饮水中镉接触致大鼠前列腺损伤和锌的保护作用

目的　研究饮水中氯化镉染毒对SD大鼠前列腺的损伤及锌的保护作用 ,并探讨镉、锌在前列腺内分布和对大鼠性激素水平的影响。方法　大鼠自由饮水染毒氯化镉 (5 0、15 0mg/L) ,镉 锌联合染毒 (15 0 3 0 0mg/L)及锌 (3 0 0mg/L) 14周后 ,取前列腺腹叶 ,观察病理及超微结构改变 ,同时测前列腺内镉、锌含量和血清性激素水平。结果　镉染毒后 ,前列腺腺体萎缩 ,上皮皱褶 ;透射电镜下见前列腺腹叶分泌细胞内质网肿胀 ,残体增多。部分细胞基质浅淡 ,细胞器缺如。与对照组相比 ,低剂量和高剂量组大鼠前列腺腹叶的器官指数显著下降 (P <0 0 5 ) ,而联合组前列腺损伤情况有所减轻。血清睾酮水平在各组间无明显改变。高剂量镉染毒促使血清中雌激素水平升高 2倍 ,并导致锌在前列腺中流失和镉在前列腺中蓄积。结论　大鼠经饮水镉染毒可直接引起前列腺分泌细胞损伤 ,并改变血清性激素水平和锌镉在前列腺中的分布。锌对镉的这种毒效应有保护作用。     

染锰大鼠肝和脑超微结构的改变

锰 (manganese ,Mn)是正常机体所必须的微量元素 ,是体内多酶的活性基因或辅助因子 ,如线粒体和叶绿体中的Mn SOD和精氨酸酶、脯氨酸酶、丙酮酸羧化酶等 ,参与许多生物化学反应 ,但吸收过量的Mn可以引起中毒[1 ] 。Mn中毒的早期表现为类神经症和自主神经功能障碍 ,如嗜睡、精神萎靡、记忆力减退等。但Mn中毒的机制至今还不清楚 ,体内外研究表明 ,Mn可以对线粒体功能产生损害[2 ,3] 。为了进一步探讨Mn中毒的机制 ,我们用氯化锰 (MnCl2 )腹腔注射染毒 ,观察了肝脏和脑组织超微结构的变化 ,以期为今后进一步研究Mn神经毒作用和Mn对线粒…     

硒对锰导致神经细胞氧化损伤的保护作用

锰是人体内所需的一种微量元素，但是长期接触锰，造成锰化合物在体内的蓄积，则会引起锰的慢性中毒，从而产生以多巴胺能神经元退行性病变为主要特征的机体损伤，出现类似帕金森病的症状。虽然锰对神经的毒作用机制尚不清楚，但是已有的研究表明，体内自由基的产生与锰的神经毒性有密切关系。慢性锰中毒可以引起机体内脂质过氧化的改变。     

锰对大鼠前列腺的毒性作用

大量动物实验证明锰（Mn）对机体存在毒性。但由于人群暴露资料的不完全，Mn对前列腺的毒性仍有待研究。2000年1月1日，我国颁布新的汽油标准。改用甲基环戊二烯羰基锰（MMT）替代四乙基铅作为新的汽油防爆添加剂，使人群，尤其是交通警察、炼油厂工人、加油站职工和繁华马路附近居民等通过大气接触Mn的机会大大增加。     

孕期锰染毒对仔鼠脑内锰,锌,铜,铁的影响

孕期锰染毒对仔鼠脑内锰、锌、铜、铁的影响杨伯宁１张德兴２檀进发１柯铭华１关雄俊３宋苏环３谢涛锰是一种有毒金属，普遍存在于自然界。锰及其化合物在现代工业中用途很广，对人体则是正常代谢所必需的一种微量元素。但过量锰进入机体可产生严重损害。在工业生产中，长...     

锌对铅致大鼠心肌氧化性损伤的保护作用

目的　探讨硫酸锌 (ZnSO4)对低水平醋酸铅 (PbAc2 )暴露的雄性SD大鼠心肌微粒体膜 (MMS)氧化性损伤保护作用的可能机制。方法　暴露组 :PbAc2 3 0mg (kg·d) ;干预组 (3个 ) :剂量为PbAc2 3 0mg (kg·d)分别 +ZnSO42 5、5、1 0mg(kg·d) ;对照组 :给等容积蒸馏水。连续灌胃 9周后断头取血分析铅、血锌含量 ;取尿液分析尿铅含量 ;取心肌制备其MMS分析Na+,K+ ATP酶 (Na泵 )、Ca2 + ATP酶 (Ca泵 )、超氧化物歧化酶 (SOD)活力、丙二醛 (MDA)含量。离体实验将大鼠MMS悬液与最终浓度PbAc2 0 4mmol L组成混合液 ,把此混合液分为 4组 ,其中 3组分别加ZnSO40 3、0 6、1 2mmol L ,37℃共同温育 30min后 ,观察ZnSO4对PbAc2 致MMS氧化性损伤的保护作用。结果　在体实验 3个染PbAc2 +ZnSO4干预组血铅平均值分别为 0 1 7、0 1 6、0 1 5μmol L;MMSMDA含量平均值分别为 2 2 8、2 1 7、2 0 7μmol g;Ca泵活性平均值分别为 1 3 1 7、1 2 98、1 2 52mmol (h.g) ,均明显低于染PbAc2 3 0mg (kg·d)组 (P <0 0 5或P <0 0 1 ) ;而 3个染PbAc2 +ZnSO4干预组血锌、尿铅含量、MMSNa泵和SOD活力平均值分别为 72、78、88μmol L ,0 33、0 36、0 39μmol L ,1 0 0 5、1 1 39、1 1 95mmol (h .g) ;1 3、1 4、1     

灯盏花素对大鼠急性肝细胞损伤的保护作用

目的探讨灯盏花素对大鼠急性肝损害的保护作用。方法取Wistar大鼠18只,随机分为Ⅰ、Ⅱ、Ⅲ3组各6只。胶原酶原位灌流法分离大鼠肝细胞后于Ⅰ、Ⅱ、Ⅲ组分别加入PBS 20mmol/L、LPS 3mg/L、LPS 3mg/L+灯盏花素20mmol/L,于施加因素后2、4、6、8、12、24h分别收集肝细胞和肝细胞培养液进行各指标测定。用透射电镜观察肝细胞形态学变化,用Fura-2-AM测定细胞内游离钙离子浓度,用[3H]油酸标记的生物膜法测定分泌型磷脂酶A2(secretory phospholipase A2,sPLA2),用Elisa法检测前列腺素E2(PGE2)的活性。结果Ⅱ组凋亡细胞与坏死细胞数均多于Ⅰ、Ⅲ组,差异均有统计学意义(P<0.01)。LPS加入肝细胞培养液2h、8h,Ⅱ组大鼠肝细胞中Ca2+浓度高于Ⅰ、Ⅲ组(P<0.05);Ⅱ组sPLA2、PGE2水平均高于Ⅰ组、Ⅲ组,差异均有统计学意义(P<0.01)。结论灯盏花素能显著抑制急性肝损害,可能与其对钙的拮抗和对sPLA2的抑制作用有关。     

对氨基水杨酸钠对锰中毒大鼠体内锰,铜水平的影响

本文报道对氨基水杨酸钠(PAS-Na)对亚急性锰中毒大鼠不同脑区,肝和血清中锰,铜含量的影响,大鼠每日ip二氯化锰15 mg·kg~(-1),连续60或84 d;接着,每日ip PAS-Na 80或120 mg·kg~(-1),连续16或21 d,结果表明,锰中毒大鼠体重增加明显减少,脑和肝中锰,铜含量明显增加,以纹状体的锰,铜含量增加最多,锰中毒后PAS—Na治疗可以使脑,肝的锰含量减少,尤以d 78时所观察到的效果更为明显,提示PAS—Na有促排锰作用。     

镉对小鼠脾脏淋巴细胞转化率的影响及锌的保护作用

镉广泛应用于电池、电镀、合金、油漆和塑料等工业,是一种在环境中极难生物降解的重金属,是环境持久性有毒物质.其可以参与大气和水循环,同时通过食物链逐级浓缩,最后以极高的浓度通过污染的食物、饮用水和吸烟等进入高等动物体内,属于疑似环境内分泌干扰物.     

锰和锗对CCl4肝损害保护作用的实验研究

实验用ＳＤ大鼠。ＣＣｌ４５００ｍｇ／ｋｇ经口染毒。每周两次。连续染毒６周。于染毒的同时分别给予锰４ｍｇ／ｋｇ和锗－１３２１０ｍｇ／ｋｇ混入饲料中喂饲。ＶｉｔＥ以１０ｍｇ／ｋｇ经腹腔注射。每周两次。每两周处死一批动物。结果显示，锰组、锗－１３２组和ＶｉｔＥ组染毒后，ＳＧＰＴ在第二周增加的幅度均低于ＣＣｌ４组，并于停止染毒后迅速下降。且锰组、锗－１３２组比ＶｉｔＥ组早两周恢复正常水平。各处理组肝匀浆中ＭＤＡ在整个观察期上升的幅度均低于ＣＣｌ４组。在染毒停止后第８周恢复正常。锰组肝匀浆中ＧＳＨ含量于整个染毒期均未见显著的下降，锗－１３２组于第４周降低显著，第８周恢复。细胞色素Ｐ４５０染毒后各组均显著降低并持续至第１０周，ｂ５值锰组和锗－１３２组分别在第四周及第六周有一最低值。均于第八周恢复。病理结果显示，锰组和锗－１３２组其纤维化、脂变的程度明显减轻。提示锰、和锗－１３２对ＣＣｌ４肝损害有一定的保护作用，其效果优于ＶｉｔＥ。     

岭回归－分光光度法同时测定党参中的痕量锰和锌

为减小最小二乘法在进行多组分光度分析时校正矩阵共线可能引起的计算误差，本文研究和改进了抗干扰能力强和适用于病态体系的岭回归模型，将其应用于党参中锰和锌的同时测定，获得满意结果。     

醋氨己酸锌抗实验性胃溃疡作用

对醋氨己酸锌的抗实验性动物胃溃疡作用进行了研究，结果表明，醋氨己酸锌显著的抑制小鼠水浸应激性胃溃疡形成，对无水乙醇所致的大鼠胃粘膜损伤具有明显的保护作用，且显著减轻幽门结扎大鼠胃粘膜的损伤，同时，对大鼠幽门结扎大后６ｈ的胃液进行分析，３００ｍｇ／ｋｇ醋氨己酸锌增加胃液分泌量，降低游离酸和总酸量，醋氨己酸锌并具有抑制胃蛋白酶活性的作用。     

二氢卟吩e_6锌的制备及对急性肝损伤的保护作用和实验性抗溃疡活性

蚕沙叶绿素粗品 ,经酸、碱降解及醋酸锌络合反应制得二氢卟吩 e6 锌 (1) ,并测定 1对吲哚美辛 (2 )诱发的大鼠胃溃疡的保护作用及对硫代乙酰胺 (3)、四氯化碳 (4 )所致小鼠急性肝损伤的防治作用。初步实验结果表明 ,ip110 0 mg/ kg,能显著降低 2诱发的大鼠胃溃疡指数 (P<0 .0 0 1)和溃疡个数 (P<0 .0 0 1) ;ip110 0 mg/ kg× 3,能显著降低小鼠 3(P<0 .0 0 5 )、4(P<0 .0 1)急性肝损伤后升高的 SGPT活性 ,提示 1有可能发展为保肝和抗溃疡新药     

Absence of an Effect of Naloxone on Ethanol Intoxication and Withdrawal Reactions

Abstract Experimental and clinical results suggest a relationship between the action of ethanol and opiates. Therefore, we have tested whether the specific morphine antagonist naloxone (2 mg/kg intraperitoneally every six hours) affects signs of severe ethanol intoxication or modifies the withdrawal syndrome following chronic ethanol intoxication in rats. Using a double blind technique, we did not find any difference between saline treated and naloxone treated animals with respect to level of intoxication and severity of withdrawal symptoms. We must therefore conclude that naloxone does not modify signs of severe ethanol intoxication or change the ethanol withdrawal syndrome in the rat. These findings do not rule out that there might be a biochemical link between actions of ethanol and opiates, but this link is probably not localized at the level of specific drug receptor interaction.     

Effect of Manganese on Neonatal Rat: Manganese Concentration and Enzymatic Alterations in Brain

Abstract Suckling rats were exposed for 15 and 30 days to manganese through the milk of nursing dams receiving 15 mg MnCl₂'4H₂0/kg/day orally and after which the neurological manifestations of metal poisoning were studied. No significant differences in the growth rate, developmental landmarks and walking movements were observed between the control and manganese-exposed pups. The metal concentration was significantly increased in the brain of manganese-fed pups at 15 days and exhibited a further three-fold increase over the control, at 30 days. The accumulation of the metal in the brain of manganese-exposed nursing dams was comparatively much less. A significant decrease in succinic dehydrogenase, adenosine triphosphatase, adenosine deaminase, acetylcholine esterase and an increase in monoamine oxidase activity was observed in the brain of experimental pups and dams. The results suggest that the developing brain may also be susceptible to manganese.     

EDTA氟碳微球对^109镉促排作用的研究

本文报告螯合剂CaNa_2EDTA氟碳微球(EDTAFM)对~(109)Cd的促排作用,并与EDTACaNa_2、Ca和Zn-DTPA金属螯合剂比较。EDTAFM对降低肝、肾、脾和肾上腺中的~(109)Cd滞留量和促进由尿液排出的效果最佳。EDTAFM能促使胎盘和胎儿组织中~(109)Cd放射性含量降低。EDTAFM在氯仿/水中的分配系数为0.051,表明镉-EDTAFM复合物是水溶性的,未见~(109)Cd在脑、心和睾丸组织中的重分布。EDTAFM是一种有前途的镉中毒治疗药物。     

杨梅多酚对大、小鼠血小板损伤的保护作用

目的 :研究杨梅多酚对大、小白鼠在化学和辐射损伤中血小板减少的影响。方法 :采用环磷酰胺和 60Co-γ射线致大、小白鼠血小板下降动物模型。结果 :杨梅多酚能提高血小板计数 ,在杨梅多酚组和病理模型对照组之间有显著性差异 (P<0.01) ;并能保护血液的止血功能。结论 :杨梅多酚对血小板损伤可起到治疗作用。     

Lithium-induced Loss of Body Sodium and the Development of Severe Intoxication in Rats

Four groups of rats were given food containing 0, 40, 70, or 100 mmol LiCl per kg dry weight, respectively. They had free access to water and 0.46 M-NaCl. This regimen was maintained for one month, and the rats did not develop lithium intoxication in spite of the high lithium dosage. The rats given lithium-containing food drank more sodium chloride solution than the control rats, and the intake increased with the lithium content of the food. Access to sodium chloride solution was then discontinued. In the two groups given the highest lithium dosages this led within four days to a marked loss of body sodium and a proportionate loss of body weight, a significant decrease of serum sodium, and the development of severe lithium intoxication. Half of the rats in these groups died within 16 days. When rats with severe lithium intoxication were given access to 0.15 M-NaCl, they drank so much of the sodium chloride solution within one hour that their body weight prior to the intoxication was re-established. The experiments indicate that administration of lithium leads to a lowered ability of the kidneys to conserve sodium and a consequent increased requirement for sodium. If this is not fulfilled, the animals lose sodium and develop severe lithium intoxication.     

Acute Alcohol Intoxication: Differences in School Levels and Effects on Educational Performance

This study examines the effects of acute alcohol intoxication on adolescents' school performance. In the 2007–2015 period, 3,317 adolescents (ages 12 to 17 years) were treated for acute alcohol intoxication, and 37 adolescents were admitted to the hospital twice. Alcohol intoxication has an overrepresentation in “low” school levels. The 37 recidivists were more often male. During the second admittance, the period of non-consciousness was longer (four versus two hours). Six recidivists had lower educational levels when measured during the second admittance. The decline in educational level between the first and second hospital admittance suggests the negative impact of alcohol intoxication on school performances. Additional research is needed on the causal relation between (heavy) alcohol use and child development.     

Effects of Zinc Acetate Hydrate Supplementation on Renal Anemia with Hypozincemia in Hemodialysis Patients

Introduction and Aims: This study examined whether zinc supplementation with zinc acetate hydrate improved renal anemia with hypozincemia in patients undergoing hemodialysis. Methods: The study participants included 21 patients undergoing hemodialysis who presented with a serum zinc level < 60 mg/dL and who were administered zinc acetate hydrate at 50 mg (reduced to 25 mg, as appropriate) for 6 months. Patients with a hemorrhagic lesion, acute-phase disease (pneumonia or cardiac failure), or hematologic disease and those whose treatment was switched from peritoneal dialysis to hemodialysis were excluded. The changes in the erythropoietin resistance index (ERI) before and after zinc acetate hydrate administration were examined. ERI was defined as the dose (IU) of erythropoiesis-stimulating agent (ESA)/week/body weight (kg)/hemoglobin content (g/dL). The differences between the two groups were analyzed using the Wilcoxon signed rank sum test, and p < 0.05 was considered statistically significant. Results: The study participants included 19 men and 2 women aged 41–95 years (mean ± standard deviation (SD): 67.1 ± 13.6). The changes in the values of parameters measured before and after zinc acetate hydrate administration were as follows: Blood Hb did not change significantly, from 10.0–13.6 g/dL (11.5 ± 1.0 g/dL) to 10.2–12.4 g/dL (11.4 ± 0.7 g/dL); serum zinc concentration significantly increased, from 33.0–59.0 mg/dL μg/dL (52.4 ± 7.6 mg/dL μg/dL) to 57.0–124.0 mg/dL μg/dL (84.1 ± 16.3 mg/dL μg/dL; p < 0.01); the ESA dose significantly decreased, from 0–12,000 IU/week (5630 ± 3351 IU/week) to 0–9000 IU/week (4428 ± 2779; p = 0.04); and ERI significantly decreased, from 0.0–18.2 (8.1 ± 5.1) to 0.0–16.0 (6.3 ± 4.3; p = 0.04). Conclusions: Zinc supplementation increased the serum zinc concentration and significantly reduced the ESA dose and ERI, suggesting that a correction of hypozincemia contributes to lessening renal anemia in these patients.