锌对Caco2细胞ZIP4 mRNA表达的影响

目的研究锌对Caco2细胞ZIP4mRNA表达的影响及其规律。方法通过锌特异螯合剂TPEN建立低锌Caco2细胞模型,RT-PCR法获得ZIP4cDNA片断,10μmol/LTPEN培养基诱导后,分别检测0、2、4、6、8和10h时点ZIP4mRNA的表达,及0、2·5、5、7·5、10μmol/LTPEN培养基诱导6h,检测各浓度组ZIP4mRNA的表达。结果RT-PCR获得单一条带的片断,大小与设计一致,获得正确的ZIP4cDNA片断,随着低锌时间的增加,ZIP4mRNA表达也升高,6h达到峰值;随着TPEN浓度的升高,ZIP4mRNA表达也随之升高。结论ZIP4mRNA表达受锌的调控,提示可能参与小肠对锌的吸收。     

辛酸、癸酸和硬脂酸对ApoE~(-/-)小鼠肠道中外源性胆固醇吸收的影响

目的探索辛酸(C8∶0)、癸酸(C10∶0)和硬脂酸(C18∶0)对小鼠肠道外源性胆固醇吸收的影响。方法将Apo E-/-小鼠按血清总胆固醇(total cholesterol,TC)水平随机分为3组,分别用含2%的辛酸、癸酸或硬脂酸的高胆固醇饲料喂养16周。分别在实验开始、第8周和第16周时检测血脂及脂蛋白相关指标,在干预16周后,空腹灌胃~3H-胆固醇,检测灌胃后1 h和4 h小鼠空肠、回肠和结肠段肠腔内容物中的~3H-胆固醇含量,并检测灌胃后0.5、1、2和4 h小鼠血中3H-胆固醇含量。结果在干预第8周时,C8∶0组血清TC和低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-c)水平显著低于C18∶0组(P0.01);干预第16周时,C8∶0组及C10∶0组血清TC和LDL-c水平均显著低于C18∶0组(P0.01)。采用~3H-胆固醇灌胃1 h后,C8∶0组空肠中~3H-胆固醇含量显著低于C18∶0组(P0.05);肠腔内容物中~3H-胆固醇含量在灌胃后1 h(P0.05)和4 h(P0.01)均显著高于C18∶0组;C8∶0组灌胃后0.5 h和2 h血中~3H-胆固醇含量均显著低于C18∶0组(P0.01),灌胃4 h后血中~3H-胆固醇浓度的曲线下面积显著低于C18∶0组(P0.05)。结论辛酸可通过减少小鼠肠道中外源性胆固醇吸收,改善血胆固醇浓度。     

锌对骨发育影响的体外研究

目的　研究锌对骨发育的影响。方法　将 1 6 d孕龄的小鼠 (每组 1 2只 )脱颈椎处死 ,无菌条件下切下胎鼠的前肢分 5组 ,分别在基础培养基 (Zn2 + 浓度为 2 0 μmol/L)及基础培养基中加终浓度为 2 0 μmol/L的 Zn2 +络合剂 (TPEN) ,及基础培养基中加 Zn SO4 至 Zn2 +浓度分别为45 μmol/L、70 μmol/L、1 2 0 μmol/L的培养基中培养 6 d。结果　 1 .培养后的胎鼠右肢与未培养左肢相比 ,其长骨长度、骨组织密度均有所增加 ;组织学分析显示 :骨组织呈活跃增殖分化相 ,骨小梁增加 ,骨基质深染。2 .生化指标及 4 5Ca示踪显示 :培养基中缺锌和在培养基中补充 Zn2 + 至 Zn2 + 浓度1 2 0μmol/L时 ,骨组织中骨钙素 (OC)和 4 5Ca含量减少 ,碱性磷酸酶 (AKP)活性降低 (P<0 .0 5 ) ;当在培养基中补充 Zn2 + 至 Zn2 + 浓度 45μmol/L、70μmol/L时 OC合成量 ,骨组织对钙的吸收及AKP活性增加 (P<0 .0 5 )。 3 .形态学指标 :X- ray显示 ,培养液中缺锌和锌浓度为 1 2 0 μmol/L时 ,长骨长度和密度与对照组相比 ,长骨长度较短 ,骨密度降低 ;当在培养液中 Zn2 +浓度分别为 45μmol/L和 70 μmol/L时 ,与对照组相比 ,长骨长度及其骨密度有所增加。结论　锌参与骨组织发育的生理和生化过程 ,锌缺乏 /过量时均可影响骨的正常     

Zeeman火焰原子吸收法直接测定人血红细胞中的锌

Zeeman火焰原子吸收法 (ZFAAS)测定人血红细胞 (RBC)样品中锌。采用低渗 Triton x- 1 0 0冷溶液和超声波联用溶血技术替代常规的样品酸湿消化方法 ,RBC样品只需经简单稀释后即可用 ZFAAS直接测定其中的锌含量 ,避免了因对 RBC样品采用复杂冗长的酸湿消化法易引起的锌的污染和丢失问题。该法锌的最低检出限为 0 .0 0 5 μg/ml;对锌浓度为 1 3 3 .9、1 5 5 .8和 1 6 8.0μmol/L的 RBC样品测得的精密度分别为 4.1 %、2 .7%和 1 .9% ;回收率为95 .5 %～ 1 0 1 .0 % ;对同一混合 RBC样品中锌的测定结果与常规的酸湿消化法测得的结果十分吻合。本法已成功地应用于临床和医学实验研究工作中对 RBC样品中锌的测定     

不同剂量锌缺乏对小鼠及其胚胎发育的影响

目的 :　用昆明种雌性小鼠建立成不同程度缺锌动物模型 ,研究不同程度锌缺乏和孕早期补锌对小鼠及其胚胎发育的影响 ,并探求其发育毒性作用的阈剂量。方法 :　实验分两阶段进行。实验一用 36只初断乳 1 4～ 1 8g小鼠 ,分为低锌 (ZD)、中锌 (ZM)、常锌 (ZN)三组 ,喂饲含锌分别为 3.0± 0 .5、1 5、30 mg/kg的饲料 ,经 50 d喂养平均体重达 30 g后交配。实验二选用 80只 ,2 5～ 30 g成熟小鼠 ,随机分为低锌组 [ZD,饲料含锌 (3.0± 0 .5) mg/kg];低锌补锌组 (ZS,于孕第 7d将低锌饲料换为含锌 30 mg/kg的常锌饲料 ) ;边缘缺锌组 (MD,饲料含锌 9mg/kg) ;常锌组(ZN,饲料含锌 30 mg/kg)。 2 5d锌耗竭性喂养后交配。所有孕鼠于妊第 1 8d活杀。结果 :　实验一 :低锌组小鼠锌水平显著低于常锌组 (P<0 .0 5) ,有典型缺锌症状 ,几乎全部出现生长抑制 ,58.33%的小鼠衰竭死亡 ,存活小鼠亦不能正常交配妊娠。 1 5mg/kg剂量组小鼠则生长发育良好 ,各项指标与常锌组间无异 (P>0 .0 5)。实验二 :ZD组小鼠血清碱性磷酸酶 (AKP)活性 ,股骨锌含量显著低于 ZN组 (P<0 .0 1 ) ;该组小鼠胚胎有明显发育不良 ,畸胎及死胎出现率显著高于 ZN组 (P<0 .0 1 )。ZS组小鼠在孕第 7d补锌后活胎仔大小已趋正常 (P>0 .0 5) ,畸胎出现率与 ZD?     

610例血清锌正常值研究

用火焰原子吸收法对 6 1 0例中小学生血清锌含量进行了测定。测定结果 :1 4岁以下年龄段血清锌为 86 .9μg/1 0 0 ml,1 7岁年龄段血清锌为 95 .81 μg/1 0 0 ml,7、1 4岁年龄段间无差异 ,但 7、1 4岁与 1 7岁年龄段间有差异。以此制定出嘉峪关市区人体血清含量的正常值。     

硒和锌对人食管癌细胞株Eca109生长增殖影响的血清生理学研究

目的观察不同剂量硒、锌灌胃大鼠血清对人食管癌细胞株Eca109生长增殖的影响。方法将SD大鼠随机分为7组(基础饲料组、低硒组、高硒组、低锌组、高锌组、低硒低锌组、高硒高锌组),每组8只。喂养30天后取大鼠血清培养人食管癌细胞株Eca109和人正常肝上皮细胞株HL7702。用AAS法分别测定各组大鼠血清硒、锌;采用MTT法、3H-TDR掺入实验研究不同浓度硒、锌灌胃大鼠血清对两株细胞生长增殖的影响。结果 (1)基础饲料组血清硒、锌水平最低,高锌组血清锌最高;高硒高锌灌胃组大鼠血清硒水平最高,低硒低锌灌胃组血清硒水平次之,均明显高于基础饲料组;而此两组大鼠血清锌与基础饲料喂饲组大鼠血清锌水平差异无统计学意义(P>0.05);(2)与小牛血清对照组相比,只有高硒高锌灌胃组大鼠血清从第72h起抑制癌细胞生长(P<0.05),其余各组均促进食管癌细胞的生长;且该组大鼠血清也抑制肝细胞生长(P<0.05);(3)高硒高锌灌胃组大鼠血清明显抑制食管癌细胞DNA合成(P<0.05),其余各组与对照组作用相近,但该组对肝细胞DNA合成的抑制作用也最强。结论硒、锌在吸收、代谢等方面可能存在相互抑制作用;血清硒、锌含量较低会促进人食管癌细胞的增殖,而增加硒、锌的摄入可提高血清硒、锌的含量且可能抑制癌细胞的增殖。     

锌和某中草药制剂拮抗铅毒作用的实验研究

目的研究锌和某中草药制剂对铅染毒小鼠某些生化指标的影响。方法选取60只健康雄性昆明种小鼠随机分成5组:治疗1组、治疗2组、治疗3组、阳性对照组、阴性对照组,每组12只。前4组用2 g/L醋酸铅水溶液腹腔注射染毒,1次/d,连续染毒35 d。阴性对照组腹腔注射等容积的生理盐水。染毒14 d后,开始灌胃给药治疗。治疗1组单独给予锌、治疗2组给予锌加中草药制剂、治疗3组单独给予中草药制剂,阳性对照组和阴性对照组灌胃给予等量的蒸馏水,1次/d,直至实验结束。实验开始和实验结束均称量各实验组小鼠体重并测定血红蛋白(Hb)。实验结束后,测定各实验组小鼠血清铅、锌、钙、尿素和丙氨酸氨基转移酶(ALT),测定脑钙、NO含量、乙酰胆碱酯酶(TchE)活力、谷胱甘肽过氧化物酶(GSH-Px)活力和脑、肝匀浆对超氧阴离子(O2.)清除率。结果治疗1组、治疗2组、治疗3组、阳性对照组和阴性对照组血铅分别为(0.070 9±0.012 9),(0.052 2±0.051 8),(0.054 7±0.017 5),(0.119 0±0.027 2),(0.010 3±0.002 6)mol/L,阳性对照组明显高于其他各组;血清锌分别为(0.096 8±0.038 5),(0.084 9±0.010 3),(0.091 1±0.031 8),(0.023 5±0.037 2),(0.061 8±0.003 1)mol/L,阳性对照组明显低于治疗2组和治疗3组;脑NO分别为(13.66±3.43),(12.85±4.70),(15.80±4.40),(23.03±7.80),(12.59±3.90)μmol/L,阳性对照组明显高于其他各组;脑钙分别为(1.9±0.1),(1.0±0.2),(1.1±0.2),(0.6±0.2),(2.2±0.3)mol/L,阳性对照组明显低于其他各组;脑TchE分别为(2.67±0.69),(5.95±1.59),(6.08±1.65),(6.21±0.28),(2.86±0.99)U/mg蛋白,阴性对照组和治疗1组明显低于其他各组;其余指标,血清ALT、尿素、钙含量、Hb、O2.清除率,阳性对照组与阴性对照组、治疗组之间均有明显差异。结论锌和某中草药制剂对铅染毒小鼠部分生化指标有明显的促进恢复作用。     

锌和维生素C对运动训练小鼠的协同抗氧化作用

目的 研究锌与维生素C对运动训练小鼠的协同抗氧化作用.方法 将昆明种小鼠随机分为5组,每组6只,即生理盐水对照组、运动对照组、运动锌组、运动维生素C组、运动锌与维生素C联合组.运动锌组、运动维生素C组、运动锌与维生素C联合组分别每日按200 mg/kg灌胃相同剂量的锌提取液、维生素C液、锌和维生素C混合液,灌胃体积为0.2 ml/kg,生理盐水对照组、运动对照组分别灌胃相同剂量的生理盐水.3周后测定各组小鼠血液、肝和脑组织的超氧化物歧化酶(super-oxide dismutase,SOD)的活力和丙二醛(malondialdehyd,MDA)的含量.结果 与运动对照组比较,运动锌组、运动维生素C组、运动锌与维生素C联合组小鼠血清、肝和脑组织的SOD活力显著增强,MDA含量明显降低,差异均有统计学意义(P＜0.05),其中运动锌与维生素C联合组的结果更明显.结论 锌和维生素C对运动训练小鼠有良好的协同抗氧化能力.     

不同剂量的锌对急性酒精性肝损伤的作用

目的:探讨不同剂量的锌对酒精造成小鼠急性肝损伤时MDA;SOD;GSH-Px的影响.方法:小鼠随机分组后喂饲不同剂量的锌30天后,各加锌组与模型对照组给予56%高度乙醇(12ml/kg·bw) 灌胃,造成急性肝损伤模型,禁食12h后处死动物,取小鼠血清测定其SOD、MDA、GSH-Px的活性.结果:加锌组MDA值显著降低,而SOD、GSH-PX显著升高,与模型对照组有显著性差异.结论:添加锌能够提高急性酒精肝损伤小鼠的抗氧化能力,从而对肝脏起到保护的作用.     

Contribution of the cecum and colon to zinc absorption in rats

We examined the role of the large intestine in zinc absorption in rats in three separate experiments. In the first experiment, we examined apparent zinc absorption in rats fed diets containing graded levels of zinc carbonate (0.015-0.535 mmol Zn/kg diet) and evaluated zinc status on the basis of the zinc concentrations in serum and several tissues. The zinc absorption and the serum zinc concentration increased with the zinc content of the diet up to 0. 153 mmol Zn/kg diet. Femoral and pancreatic zinc levels increased linearly up to 0.229 mmol Zn/kg diet. In the second experiment, a zinc carbonate suspension was administered into the cecum via an implanted cannula or into the stomach via an orogastric tube, and the rats were fed diets with or without a highly fermentable fiber, guar gum hydrolysate (GGH, 50 g/kg diet), with coprophagy prevention. The amount of instilled zinc corresponded to the amount of zinc ingested as a component of the diet by the rats of a control group, 0.229 mmol Zn/kg diet. Apparent absorption of cecally instilled zinc was approximately half that observed when zinc was administered into the stomach in both diet groups. Serum and femur zinc concentrations in the cecum-administered groups were approximately 50 and 25% lower, respectively, than those in rats administered zinc into the stomach. The results demonstrate that, in vivo, the absorptive efficiency in the large intestine is not sufficient to satisfy the rat's zinc requirement and does not change when the luminal environment is substantially altered by feeding GGH. In Experiment 3, the effects of cecocolonectomy on zinc absorption were examined in rats with gastric acid suppression. In the cecocolonectomized groups, serum zinc concentration was lower as a result of treatment with a proton pump inhibitor, omeprazole, than in vehicle-treated rats, but not in sham-operated groups. These findings suggest that the cecum and colon contribute to zinc absorption when absorption in the small intestine is impaired.     

锌和游离叶酸吸收的相互影响

目的：研究锌和游离叶酸吸收的相互影响。方法：７２只Ｗｉｓｔａｒ雄性离乳大鼠随机分成九组，分别饲以不同锌和游离叶酸配比的饲料，喂养２４天，观察各组大鼠血清锌浓度，股骨锌含量及大鼠粪锌排出率变化。结果：上述指标不受饲料中叶酸含量的影响。低锌低叶酸组大鼠血清叶酸水平显著低于锌正常低叶酸组，而中高叶酸组血清叶酸水平不受饲料中锌含量的影响。相关分析也显示大鼠血清叶酸水平和血清锌水平无相关关系。结论：本实验剂量（４～４０ｍｇ／ｋｇ饲料）游离叶酸的补充不影响锌的吸收。缺锌不利于游离叶酸的吸收     

不同抗氧化活性水果汁对老龄大鼠抗氧化功能的干预作用

目的　观察不同抗氧化活性水果汁对老龄大鼠抗氧化功能的干预作用,为进一步研究水果抗氧化抗衰老有效成分提供理论依据。方法　自然衰老Wistar大鼠 30只分为 3组,分别灌胃石榴汁 3 2ml、苹果汁 2 4ml和蒸馏水 3 2ml,实验周期 4周,实验结束后测定血清抗氧化物质含量、抗氧化酶活性、血清及尿中自由基氧化产物、外周血淋巴细胞DNA损伤等有关指标。结果　石榴汁干预组老龄大鼠血清抗氧化活性 ( 0. 90±0. 13 ) mmol/L明显高于对照组的 ( 0 .79±0 .10 )mmol/L;血清羰基含量显著降低,与对照组比较差异具有统计学意义;血清ox LDL含量 ( 2. 03±0 .43)μmol/L明显低于对照组(3. 04±0. 52)μmol/L;彗星试验显示外周血淋巴细胞DNA损伤率及尾长 /总长比值降低,显著低于对照组;石榴汁干预对血清VC和VE浓度、抗氧化酶活性、MDA含量及尿 8 OH dG排出量均未见影响。苹果汁干预组除淋巴细胞DNA损伤减轻外,其他指标均未见显著变化。结论　抗氧化活性较强的石榴汁能够明显改善老龄大鼠抗氧化功能,而抗氧化活性较低的苹果汁作用较弱,水果中多酚类物质可能是其主要抗氧化功能物质。     

Inhibitory Effects of Tart Cherry (Prunus cerasus) Juice on Xanthine Oxidoreductase Activity and its Hypouricemic and Antioxidant Effects on Rats

The aim of this study was to investigate the effect of tart cherry juice on serum uric acid levels, hepatic xanthine oxidoreductase activity and two non-invasive biomarkers of oxidative stress (total antioxidant capacity and malondialdehyde concentration), in normal and hyperuricemic rats. Tart cherry juice (5 ml/kg) was given by oral gavage to rats for 2 weeks. Allopurinol (5 mg/kg) was used as a positive control and was also given by oral gavage. Data showed that tart cherry juice treatment did not cause any significant reduction in the serum uric acid levels in normal rats, but significantly reduced (P<0.05) the serum uric acid levels of hyperuricemic rats in a time-dependent manner. Tart cherry juice treatment also inhibited hepatic xanthine oxidase/dehydrogenase activity. Moreover, a significant increase (P<0.05) in serum total antioxidant capacity was observed in tart cherry juice treated-rats in both normal and hyperuricemic groups. The oral administration of tart cherry juice also led to a significant reduction (P<0.05) in MDA concentration in the hyperuricemic rats. Although the hypouricemic effect of allopurinol, as a putative inhibitor of xanthine oxidoreductase, was much higher than that of tart cherry, it could not significantly change anti-oxidative parameters. These features of tart cherry make it an attractive candidate for the prophylactic treatment of hyperuricaemia, particularly if it is to be taken on a long-term basis. Further investigations to define its clinical efficacy would be highly desirable.     

Use of EDTA to produce zinc deficiency in the pregnant rat.

The effectiveness of EDTA in reducing the endogenous zinc supply in pregnant rats was determined by two experiments. In experiment 1, a high level of zinc (100 ppm) was given to rats days 15 through 17 of gestation. In experiment 2, a low level of zinc (3 ppm) was given from days 1 through 17. On day 18, half the rats were given EDTA in two intraperitoneal injections 6 hours apart with or without zinc supplementation. The -Zn + EDTA group lost weight continuously after the injections, had increased hematocrit levels prior to parturition,and showed greater stress at parturition than did the -Zn group. Weight gains, hematocrit level, and parturition in the +Zn + EDTA group did not differ significantly from those of the +Zn controls. Spleen weights were decreased in the -Zn + EDTA and -Zn groups and zinc concentration in the spleen increased in the -Zn + EDTA group. Iron concentration decreased in the spleen and increased in the liver of EDTA-treated rats. Use of EDTA to remove endogenous zinc appears to offer a mechanism for study of the effects of short-term zinc supplementation at critical periods in the pregnant zinc-deficient rat.     

Toxicity of zinc oxide nanoparticles through oral route

This experiment was aimed to determine the significance of dose by comparing acute oral toxicological potential of nano-sized zinc oxide (20 nm) with its micro-sized zinc oxide. Sprague Dawley rats, 8 to 9 weeks old, were administered with 5, 50, 300, 1000 and 2000 mg/kg body weight (b.w.) of nano- and micro-sized zinc oxide suspended in distilled water once through oral gavage. The effects of the micro- and nano-sized zinc oxide on biochemical and hematological parameters were analyzed on day 14 of administration. The organs were collected for histopathology. Interestingly, inverse dose-dependent increase was noted in aspartate aminotransferase, alanine aminotransferase serum levels of nano-size zinc oxide groups when compared with their micro-sized zinc oxide. Clotting time was effected in all the male groups of nano-size zinc oxide, except in 1000 mg/kg b.w. The incidences of microscopic lesions in liver, pancreas, heart and stomach were higher in lower doses of nano-size zinc oxide compared to higher dose. However, the incidences of above lesions were higher in rats treated with a high dose of micro-sized zinc oxide. We conclude that nano-size zinc oxide exhibited toxicity at lower doses, thus alarming future nanotoxicology research needs to be focused on importance of dose metrics rather following the conventional methods while conducting in vivo experiments.     

Effect of zinc status on salivary zinc concentrations in the rat.

Three experiments were done to determine whether salivary zinc concentration is a more sensitive indicator of zinc status than plasma zinc. Weanling male rats fed a low zinc (less than 1 ppm) diet for 5 weeks with or without zinc (100 ppm) in the drinking water had salivary zinc concentration of 0.19, 0.16, and 0.20 microgram/ml for the zinc-deficient, zinc-supplemented restricted-intake, and zinc-supplemented ad libitum-fed groups, respectively. Combined values for male and female rats after 4 weeks of the same treatments in experiment 2 were 0.60, 1.2 and 0.44 microgram/ml. Saliva collected on day 22 of pregnancy contained 0.30 and 0.24 microgram/ml from zinc-supplemented and zinc-deficient rats, respectively. Salivary zinc concentrations in the deficient rats did not differ from those of the zinc-supplemented ad libitum-fed controls in any of the experiments. Salivary zinc concentration in the zinc-supplemented restricted-intake group in experiment 2 was significantly higher than that in the other two groups. Decreases in serum, bone, and fetal zinc concentrations indicated that the rats were definitely zinc-deficient. Since zinc concentration of mixed saliva in the rat was not decreased by even a severe zinc deficiency, salivary zinc does not appear to be as good an indicator of zinc status as plasma zinc.     

缺锌对大鼠胃癌发生率的影响

对Ｗｉｓｔｅａｒ大鼠做缺锌饲养并以Ｎ－甲基－Ｎ′硝基－Ｎ亚硝基胍（ＭＮＮＧ）作为致癌剂，观察缺锌对大鼠胃癌发生率的影响。结果显示，缺锌组动物１００％呈现前胃粘膜中度或高度增生；而对照组上皮增生发生率仅５２．５％，中、重度增生者为１５％；两组动物胃粘膜增生的严重程度及发生频率有显著差别。实验组２例大鼠胃腺区发生非典型增生，对照组无此种现象。结果还显示，缺锌大鼠发生前胃癌的危险性增加。两组差异显著（Ｐ＜０．０１）。提示适量锌具有保护胃粘膜，抑制肿瘤发生的作用；缺锌是导致胃癌发生率升高的危险因素。     

Hyperglycemic action of zinc in rats

The effect of zinc on serum glucose, insulin and glucagon as well as liver glycogen was investigated in normal, adrenalectomized (ADX), and diabetic rats. Serum glucose was significantly elevated within 15 minutes after intraperitoneal administration of zinc (25 mumol) but returned to normal limits within 4 hours. Similar effects on serum glucose were noted with orally administered zinc. Significant depletion of hepatic glycogen in zinc-treated rats suggests glycogenolysis was responsible at least in part for the increased blood glucose. Adrenalectomy completely eliminated the hyperglycemic response to this metal, whereas adrenergic blockade with phenoxybenzamine and propranolol was effective in preventing hyperglycemia. The hyperglycemic response to zinc was not eliminated in diabetic rats. Administration of dexamethasone, alone or in combination with zinc, was unable to change serum glucose concentrations in ADX rats. Plasma glucagon was significantly elevated within 15 minutes but was reduced 6 hours after zinc treatment. Insulin was significantly depressed within 30 minutes after administration of zinc and eventually increased over controls by 4 hours after treatment. These data suggest that the hyperglycemic response to zinc depends on a mechanism, requiring an intact adrenal gland, which acts to produce a rapid alteration in blood glucose.     

Reversibility of testicular atrophy induced by Di(2-ethylhexyl) phthalate in rats

Previous studies have shown that di(2-ethylhexyl) phthalate (DEHP) results in atrophy of testes and accessory sex organs accompanied by a decreased testicular concentration of zinc in rats. An experiment was performed to determine whether those changes in rat testes are reversible changes. Young Wistar male rats were administered 2.0 g/kg of DEHP for 14 days. At that time, one-half of the rats were killed for determination of zinc and testosterone concentrations in the testis, liver, and serum, and organ weights. The remaining rats were maintained for additional 45 days without further DEHP administration. Testicular weight of rats administered DEHP over the 14-day period was significantly less than that of the control animals, and testicular testosterone content and zinc concentrations were less than those of the control animals. At the end of the 45-day recovery phase, serum testosterone concentration returned to the control level, but testicular zinc concentration and testosterone content were still lower than those of the control animals. In addition, testicular weight of DEHP-treated rats was lower than that of the control animals and histologically, only a small number of seminiferous tubules showed spermatogenesis. These results indicate that, morphologically, DEHP-induced testicular atrophy appears to be of limited reversibility.