小鼠肾血管球滤过膜发育的电镜研究

目的研究发育中小鼠血管球滤过膜的变化。方法应用透射电镜观察胚胎和新生小鼠血管球滤过膜的超微结构。结果在肾小体的发育过程中,足细胞形状明显变薄,足突数量逐渐增多,其形状逐渐窄小,足突间裂孔和裂孔膜出现;足细胞下、内皮细胞下先后出现基膜,而后两种基膜融合形成一层较厚的基膜。随着毛细血管袢的不断增生,在足细胞下方出现新合成的环状或袋状的基膜片段;内皮细胞形状也明显变薄。出现大量内皮孔。结论在小鼠肾小体的发育过程中,足细胞和内皮细胞逐渐分化成熟,基膜最早来源于足细胞。随后内皮也参与合成基膜,发育晚期基膜的合成和更新主要由足细胞来完成。     

大鼠肾小体发育中滤过屏障超微结构的演变

目的:探讨大鼠肾小体发育中滤过屏障超微结构的变化规律。方法:采用光镜、电镜技术,并结合体视学分析方法,对不同发育阶段大鼠滤过屏障超微结构的变化进行形态学观察和体视学测量。结果:在肾小体发育过程中,足细胞和内皮细胞的形状逐渐低平,内皮孔增多,足突及裂孔大量分化增多;足细胞下先出现电子密度较低的基膜,随后内皮细胞下才出现基膜,以后,二者融合形成一层电子密度较高的血管球基膜。结论:在大鼠肾小体的发育过程中,足细胞比内皮细胞先分泌基膜,然后二者融合形成血管球基膜。     

慢性镉中毒小鼠肾脏的超微结构观察

透射电镜下观察10只慢性镉中毒小鼠肾脏的超微结构变化，结果表明肾小体和近曲小管上皮细胞的超微结构均受损伤，肾小体，毛细血管内皮细胞肿胀，增厚，血管系膜增生，血管球基膜增厚或分裂成层，基膜和内皮细胞之间或基膜的分裂之间有电子致密物沉积，近曲小管上皮细胞，胞核变形，固缩，线粒体肿胀，嵴断裂，脱落，细胞游离面微绒毛肿胀，变形，排列紊乱，细胞基底面质膜内褶减少或消失，这些超微结构的改变与某些类型肾小球肾炎的病理特征相似。     

维生素E对慢性染镉肝细胞凋亡的拮抗作用

目的　探讨维生素E(vitaminE ,VE)对慢性染镉肝细胞凋亡的拮抗作用。方法　健康昆明种小鼠 75只 ,体重 2 8g～ 32g ,随机分 3组 :染镉组 (Cdcl2 2mg·kg-1,皮下注射 ,每周 2次 ,共 3个月 )、VE +镉组 (染镉同时给VE 10mg·kg-1·d-1,灌胃 )、正常对照组 (注射等量生理盐水 )。采用免疫组化细胞凋亡染色 (Tunel法 )结合形态计量分析 ,观察 3组小鼠肝细胞凋亡的形态和数量改变。结果　 (1)染镉组小鼠肝细胞可见较多的细胞凋亡 ,VE +镉组肝细胞凋亡数量较少 ;细胞计数表明 ,VE +镉组细胞凋亡数量比染镉组明显减少 (P <0 0 1) ,而与正常对照组相比无显著性差异 (P >0 0 5 )。 (2 )凋亡肝细胞主要有以下形态特点 :①细胞胞体变小 ;②细胞核核仁消失 ,染色质浓缩边集于核膜下 ,核呈环状 ,晚期核固缩、变小 ,深染、致密度高。形态计量分析表明 ,凋亡肝细胞核的平均截面积、平均表面积、平均截面周长、体积密度等形态参数值均较正常肝细胞核明显减小 ,有显著性差异 (P <0 0 1) ;③核碎裂 ,形成凋亡小体。结论　VE对镉所致的肝细胞凋亡有抑制作用。     

维生素E对镉中毒小鼠睾丸生精细胞保护作用的形态学研究

目的探讨维生素E(VitaminE,VE)对慢性镉中毒小鼠睾丸生精细胞损伤的保护作用。方法3月龄昆明种雄性小鼠60只,随机分3组:镉组(每次CdCl22mg/kg,皮下注射,每周2次,共3个月),VE组(染镉同时给VEl0mg·kg-1·d-1,灌胃)和正常对照组(注射等量生理盐水),用光镜、电镜观察生精细胞形态变化,并对精原细胞和精子的超微结构进行立体定量分析。结果(1)与正常对照组比较,镉组小鼠睾丸均受损,根据受损程度可分为轻、中、重3型;精原细胞胞核和精子头内细胞核的平均截面积、平均体积和平均表面积等形态参数值均显著缩小(P<0.05);(2)VE组:大部分小鼠睾丸的形态结构接近正常,仅少部分小鼠的睾丸受到轻、中型损伤;精原细胞胞核和精子头内细胞核的平均截面积、平均体积和平均表面积等形态参数值与正常对照组的相应值接近,无显著性差异(P>0.05)。结论VE对镉引起的小鼠生精细胞形态的损伤有一定保护作用。     

小鼠肾小体发育中的细胞形态学变化

目的：探讨小鼠肾小体发生和发育过程中各种细胞的形态变化。方法：应用组织培养、后肾移植和光、电镜技术对发育不同阶段的肾小体进行观察。结果：胚龄13d后肾尚未出现肾小体时,经培养5d,或移植到受鼠5d后出现了成熟的肾小体的结构。电镜下观察表明：上皮基膜先于内皮基膜出现,随后两层膜融合。早期内皮细胞无核部分是连续的,无小孔结构。在发育过程中,小孔结构增多。早期足细胞有两种类型,明型和暗型,细胞基部伸出小突起并穿过基膜与内皮细胞紧贴。结论：血管球来源于内源性后肾细胞。发育过程中足细胞与内皮有结构上的接触,上皮基膜先于内皮基膜出现,足细胞有两型。     

小鼠肾小体发育中血管球毛细血管的分化

目的:探讨小鼠肾小体发育中血管球毛细血管内皮细胞的演变及毛细血管立体计量学的变化规律.方法:采用光镜、电镜技术,并结合体视学分析的方法,对不同发育阶段小鼠血管球毛细血管内皮细胞的演变及毛细血管立体计量学变化进行形态学观察和体视学测量.结果:在小鼠肾小体发育过程中,毛细血管内皮细胞的形状逐渐低平,内皮孔增多;从胚龄16 d到生后40 d,小鼠毛细血管的长度和表面积大约增大了64倍,体积大约增大了85倍.结论:在肾小体发育过程中,血管球毛细血管内皮孔的增多和血管球毛细血管的增大,为肾小体的滤过功能逐渐成熟提供了形态结构基础.     

VitE慢性镉中毒小鼠生精细胞影响的形态观察及立体定量分析

昆明种雄性小鼠 75只随机分成三组 :镉组(2 mg/kg/次 ,皮下注射 ,2次 /周 ) ;镉 Vit组 (染镉同时给 Vit E10 mg/ kg/　天 )和正常对照组 (注射等量生理盐水 )。 3月后取睾丸按常规制成 HE染色切片和超薄切片 ,分别用光镜和 H- 6 0 0型透射电镜观察 ,并用Bia Mias图像分析软件 ,P- 计算机图像分析系统对各组精原细胞和精子的部分超微结构进行了立体定量分析。结果如下 :1.镉组小鼠睾丸均受损 ,根据受损程度可分三型。轻型 :有散在少量的生精细胞变性、坏死。变性细胞的胞质内细胞器肿胀 ,核体积略增大 ;坏死细胞的核固缩、溶解 ,胞质内…     

电针“足三里”穴对肾小体及肾小管超微结构的作用

电针“足三里”穴引起肾小体过滤膜通透性增强,表现为毛细血管内皮小孔轻度扩张、基膜增厚、密度变浅。但足细胞裂孔直径未改变,同时,肾小管机能活性升高。近端与远端小管曲部上皮微绒毛加长、顶端小泡及溶酶体数目增多、基底皱褶伸长。近小球体细胞合成肾素的机能亦增加。总之,针刺后肾脏的过滤、重吸收、排泄及分泌功能均加强。本文还探讨了针刺镇痛与肾超微结构变化之间的相互关系、联系方式及其机能调整等问题。     

肾基膜来复红染色法的改良

肾小体的基膜位于足细胞与内皮的细胞之间,是由胶原蛋白和糖胺多糖组成的较厚的膜,是滤过屏障的主要组成部分,在生理机能上有着重要的意义.目前显示肾基膜有多种方法,在众多的染色法中,多数学者认为来复红染色法较简便,乐于接受,是较常见的显示肾基膜的一种方法,但其缺点是染色时间颇长,且药品不易得到,我们经多次实验观察,用醛品红代替来复红,获得了良好的效果,现将改良方法介绍如下.     

镉对慢性镉中毒小鼠黑质神经元的损害及维生素C的拮抗作用

目的研究维生素C（VC）对慢性镉中毒小鼠黑质神经元的保护作用。方法将75只雄性昆明种小鼠随机分为3组,每组25只。镉中毒组皮下注射氯化镉（CdCI：）,每周2次,每次2mg／kg,VC加镉组（VC组）上述方法和剂量染镉外,VC按每次25mg稀释后灌胃,正常组同时给予生理盐水。3个月后对小鼠进行Y型迷宫学习能力检测,并通过光镜及透射电镜观察小鼠黑质神经元的细微结构。结果Y型迷宫检测显示,VC组与镉中毒组相比,小鼠的学习、记忆能力均降低,差异有统计学意义（P〈0．05）;与正常组比较,差异无统计学意义（P〉0．05）。光镜和电镜结果显示,VC组小鼠中脑黑质区结构接近正常组,与镉中毒组比较有明显差异。结论抗氧化剂VC对慢性镉中毒组小鼠黑质神经元有显著的保护作用。     

The Prenatal Toxic Effect of Methylmercury on the Development of the Appendicular Skeleton of Rat Fetuses and the Protective Role of Vitamin E

Methylmercury (MeHg) is an environmental contaminant that is found in many ecosystems. Many studies reported that MeHg toxicity is accompanied by increased lipid peroxidation that may lead to oxidative damage to DNA, RNA, and proteins. Vitamin E is considered as the most effective antioxidant preventing lipid peroxidation. The aim of this study was to evaluate the effects of MeHg exposure during pregnancy on the development of the appendicular skeleton in rat fetuses and whether vitamin E administration could reduce this toxicity. Positively mated adult female Sprague–Dawley rats were used and divided into the following experimental groups: control group, received only deionized water, and four MeHg treated groups received 1 mg of MeHg/kg/d, 2 mg of MeHg/kg/d, 1 mg of MeHg/kg/d plus 150 mg of vitamin E/kg/d, and 2 mg of MeHg/kg/d, plus 150 mg of vitamin E/kg/d starting from Day 0 of gestation. On Day 20 of gestation, the fetuses from the pregnant rats were extracted and the fetal growth parameters were evaluated. Skeletal evaluation of ossification of both fore‐ and hind‐limbs, and coxal bones were undertaken. Results showed that treatment with MeHg caused adverse effects on fetal growth parameters and ossification of the bones. The coadministration of vitamin E with MeHg revealed an improvement in these parameters. These results suggest that vitamin E may ameliorate some aspects of MeHg developmental toxicity. The underlying and human health implications warrant further investigations. Anat Rec, 2012. © 2012 Wiley Periodicals, Inc.     

Amelioration of alloxan-induced diabetic keratopathy by beta-carotene

This study was undertaken to assess the anti-keratopathy activity of β-carotene in experimentally-induced diabetic animal model. The rats were divided into four groups as following: G1, normal control group; G2, β-carotene control group (50 mg/kg b.wt.); G3, diabetic group which was injected intraperitoneally with a single dose (100 mg/kg b. wt) of alloxan (ALX) and G4, diabetic rats treated with β-carotene which was injected with ALX as G3, and then received a daily oral dose of β-carotene (50 mg/kg b.wt.) for 3 months. ALX injection caused elevated levels of serum glucose in diabetic group. Moreover, histopathology revealed relatively thick corneal epithelium, ill-defined Bowman's membrane, widely spaced stromal layers and relatively thick Descemet's membrane. Electron microscopic studies showed vacuolated cytoplasm, partial loss of hemi-desmosomes and disorganized collagen fibrils with focal lysis of stromal layer. Oral gavage of β-carotene to diabetic rats for 3 months significantly decreased serum glucose level and ameliorated histopathological, immunohistochemical and ultrastructural results. Consequently, β-carotene exerted anti-keratopathy effects and ameliorated the corneal changes in diabetic rats via its hypoglycemic and antioxidant mechanisms.     

Vitamin E reversed nicotine-induced toxic effects on bone biochemical markers in male rats

Introduction

Vitamin E is beneficial in restoring bone histomorphometric parameters in nicotine-treated rats. This study determined the effectiveness of 3 forms of vitamin E in restoring bone metabolism in nicotine-treated rats.

Material and methods

Thirty-five male Sprague-Dawley rats were divided into 5 groups: (1) control (C), (2) nicotine cessation (NC), (3) α-tocopherol (ATF), (4) tocotrienol-enhanced fraction (TEF) and (5) γ-tocotrienol (GTT). Treatment was carried out for 4 months. The control group was administered normal saline and olive oil throughout the treatment period while treatment for groups 2-5 was performed in 2 phases. In the first phase, the groups received nicotine 7 mg/kg intraperitoneally for 2 months. The following 2 months, group 2 received normal saline and olive oil while groups 3-5 received ATF, TEF or GTT, 60 mg/kg orally. Pre-treatment and post-treatment serum was collected for bone biochemical marker measurement using the ELISA method.

Results

Nicotine increased serum bone-resorbing cytokines (interleukin-1 and interleukin-6) and the bone resorption marker pyridinoline (PYD) while reducing the bone formation marker osteocalcin after 2 months of nicotine treatment. The parameters failed to improve after nicotine was stopped for 2 months. Supplementation with the 3 forms of vitamin E improved the parameters, i.e. reduced the cytokines and pyridinoline as well as increased the osteocalcin. In addition, the TEF and GTT groups had a higher level of osteocalcin than the control group.

Conclusions

Nicotine impaired bone metabolism and cessation of nicotine treatment did not reverse the effects. Vitamin E, especially the tocotrienols, restored bone metabolism that was impaired due to nicotine.     

Ameliorating effect of vitamin C on murine sperm toxicity induced by three pesticides (endosulfan, phosphamidon and mancozeb)

The ameliorating effect of vitamin C (injected intraperitoneally)was evaluated against changes in sperm count and sperm headmorphology in mice fed either 3, 6 or 1000 mg/kg body wt/dayendosulfan, phosphamidon or mancozeb, respectively. The animalsreceived aqueous preparations of the pesticides and/or vitaminC once daily for 35 consecutive days. All three pesticides,irrespective of their chemical nature, significantly decreasedthe sperm count, as well as increased the frequency of spermwith aberrant head morphology. Out of the three doses of vitaminC used the middle and higher ones (20 and 40 mg/kg body wt/day,respectively) afforded comparatively more significant amelioration.The lower dose (10 mg/kg body wt/day) of this vitamin (quantitativelyequivalent to the human therapeutic dose according to body weight)was least efficacious in both the tests. However, ameliorationwas never up to the control level in any case. Vitamin C doses,when administered alone, did not produce any adverse effecton sperm count and sperm head morphology. ¹To whom correspondence should be addressed     

A Biochemical and Histopathologic Study Showing Protection and Treatment of Gentamicin-Induced Nephrotoxicity in Rabbits Using Vitamin C

Gentamicin and vitamin C have been proposed as nephrotoxic and antioxidant, respectively. This study involved biochemical and histopathologic investigation showing protection and treatment of gentamicin-induced nephrotoxicity in rabbits using vitamin C for 26 days hypothesizing that whether vitamin C would inhibit or decrease the raised serum urea and creatinine levels. This study was conducted on 25 healthy male albino rabbits (average weight 1.5±0.2 kg), classified into 5 groups: group A, B, C, D and E for nephrocurative (study-I) and nephroprotective (study-II) studies. Control group of rabbits (group A) received only the vehicle of gentamicin ampoule. In study-I, gentamicin sulphate (GS 80 mg/kg, i.m.) was administered to group B and C rabbits for ten days, then group C rabbits received vitamin C 250 mg/Kg for remaining 16 days. Group D and E received GS 80 mg/kg and GS 80 mg/kg i.m.-vitamin C 250 mg/kg orally, respectively during whole period (26 days) of study-II. After 26 days, various biochemical parameters, i.e. serum creatinine, blood urea nitrogen (BUN), and serum antioxidant activity, and histopathologic investigations were made. Nephrotoxicity was observed in rabbit groups B, C and D as evident from significant (p<0.05) high levels of serum creatinine and BUN and low serum antioxidant levels as compared to the levels of control group. Decrease in the levels of serum creatinine and BUN along with the increase in serum antioxidant activity was observed after vitamin C treatment in group C. While, renal-protective role of vitamin C was seen in group E as compared to the control. In conclusion, Gentamicin induced nephrotoxicity can be attenuated or treated using vitamin C.     

Vitamin E ameliorates alterations to the articular cartilage of knee joints induced by monoiodoacetate and diabetes mellitus in rats

We recently reported an animal model of osteoarthritis (OA) induced by a combination of the chondrocyte glycolysis inhibitor, monoiodoacetate (MIA) and the agent that induces diabetes mellitus, streptozotocin (STZ). Here we investigated the potential protective effect of the antioxidant and anti-inflammatory agent, vitamin E against MIA+STZ-induced OA. Therefore, rats were either injected once with MIA (2 mg/50 μL) + 65 mg/kg STZ before being sacrificed after 8 weeks (model group) or were treated immediately after MIA+STZ injections with vitamin E (600 mg/kg; thrice a week) before being sacrificed after 8 weeks (treatment group). Using scanning and transmission electron microscopy examinations, we observed in the model group a substantial damage to the articular cartilage of the knee joint as demonstrated by the destruction of the chondrocytes, territorial matrix, disrupted lacunae, collagen fibers, and profound chondrocyte ultrastructural alterations such as degenerated chondrocyte, irregular cytoplasmic membrane, damaged mitochondria and rough endoplasmic reticulum, vacuolated cytoplasm, presence of lipid droplets and different sizes of lysosomes, which were substantially but not completely protected by vitamin E. H&E stained sections of knee joint articular cartilage showed that MIA+STZ induced damage to the chondrocyte and territorial matrix. Vitamin E also significantly (p < .05) inhibited MIA+STZ-induced blood levels of the inflammatory biomarkers, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) that are known to be modulated in OA and diabetes. We conclude that vitamin E protects against MIA+STZ-induced knee joints injuries in rats, which is associated with the inhibition of biomarkers of inflammation.     

Vitamin E protects mice against Diplococcus pneumoniae type I infection

Vitamin E protects nonimmunized and immunized mice against fatal Diplococcus pneumoniae type I (DpI) infection. A dietary supplementation of 180 mg of dl-alpha-tocopheryl acetate per kg of diet increased survival of nonimmunized mice from 20 to 80% when challenged with 20 organisms, and of mice immunized with 0.5 ng of DpI polysaccharide from 15 to 70% when challenged with 20,000 organisms. The phagocytic index of immunized mice was four times higher in the 180-mg vitamin E group than in the control group. Both the survival and phagocytic index revealed a biphasic dose response, indicating a cause-effect relationship between phagocytosis and survival. Vitamin E also significantly increased the rate of carbon clearance from blood, indicating a general increase in phagocytic activity. The data indicated that increased macrophage activity probably aided by increased antibody production was the principal reason for increased protection.