal injection of [³²P]orthophosphate, [Me?¹⁴ C]choline or [2?³H]glycerol. Significant increases in liver microsomal phospholipid content after the administration of either PCBs or phenobarbital indicated the actual proliferation of endoplasmic reticulum membranes. The rate of both [³²P] and [¹⁴C] incorporations into microsomal choline-containing phospholipids, such as phosphatidylcholine, sphingomyelin and lysophosphatidylcholine, was reduced to one fifth by PCBs administration compared with control animals. The incorporation of [³²P]orthophosphate into phosphatidylethanolamine or other phospholipid classes was less or not affected, respectively, by PCBs administration. The specific inhibitory effect of PCBs on the incorporation into cholinecontaining phospholipids was not observed when [2?³-H]glycerol was used as a precursor. Phenobarbital administration, however, increased significantly the rate of [³²P] incorporation into liver phospholipids, especially phosphatidylcholine. It is suggested that the increase in microsomal phospholipid content by PCBs administration is not due to the stimulation of synthesis but to the inhibition of the catabolism of membrane phospholipids and that the increase in content caused by phenobarbital is due at least in part, to the stimulation of synthesis. The possible site(s) of PCBs-induced inhibition of phospholipid biosynthesis in rat liver is discussed.     

Guanidination of notexin promotes its phospholipase A2 activity-independent fusogenicity on vesicles with lipid-supplied negative curvature

To address the requirement of phospholipase A₂ (PLA₂) activity in membrane fusion events and membrane perturbation activity of notexin and guanidinated notexin (Gu-notexin), the present study was conducted. Notexin and Gu-notexin did not show PLA₂ activity after the removal of Ca²⁺ with EDTA. Metal-free notexin and Gu-notexin were found to induce membrane leakage and fusion of phospholipid vesicles. Fusogenic activity of native and modified notexin correlated positively with their membrane-damaging activity underlying the deprivation of PLA₂ activity. Compared with Ca²⁺-bound Gu-notexin, fusogenicity of metal-free Gu-notexin was notably increased by incorporation of cholesterol, cholesterol sulfate, phosphatidylethanolamine, α-tocopherol and phosphatidic acid that supplied negative curvature into phospholipid bilayer. The ability of Gu-notexin to induce membrane fusion of vesicles with lipid-supplied negative curvature was higher than that of notexin regardless of the absence or presence of Ca²⁺. Consistently, metal-free Gu-notexin markedly induced membrane fusion of red blood cells (RBCs) compared with metal-free notexin, and fusion activity of metal-free Gu-notexin on cholesterol-depleted RBCs notably reduced. Compared with notexin, Gu-notexin highly induced uptake of calcein-loaded phosphatidylcholine (PC)/cholesterol and PC/cholesterol sulfate vesicles by K562 cells in the presence of EDTA. Taken together, our data suggest that notexin and Gu-notexin could induce vesicle leakage and fusion via a PLA₂ activity-independent mechanism, and guanidination promotes PLA₂ activity-independent fusogenicity of notexin on vesicles with lipid-supplied negative curvature.     

Effect of scorpion (Leiurus Quinquestriatus H and E) venom on lipid metabolism.

Injection of rats with a sublethal dose (200 μg per kg) of Leiurus quinquestriatus venom, induces an increase in the total lipid, cholesterol and phospholipid content of the liver. In the serum an increase in the free and esterified cholesterol, esterified fatty acids, phosphatidylcholine, phosphatidylethanolamine and a decrease in free fatty acids, sphingomylin and lysolecithin was demonstrated. An increase in the albumin, alpha₁-and alpha₂-globulins, and a decrease in the beta and gamma globulins of the serum was also observed.     

Effects of delta 9-THC on human platelet phospholipids

The possible change in Platelet lipids after smoking delta 9-THC was studied in chronic hashish users. The fluctuations of total phospholipid content is related to alterations of individual phospholipids. Changes in phosphatidylcholine, phosphatidylinositol and phosphatidylethanolamine are discussed in relation to membrane derangement leading to the increased rate of platelet lysis and aggregation under high doses of the drug.     

Neurochemical changes on oxidative stress in rat hippocampus during acute phase of pilocarpine-induced seizures

Using the epilepsy model obtained by systemic administration of pilocarpine in rats in the present study we investigated the changes caused by seizures on content and species of gangliosides and phospholipids, as well as on cholesterol concentration, glutathione reduced contents, Na⁺, K⁺-ATPase activity and lipid peroxidation levels in rat hippocampus. Wistar rats received pilocarpine hydrochloride (400 mg/kg, i.p., pilocarpine group), and other group received 0.9% saline (i.p., control group). Results showed that seizures significantly decreased the total content of lipids and glutathione reduced concentration in rat hippocampus. We also observed that seizures significantly reduced the absolute quantity of the major brain gangliosides (GM1, GD1a, GD1b and GT1b) and phospholipids (sphingomyelin, phosphatidylcholine and phosphatidylethanolamine). Our data also showed a decreased Na⁺, K⁺-ATPase activity and an increased TBARS levels in hippocampus of seized rats. If confirmed in human beings, these data could suggest that the alteration in lipid composition, Na⁺, K⁺-ATPase activity, glutathione reduced content and TBARS levels caused by seizures might contribute to the neurophysiopathology of seizures observed in epileptic patients.     

Exposure of human red blood cell membrane phospholipids to snake venom phospholipases. A--II. Hydrolysis of substrates in intact and resealed cells by phospholipase from ringhals (Hemachatus haemachates) venom: effect of calcium ions

Hydrolysis of substrates in intact and resealed cells by phospholipase from Ringhals (Hemachatus haemachates) venom: Effect of calcium ions. Toxicon16, 153–161, 1978. The accessability of glycerophospholipids in intact and in resealed human red cells to the action of Ringhals phospholipase A has been compared in isotonic and in hypotonic conditions, both with and without addition of Ca²⁺. Normal red cells in hypotonic media exposed prior to hemolysis, up to 70% of the membrane phosphatidylcholine, 20% of the phosphatidylethanolamine and about 5% of the phosphatidylserine to the action of the enzyme. The rate of hydrolysis of individual substrates in red cells in non-hemolytic conditions differs from the characteristic substrate preference of the enzyme. It is concluded that, in the outer half of the intact membrane, phosphatidylcholine is more exposed than phosphatidylethanolamine.The limit of non-lytic phospholipid degradation varies with the extent of stress exerted on the membrane by osmotic swelling and is strongly influenced by the presence of Ca²⁺ which acts both as an enzyme activator and a membrane stabilizer. Both in isotonic and in hypotonic media resealed cells differ from the normal ones by exhibiting an increased availability of the membrane glycerophospholipids, particularly phosphatidylserine and phosphatidylethanolamine, to the action of the enzyme. Moreover, while in isotonic media intact cells are not hemolyzed by the enzyme either in absence or in the presence of added Ca²⁺, the resealed cells treated with enzyme and Ca²⁺ undergo hemolysis.     

青心酮防治ApoE(-/-)小鼠主动脉粥样硬化斑块形成与脂氧素的关系

目的观察青心酮防治ApoE(-/-)小鼠主动脉粥样硬化(AS)病变形成与脂氧素的关系。方法取8只8周龄C57BL/6小鼠作空白对照组;取24只8周龄的ApoE(-/-)小鼠,♂,随机分成3组(每组8只):动脉硬化组(乙醇20 mg kg 1 d 1);青心酮组(青心酮20 mg kg 1 d 1);辛伐他汀组(辛伐他汀20 mg kg 1 d 1)。所有小鼠均以"西方类型膳食"饲养至16周。取血检测脂氧素、血脂和15-脂氧合酶蛋白的含量等;取主动脉根部行HE染色观察ApoE(-/-)主动脉粥样硬化病变情况;电镜观察斑块内皮细胞变化。Western blotting法测定血清中15-LO水平。结果青心酮组脂氧素增加,血脂含量降低,AS病灶形成减少,斑块内皮细胞损伤减轻,15-脂氧合酶含量减少。结论青心酮防治ApoE(-/-)小鼠AS病变,可能与其增加15-脂氧合酶途径产物——脂氧素有关。     

Prevention by amiodarone of phospholipid depletion in isoproterenol-induced ischemia in rats

This work was performed to study phospholipid metabolism in isoproterenol-induced ischemic heart and the possible protective effect of amiodarone (Am) and chlorpromazine (CPZ). Heart weight increased 24 h after subcutaneous injection of isoproterenol (40 mg/kg) whereas myocardial phospholipid content and creatine kinase activity decreased without modification of the cholesterol content. The phospholipid content was significantly correlated with creatine kinase activity (P < 0.001). Phosphatidylcholine, phosphatidylethanolamine and cardiolipin decreased significantly (P < 0.001) in the isoproterenol group whereas the lysophosphatidylcholine and lysophosphati-dylethanolamine content increased. The lysophosphatidylcholine/phosphatidylcholine and lysophosphatidylethanolamine/phosphatidylethanolamine ratios consequently increased to a significant degree (P < 0.01) suggesting indirectly the activation of phospholipases A in the ischemic myocardium. Free fatty acid content increased, indicating hydrolysis of phosphatidylcholine, phosphatidylethanolamine, lysophosphatidylcholine and lysophosphatidylethanolamine. Intravenous injection of Am (20 mg/kg) or intraperitoneal injection of CPZ (30 mg/kg) prior to isoproterenol injection provided complete protection against phospholipid depletion and against increase of the lysophosphatidylcholine/phosphatidylcholine and lysophosphatidylethanolamine/phosphatidylethanolamine ratios which returned to control values. Neither substance had any effect on the heart weight increase due to an edematous and inflammatory process. The total protection by both substances against phospholipid depletion was not sufficient to prevent the creatine kinase activity decrease. The improved phospholipid degradation in the ischemic myocardium is discussed in relation to the in vitro inhibitory effect of Am or CPZ on phospholipases A activity.     

Effect of long term fluoride exposure on lipid composition in rat liver

Chronic fluorosis can severely damage many systems of human body, but its pathogenesis is unclear. Normal composition and structure of cellular membrane lipids are a basic factor to maintain cell function. In this investigation, cellular membrane lipids of the liver were analysed after a long term fluoride treatment for rats and the results are discussed in order to give an explanation for the pathogenesis of this disease. Wistar rats were supplied with drinking water containing either 30 or 100 ppm fluoride (NaF) for seven months. Contents of phospholipid and neutral lipid in rat liver were analyzed by high-performance liquid chromatography, and fatty acid composition from individual phospholipids was measured by gas chromatography. Results showed that the total liver phospholipid content decreased in the rats treated with high dose of fluoride due to a lower content of phosphatidylethanolamine (PE), phosphatidylcholine (PC) and phosphatidylserine (PS). Among the fatty acid compositions of PE and PC in the livers of fluoride poisoned animals, the proportion of polyunsaturated fatty acids (20:4 and 22:6) decreased, whereas saturated fatty acids (16:0 and 18:0) increased. No changes could be detected in the amounts of liver cholesterol and dolichol. Total ubiquinone contents in rat liver were reduced by 11% in the group treated with 30 ppm fluoride and by 42% in the group treated with 100 ppm fluoride. In the subclasses of ubiquinone, both ubiquinone-9 and ubiquinoine-10 amounts decreased after fluoride treatment. These modifications of membrane lipids might be induced by oxidative stress, which might be an important factor in the pathogenesis of chronic fluorosis.