镉对大鼠胰岛素水平的影响

目的研究镉对机体胰岛素水平的影响。方法采用随机区组方法,96只SD大鼠给予不同剂量的镉(CdCl20、50、100和200mgL),饮水染毒30天、60天、90天。测定不同染毒时间大鼠血胰岛素、血液、尿液中镉含量的改变以及肝、肾和胰脏中镉含量的改变。结果染毒组大鼠在染毒30天中、高剂量组和染毒60天的中剂量组血清胰岛素水平显著降低。各剂量组大鼠血、尿和胰脏中镉含量有显著增加。但胰脏中镉含量低于肾脏和肝脏。结论镉可以在胰脏组织蓄积,引起胰岛素水平降低。     

经口镉染毒大鼠前列腺中金属硫蛋白基因表达水平的变化

目的 观察经口镉染毒对大鼠前列腺组织中锌、镉含量以及金属硫蛋白（MT）基因表达水平的影响。方法 48只大鼠随机分成8组，每组6只，其中设对照组和50、100、200mg/kg镉染毒组各2组。大鼠通过饮水给予氯化镉，并分别在染毒1个和6个月后分批（每批4组）处死大鼠。大鼠前列腺组织中锌、镉含量的测定采用原子吸收光谱法，而金属硫蛋白基因（MT－I和MT-Ⅱ）表达水平的测定采用RT－PCR的方法。结果 在镉染毒的每1个月和第6个月，随着镉染毒剂量的增加，锌在大鼠前列腺腹叶中的含量呈逐渐降低的趋势。其中在镉染毒1个月和6个月后，200mg/kg镉染毒组大鼠前列腺腹叶中锌的含量分别为9．5、8．5μg/g湿重，明显低于对照组的17．0、18．9μg/g湿重，差异有显著性（P＜0．05）。与锌相反，各染毒组大鼠前列腺腹叶和背侧叶中镉的含量均明显高于对照组，尤以背侧叶增高的幅度更明显。MT－I和MT－Ⅱ在前列腺腹叶的表达水平随着镉染毒剂量的增大而呈逐渐降低趋势；在染毒第1个月和第6个月，200mg/kg镉染毒组的MT－I基因相对表达丰度为0．410和0．339，MT－Ⅱ基因相对表达丰度为0．100和0．112，均明显低于对照组MT－I（0．760，0．830）和MT－Ⅱ（0．429，0．439）相对表达丰度，差异有显著性（P＜0．01）。显著 经口镉染毒能影响大鼠前列腺组织中锌、镉的含量和MT基因表达的水平。     

亚慢性铅镉联合染毒对SD大鼠血液生理生化指标的影响

目的研究亚慢性铅镉联合染毒对SD大鼠血液生理生化的影响。方法将80只健康SD大鼠,随机分成3个试验组和1个对照组,每日对各试验组大鼠经口给予29.96、89.88和269.65 mg/kg铅镉混合溶液,对照组自由饮水,持续灌胃90 d。每30 d采集一次血液,测定血液生理生化指标。结果与对照组相比,各试验组大鼠血液白细胞总数、红细胞总数和血红蛋白含量总体呈现先上升后下降的显著变化;谷草转氨酶活性、谷丙转氨酶活性和尿素含量持续显著上升;血糖和总胆固醇含量最高剂量组显著下降,甘油三酯含量表现为最低剂量组显著上升;总蛋白、白蛋白、球蛋白、肌酐含量无显著变化。同时,各剂量组大鼠肝细胞和肾小管上皮细胞出现不同程度的颗粒变性、水泡变性和细胞坏死。结论亚慢性铅镉联合暴露对大鼠的血液生理生化指标有显著影响,长期低剂量铅镉联合染毒后可引起动物机体不同程度的肝功能和肾功能损伤。     

氧化镉粉尘致大鼠肾毒性的实验研究

本文通过气管注入式染毒探讨了氧化镉粉尘对大鼠的肾毒性。以尿蛋白、尿酶(NAG、LDH、ALP)及肾皮质镉含量为观察指标,实验结果得出:染毒后3个月,100mg剂量组各指标改变最显著,各指标的相关系数均有统计学意义;染毒后6个月,100mg及50mg两组出现了明显作用,尿蛋白、尿NAG及LDH活性显示了剂量-效应关系,肾皮质镉含量也出现了相应的增高。作者认为,难溶性的氧化镉粉尘经呼吸道染毒对大鼠肾脏也有损害作用。     

大鼠体内镉负荷与尿金属硫蛋白关系的实验研究

[目的]分析大鼠尿金属硫蛋白(UMT)与体内镉负荷的关系,探讨UMT作为镉接触性生物标志物的可行性。[方法]24只SD大鼠分为4组,分别皮下注射给予0、0.5、1.0、2.0mgCd/kg体重CdCl27d。原子吸收分光光度法(AAS)测定肝脏、肾脏、胰脏、尿液、血液中镉的含量;比色法测定尿N-乙酰-β-D-氨基葡萄糖苷酶(UNAG)水平;酶联免疫吸附法(ELISA)检测UMT的含量。[结果]镉染毒大鼠血镉、尿镉、肝镉、肾镉、胰镉含量随染镉剂量的增加而明显增加,与对照组相比差异有统计学意义(P<0.05);各染镉组大鼠UNAG水平未见明显改变(P>0.05);UMT含量随着染镉剂量的增加而明显增加(P<0.05),并且与肝镉、肾镉、胰镉、血镉、尿镉含量呈明显正相关,相关系数分别为0.703、0.815、0.691、0.654、0.641(P<0.01)。[结论]UMT与体内镉负荷指标间存在较好的一致性,能反映机体镉负荷水平,可作为镉接触生物标志物。     

急性镉染毒大鼠血和尿指标与肾形态学改变的关系

目的 观察急性镉中毒大鼠尿液、血清指标与肾病理学改变的关系,以判断.肾功能损害Ζ的程度.方法 将SD健康雄性大鼠随机分成空白对照组和高、中、低3个剂量染镉组(染毒剂量分别为1.6、0.8、0.4 mg/kg,每天1次,连续染毒5 d),每组6只动物.分别测定各组血肌酐(Cr)、尿素氮(BUN)、尿β-N-乙酰葡萄糖苷酶(NAG)、肾皮质镉含量;光学显微镜、电子显微镜下观察肾组织形态学变化.结果 3个染镉组中,高剂量组血Cr及尿NAG水平较对照组升高,差异有统计学意义(P＜0.05),病理学观察相应出现肾小球萎缩,大量近曲小管上皮细胞明显肿胀,部分坏死,管腔狭窄甚至消失;尿NAG动态观察发现,中剂量组在第5天出现峰值,与对照组比较,差异有统计学意义(P＜0.05),该组可见到部分肾近曲小管上皮细胞肿胀变性,管腔萎缩.结论 急性染镉引起的肾功能生化指标变化与组织形态学变化一致,中、低剂量组的损伤为可逆的.     

亚慢性镉染毒致大鼠心脏损伤探讨

目的 观察氯化镉(CdC12)亚慢性染毒对大鼠心脏组织的损伤作用.方法 96只SD大鼠随机分成镉高剂量组、中剂量组、低剂量组和生理氯化钠对照组,每组24只,雌雄各半,给予CdCl2腹腔注射,每天1次,每周5d,连续14周.测定大鼠心脏组织中镉水平和脏器系数的变化,现察其心肌组织病理学改变.结果 镉染毒雄性大鼠心脏镉水平在高剂量组、中剂量组和低剂量组分别为5.764、2.450和0.789 μg/g,分别是对照组的 115.28、49.00和15.78倍;而雌性大鼠心脏镉水平在上述3个剂量组分别为5.147、2.180和1.219μg/g,分别是对照组的102.94、43.60和24.38倍,差异均有统计学意义(P<0.01).两性大鼠心脏脏器系数均随着镉染毒水平的增加而有不同程度的升高,有明显的剂量依赖关系(P<0.01)0所有染毒大鼠心脏组织出现不同程度的形态结构改变,主要有心肌纤维排列疏松,间陈增宽,细胞核固缩、碎裂、崩解,甚至心肌坏死,这些病理学改变随着镉染毒水平的增加而更加明显.结论　亚慢性镉染毒可引起大鼠心脏组织内镉蓄积,导致染毒大鼠心肌坏死等明显的组织病理学改变.     

镉对雌性大鼠体重变化和卵巢脏器系数的影响

目的 本文旨在研究镉对雌性大鼠体重变化和卵巢脏器系数的影响,为进一步开展镉的雌性毒性实验研究提供依据。方法 清洁级SD系雌性成年大鼠按体重分层随机分成高、低剂量组和对照组,染镉剂量分别为1.0、0.25和0.0 mg/kg,腹腔注射染毒,1次/d,每周5 d,连续6周。观察各组大鼠体重变化和卵巢重量并计算其脏器系数。结果 高剂量组大鼠在染毒1周后体重已出现增长缓慢,其增长率显著小于对照组(P<0.05),在经过一段时间的适应性体重增长后,在染毒4周后,高剂量组大鼠体重增长仍明显滞缓,增长率小于对照组,但差异无显著性;染毒的1、2、5、6周体重均明显低于对照组(P<0.05)。而染毒6周后的各染毒剂量组大鼠的双侧卵巢重量和脏器系数与对照组差异无显著性。结论 镉对动物体重变化的影响是镉对机体毒性较早出现的表现之一,镉对卵巢可能尚未造成明显的器质性病理改变。     

镉对大鼠雌性性腺毒性研究

目的　镉的雌性性腺生殖毒性研究颇少见。本文通过亚慢性镉染毒,观察了镉对大鼠的雌性性腺毒性。方法　随机将动物分四组,染镉剂量分别为１ 、０－５ 、０－２５ 和０ ｍｇ／ｋｇ 体重。腹腔注射染毒,每日一次,每周５ 天,连续６ 周。结果　镉染毒各剂量组大鼠卵巢镉含量均显著高于对照组;高、中剂量染毒组大鼠动情周期均比对照组显著延长;高、中剂量染毒组大鼠闭锁卵泡构成比显著高于对照组。结论　卵巢同肾脏一样,也是镉的重要的靶器官之一。镉的雌性性腺生殖毒性可表现为动情周期的明显延长,卵巢细胞生长发育过程的明显障碍     

镉对雌性大鼠血清FSH、LH水平的影响

目的 研究镉对雌性大鼠血清FSH(促卵泡激素)、LH(黄体生成激素)水平的影响。方法 以不同剂量镉(分别为0、0.25(或0.5)mg/kg、1.0mg/kg)对雌性大鼠进行亚急性、亚慢性注射染毒。一批大鼠染毒7、14d后测定血清中的LH、FSH的变化;另一批大鼠染毒30d后测定血清中LH、FSH含量。结果 染毒7、14d天大鼠血清FSH、LH含量高、低剂量组与对照组比较差异均无显著性(P>0.05);染毒30d,各剂量组大鼠血清中LH、FSH仍未见显著差异(P>0.05)。结论 在本实验条件下,染镉雌性大鼠血清FSH、LH水平未见明显变化。结论镉亚急性及亚慢性染毒,尚未造成雌性大鼠垂体功能损伤,抑或存在损伤仍能通过垂体的代偿功能而维持FSH、LH在正常水平范围。     

Effects of camostat, a synthetic protease inhibitor, on endocrine and exocrine pancreas of the rat

The effects of chronic oral treatment of rats with 400 mg/kg body weight camostat, a synthetic protease inhibitor, on weight gain and both pancreatic exocrine and endocrine secretion were studied and compared with pair-fed controls. Administration of camostat was found to result in a lower weight gain than in untreated rats fed ad libitum because of reduced food intake. The pancreas of treated rats showed hypertrophy and hyperplasia with significantly higher total contents of amylase, lipase, trypsinogen and chymotrypsinogen than that of pair-fed controls. The specific activity of lipase, trypsinogen and chymotrypsinogen remained unchanged but the specific activity of amylase was significantly lower than in pair-fed controls. Stimulation of pancreatic enzymes with CCK 8 in treated rats resulted in a greater output of proteases, no difference in secretion of lipase and a lower secretion of amylase than in pair-fed rats. Glucose-dependent insulin secretion was also significantly lower in camostat-treated rats than in controls. This effect could be reversed by gastric inhibitory polypeptide. After termination of treatment with camostat all enzymes were normalized within 14 d. Our results on the hypertrophied pancreas of rats suggest preferential synthesis and secretion of protease at the expense of amylase and diminished sensitivity of insulin to stimulation by glucose. All effects of camostat on the pancreas were reversible.     

I.v. hypertonic glucose stimulates the exocrine pancreas in rat

BACKGROUND: Pancreatic atrophy and dysfunction resulting from parenteral nutrition (PN) may be explained by several mechanisms; one of the important factors is the nutrient in the circulation, which affects the pancreatic growth and secretion. The effect of nutrients on the pancreatic exocrine still has controversies. The aim of the present study is to better understand the effect of i.v. glucose on the exocrine pancreas stimulated by cholecystokinin during the parenterally fed condition. METHODS: Two mixed solutions consisting of 30% and 50% glucose, respectively, were used. Thirty male Sprague-Dawley rats were randomly divided into 5 groups, including a control group; a freely fed group received cholecystokinin; 2 groups were infused with 30% and 50% glucose, and a group was infused with 50% glucose with cholecystokinin. The body weight and pancreatic contents were measured after 10 days. RESULTS: The body weight in all groups was increased but lower than in the freely fed rats. I.v. glucose caused a decrease in the pancreatic weight, the amount of the pancreatic protein and DNA, and the level of amylase but elevated the level of trypsin in all treated groups. The enzymes were elevated after infusion of cholecystokinin with glucose, but they were lower than in freely fed animals with cholecystokinin. Compared with 30% glucose, 50% glucose elevated the level of amylase but did not affect the level of trypsin. CONCLUSIONS: I.v. glucose results in atrophy of the exocrine pancreas, elevates the amylase in pancreas, but suppresses the stimulatory effect of cholecystokinin on the exocrine pancreas.     

硒和维生素E缺乏对大鼠胰腺腺泡功能的影响

饲予大鼠克山病病区粮引起血清淀粉酶与脂肋酶活性阵低，胰腺腺泡合成淀粉酶与脂肪酶的能力减弱，并伴有胰腺ＧＳＨ－Ｐｘ活力明显下降，ＬＰＯ合量升高，硒含量明显减少。在病区粮中补一定剂量晒或ＶＥ可明显提高血清淀粉酶与脂肪酶活性，增加肽腺腺泡淀粉酶与脂肪酶的合成，同时使ＧＳＨ－Ｐｘ活力升高，ＬＰＯ含量降低。此结果提示，克山病病区粮中的致病因素可引起胰腺外分泌功能的原发性损害，其机制可能与晒和ＶＥ缺乏有关。     

缺锌对大鼠复合型叶酸吸收的影响及其机理的探讨

方法：将２４只大鼠随机分成三组：缺锌组（ＺＤ）、锌正常对照组（ＺＮ）和对饲组（ＰＦ）。分别喂以缺锌（３．０８ｍｇ锌／ｋｇ饲料）、锌正常饲料（５６．２０ｍｇ锌／ｋｇ饲料），２４天后测定大鼠血清锌浓度、叶酸浓度、胰脏蛋白质含量及胰脏结合酶活性。结果：与对照组相比缺锌组上述指标均显著降低。大鼠血清叶酸水平、胰脏结合酶活性、血清锌水平成正相关；胰脏蛋白质含量和血清锌水平成正相关。结论：缺锌可降低结合酶的活性，还可能通过减少结合酶的量降低对叶酸的吸收     

Decrease in amylase (EC 3.4.21.4) synthesis in lactating rats

The amylase (EC 3.4.21.4) and trypsin (EC 3.2.1.1) activities in the pancreas in rats during pregnancy, lactation and after the weaning period, and the secretory responses to a secretagogue (caerulein) in the exocrine pancreas of lactating rats were measured. Trypsin activity increased as lactation progressed and reached twice that of unmated rats in the second half of the lactation period. The amylase activity fell before parturition and failed to recover even after the start of lactation and was significantly decreased throughout the lactation period. The total amount of pancreatic juice produced in the lactating rats was significantly greater than that of unmated rats; the amylase output was significantly less than that of unmated rats. When the pups were removed, amylase activity in the pancreas returned to the value in unmated rats. Furthermore, the amylase activity in lactating rats receiving a daily injection of insulin significantly exceeded that of normal lactating rats. These results indicate that the decrease in amylase activity in lactating rats is due to the reduction of amylase synthesis and there is a possibility that insulin is required for normal or elevated rates of amylase synthesis in lactating rats.     

Long-term effectiveness of dietary iron and ascorbic acid in the prevention and cure of cadmium toxicity in rats.

The protective and curative effects of dietary iron and ascorbic acid on chronic (180 days) cadmium toxicity in rats were examined. Growth retardation and anemia were observed in rats fed a diet containing 50 ppm of cadmium for 180 days; during this period the contents of iron in the liver, kidney, spleen, testis, intestine, and tibia decreased and the zinc contents of the liver and kidney increased, but the calcium content of bone did not change. Addition of 400 ppm of iron and 1% of ascorbic acid to the cadmium-containing diet overcame the growth retardation and anemia due to cadmium toxicity and reduced the tissue levels of cadmium; however, it did not restore the zinc contents in the liver, kidney, and bone to normal. Similar effects were observed when these compounds were added to cadmium containing diet for 90 days after feeding the cadmium diet alone for 90 days. The glutamic-pyruvic transminase and glutamic-oxaloacetic transminase activities in the plasma of rats fed the cadmium diet increased significantly and these increases were prevented by supplementing the diet with iron and ascorbic acid. Glucose, urea, and alkaline phosphatase in the plasma and glycogen in the liver were not changed by feeding the cadmium diet for 180 days. These results indicate the long-term effectiveness of supplementing the diet with iron and ascorbic-acid for preventing and curing dietary cadmium toxicity in rats.     

The distribution of tracer doses of cadmium in the normal rat

The distribution and excretion of a single tracer dose of cadmium-109 given intravenously to rats were studied in a 60-day time course experiment. The organs that accumulated the most cadmium were the liver, kidneys, and pancreas. Initial high plasma levels decreased rapidly, and most of the cadmium that remained in the blood after 24 hr was found in the red cells. In most organs and tissues a level was reached within 24 hr at which the cadmium concentration remained relatively stable. Kidney was a marked exception because the amount of cadmium found in that organ increased progressively. Excretion of cadmium was found to be predominantlyvia the feces. Twenty-five to 28% of the dose was excreted by that route in 60 days, the most rapid phase occurring during the first three days. Less than 0.15% of the dose was excretedvia the urine.     

Dietary zinc treatment for chronic copper intoxication in palm kernel cake (PKC) fed sheep

Thirty, 4 month-old male Maim x Polled Dorset crossbred sheep were allocated into 6 groups of 5 animals each. Four groups of animals were stall-fed with basal diet of 90% palm kernel cake (PKC) and 10% grass (G) for 16 weeks. One group of the animal was slaughtered at the end of the 16 weeks feeding trial (PKC group), whilst the other three groups were further fed with either the same diet (PKC+PKC group) or fed with a new diet consisting of 30% corn and 10% fish meals (CF) and grass (60%) either with (PKC+CF+Zn group) or without (PKC+CF group) zinc supplementation (500 mg/g Zn as zinc sulfate) for another 16 weeks and were slaughtered at the end of the feeding trial, The other two groups which act as controls were fed with corn (30%) and fish meals (10%) and grass (60%), and were slaughtered at weeks 16 (CF group) and 32 (CF+CF group) of the trial. The blood, right and left liver, renal cortex and medulla, pancreas, bile and urine of all animals were analysed for copper and zinc contents using an atomic absorption spectrophotometer. The liver and kidney were also fixed in 10% buffered formalin for histopathological examination. The study showed that neither clinical signs nor gross lesions of copper or zinc toxicity were observed throughout the trial. However, the copper concentration in both the right and left liver of PKC fed sheep at weeks 16 and 32 rose to about 3 times that of the controls and remained high in both the PKC+CF and PKC+CF+Zn groups. A similar pattern of copper concentration was observed in the blood. The copper and zinc contents in the renal cortex and medulla, pancreas, bile and urine remained low in all groups. The zinc content in the liver of PKC+CF+Zn group was significantly increased. Histologically, moderate hepatic lesions were observed in the PKC fed sheep at week 32. The lesions were milder in the other groups especially in the PKC+CF+Zn group. No significant renal lesions was recorded in all groups. It was concluded that the usage of dietary zinc supplementation (500 mg/g) in the treatment of PKC toxicity in sheep was unsatisfactory. The ability of Malin x Polled Dorset crossbred sheep to tolerate the high copper content in PKC at least during the first 16 weeks of the feeding trial may provide more avenue in the utilization of PKC as a major feed ingredient in sheep.