Toxic effects of Fusarium mycotoxin butenolide on rat myocardium and primary culture of cardiac myocytes.

Mycotoxin toxicosis has been implicated in the etiopathogenesis of Keshan disease (KD), an endemic cardiomyopathy prevailing in some regions of China. Butenolide (4-acetamido-4-hydroxy-2-butenoic acid gamma-lactone, CAS No. 16275-44-8), a mycotoxin produced by several Fusarium species such as Fusarium tricinctum and Fusarium graminearum, is frequently detected from the cereals in the endemic areas of KD. The present study is undertaken to investigate whether this mycotoxin can induce myocardial damage. Exposure of primary culture of cardiac myocytes to butenolide resulted in significant cytotoxicity, manifested by changes in cell morphology and decreases in cell viability. Consistent with the in vitro findings, distinct myocardial toxicity in vivo was observed after administration of rats by gavage with butenolide (10 and 20 mg/kg/day) for 2 months, and the myocardial injuries were characterized by focal necrosis of myocardium and fragmentation of myofiber. Butenolide also induced significant oxidative damage to the myocardium in vitro evidenced by a concentration-dependent lipid peroxidation in the myocardial homogenates, whereas antioxidants superoxide dismutase (SOD), N-acetylcysteine (NAC) and glutathione (GSH) provided significant protections against this oxidative effect. Taken together, these results clearly reveal that butenolide possesses the potential to induce myocardial toxicity. The present findings may reinforce the hypothesis that toxicosis by mycotoxins is one of the etiological factors for KD.     

脂肪乳剂用于酰胺类局麻药毒性反应的救治

局麻药全身毒性反应发生率低,但其导致的并发症严重.动物和离体心脏的实验研究证明脂肪乳剂能快速逆转强效酰胺类局麻药导致的心血管系统衰竭.多例成功复苏酰胺类局麻药所致心脏停搏的报道显示,脂肪乳剂可成功逆转局麻药中毒所导致的心脏和中枢神经系统衰竭.脂肪乳救治局麻药中毒的机制可能通过两个途径共同作用:降低组织中的局麻药浓度和改善心肌细胞的能量代谢.     

The Protective Role of Glutathione, Cysteine and Vitamin C against Oxidative DNA Damage Induced in Rat Kidney by Potassium Bromate

The roles of glutathione (GSH), cysteine, vitamin C., liposome-encapsulated superoxide dismutase (L-SOD) and vitamin E in preventing oxidative DNA damage and cytotoxicity in the rat kidney after administration of potassium bromate (KBrO₃) to male F344 rats were investigated by measuring 8-hydroxydeoxyguanosine (8-OH-dG), an oxidative DNA product, lipid peroxidation (LPO) levels and relative kidney weight (RKW). Combined pre- and posttreatment of animals with 2 × 800 mg/kg GSH i.p. inhibited the increase of 8-OH-dG, LPO levels and RKW caused by 80 mg/kg KBrO₃ i.p. administration. In contrast, pretreatment with 0.3 ml/kg diethylmaleate (DEM) i.p., a depletor of tissue GSH, was associated with elevation of 8-OH-dG, LPO levels and RKW after a 20 mg/kg KBrO₃ i.p. treatment, which itself caused no change. Administration of KBrO₃ itself reduced renal non-protein thiol levels, but this was inhibited by the two doses of exogenous GSH. Combined treatment with DEM and KBrO₃ lowered the non-protein thiol level in the kidney more than did DEM treatment alone. Protective effects against the oxidative damage caused by KBrO₃ were also observed for pre- and posttreatment with 400 mg/kg cysteine i.p., another sulfhydryl compound, and daily i.g. application of 200 mg/kg vitamin C for 5 days. However, no influence was evident after pre- and posttreatment with 18,000 U/kg L-SOD i.p. or daily i.g. 100 mg/kg of vitamin E for 5 days. The results suggest that intracellular GSH plays an essential protective role against renal oxidative DNA damage and nephrotoxicity caused by KBrO₃.     

脂肪乳剂在重症急性胰腺炎营养治疗中的安全性及有效性分析

目的 :探讨脂肪乳剂应用于重症急性胰腺炎的安全性和有效性。　方法 :回顾分析重症急性胰腺炎病人肠外营养治疗期间 ,应用脂肪乳剂的影响。 74例重症急性胰腺炎病人行肠外营养治疗 ,按静脉营养液是否含脂肪乳剂分为脂乳组和非脂乳组。　结果 :脂乳组肠外营养治疗后清蛋白、前白蛋白改善显著 (P <0 .0 1 ) ,非脂乳组则无显著变化 (P >0 .0 5 ) ,脂乳组较非脂乳组改善明显 (P <0 .0 1 ) ;血清肌酐、尿素氮等在脂乳组治疗后下降明显 (P <0 .0 5 ) ,较非脂乳组改善显著 (P <0 .0 5 ) ;营养治疗结束后 ,脂乳组高血糖症状明显得到控制 (P <0 .0 1 ) ,而非脂乳组效果不佳 (P >0 .0 5 ) ,脂乳组优于非脂乳组 (P <0 .0 5 ) ;血淀粉酶均有下降 ,脂乳组未见异常增高。　结论 :重症急性胰腺炎病人输注脂肪乳剂安全有效 ,有助于恢复正氮平衡     

Lipid Peroxidation and Vitamin E in Red Blood Cells and Plasma in Hemodialysis Patients Under rhEPO Treatment

Abstract: Lipid peroxidation, measured by malonyldial-dehyde (MDA) and vitamin E in red blood cells (RBC) and plasma, was investigated in 25 hemodialysis (HD) patients before and after 6 months rhEPO therapy. RBC-MDA was significantly elevated, but plasma MDA was in the reference range. After recombinant human erythro-poietin (rhEPO) treatment, the MDA level was significantly decreased in both compartments. Marked vitamin E deficiency was established in RBC as well as in plasma. rhEPO therapy restored vitamin E levels in both compartments. Our data suggest a possible positive rhEPO-antioxidant effect in HD patients.     

煤石英对大鼠肺泡巨噬细胞氧化系统的影响

利用染煤石英混合粉尘大鼠作为实验模型，研究在实验性大鼠煤矽肺形成过程中肺泡巨噬细胞氧化和抗氧化系统的改变。结果表明在染煤石英粉尘７天，脂质过氧化产物有轻度升高，至３０天时己恢复正常，超氧化物歧化酶在染尘后７天降低，以后恢复至正常，而还原型谷胱甘肽和谷胱甘肽过氧化物酶升高明显，这与石英所致肺泡巨噬细胞的变化明显不同，说明脂质过氧化反应在煤矽肺形成过程中作用不明显。     

肉苁蓉多糖对衰老小鼠脂质过氧化的影响

目的:研究肉苁蓉多糖(polysacchridesofcistanchedeserticolaY.C.Ma,PCD)对亚急性衰老小鼠的抗 脂质过氧化作用。方法:使用D 半乳糖造成小鼠亚急性衰老模型,观察PCD对亚急性衰老小鼠血液和肝脏组 织中超氧化物岐酶(SOD)、脂质过氧化物(LPO)的含量的影响。结果:灌服肉苁蓉多糖衰老小鼠的血液和肝脏 组织中SOD明显高于模型组(P<0.05);LPO的含量明显低于模型组(P<0.05)。结论:肉苁蓉多糖具有明显 的抗脂质过氧化功能,防止亚急性衰老小鼠的组织脂质过氧化损伤。     

表没食子儿茶素没食子酸酯对缺血再灌注损伤大鼠心肌脂质过氧化及心肌酶活性的影响

目的：观察表没食子儿茶表没食子酸酯（EGCG）对缺血再灌注损伤大鼠心肌脂质过氧化及心肌酶活性的影响。方法：雄性Wistar大鼠50只分为5组，假手术组、缺血再灌注组（IR），丹参（SM，100mg/kg）组，EGCG1（10mg/kg)组和EGCG2（20mg/kg）组，每组10只动物，采用结扎大鼠左冠状动脉前降支30min后再灌注60min的方法建立在体缺血再灌注损伤模型，分别测定心肌丙二醛（MDA）含量，超氧化物歧化酶（SOD）及ATP酶活性和血浆乳酸脱氢酶（LDH）水平。结果：与假手术组比，IR组大鼠心肌MDA及血浆LDH明显升高，SOD及ATP酶活性则显著降低（P＜0．01）；EGCG和SM均能显著，降低MDA与LDH，明显增加SOD与ATP酶活性（与IR组比，P＜0．01），并且EGCG（20mg/kg)，降低MDA与LDH的作用较SM（100mg/kg)更明显（P＜0．05）。结论：EGCG通过抑制脂过氧化反应和提高心肌SOD与ATP酶活性，对大鼠缺血再灌注损伤心肌有显著的保护作用。     

脂肪乳剂对健康人外周血单个核细胞磷脂脂肪酸组成的影响

目的探讨脂肪乳剂对健康人免疫细胞脂肪酸组成的影响。方法采用毛细管气相色谱法检测8名健康志愿者连续7天外周静脉输注脂肪乳剂(20%intralipid)后,外周血单个核细胞磷脂脂肪酸谱的变化。结果静脉输注脂肪乳剂对健康人外周血单个核细胞数量、肝功能和血脂无影响,软脂酸(C16∶0)、油酸(C18∶1N9)比例在单个核细胞磷脂酰乙醇胺(PE)中明显增加(P<0.05,P<0.01);硬脂酸(C18∶0)减少(P<0.05);亚麻酸(C18∶3N3)、软油酸(C16∶1N7)在磷脂酰胆碱(PC)中明显增加(P<0.05),而其余脂肪酸均未发生明显改变。饱和脂肪酸与不饱和脂肪酸的比值(S/U)和脂肪酸的不饱和指数(UI)在单个核细胞PE、PC中均保持不变。结论脂肪乳剂不可能通过影响免疫细胞磷脂脂肪酸组成的途径对免疫功能产生影响。