Fertility of female mice fed coumestrol and diethylstilbestrol

Abstract

Coumestrol, a compound produced by various legumes which exerts estrogen‐like activity in animals, and diethylstilbestrol (DES) were studied as chemical agents for controlling reproduction in mice. Female mice were fed control diets or diets containing 100 ppm coumestrol for eight days. Female mice were exposed to males and reproductive tracts examined 14 days later. Litter size was not affected by 100 ppm dietary coumestrol but feed consumption was reduced 17%. Similar trials were conducted with mice fed 1 ppm DES. Vaginal plugs were present in 50% of the females fed 1 ppm DES, but no fetal pups were present. Feed intake was reduced 37% by the DES. Levels of 0, .1, .25, .50, .75 and 1.0 ppm DES were compared in two strains of mice, Swiss and ICR. Reproduction in both strains was totally inhibited by all DES treatments. The use of DES to control rodent populations warrants further investigation.     

甲醛经口染毒致小鼠脏器损伤和炎症反应的研究

为探讨在单独染毒和卵清蛋白(OVA)联合致敏的条件下,甲醛灌胃染毒对小鼠造成的毒性效应,将雄性Balb/c小鼠随机分为7组:对照组(蒸馏水组);OVA致敏组;2mg/(kg·d) FA(甲醛)组;20mg/(kg·d) FA组;200mg/(kg·d) FA组;200mg/(kg·d)FA+ OVA组;200mg/(kg·d) FA+ OVA +MT(褪黑素)组,以蒸馏水和不同浓度甲醛溶液灌胃,连续21d. OVA致敏组,200mg/(kg·d) FA+ OVA组,200mg/(kg·d) FA+ OVA +MT组在第6,13,20d进行腹腔注射OVA致敏;此外,200mg/(kg·d) FA+ OVA +MT组,每天用1.0mg/mL褪黑素灌胃小鼠(小鼠灌胃剂量10mg/(kg·d)),连续21d.检测肝,肾和肺组织中活性氧自由基(ROS),丙二醛(MDA)和还原型谷胱甘肽(GSH)的含量,并采用ELISA法检测肝组织中IL-4和IFN-γ的水平.结果表明,与对照组相比,甲醛浓度为200mg/(kg·d),小鼠肝脏ROS含量增加(P<0.05),MDA含量增加以及小鼠肾脏GSH含量降低,均有显著性差异(P<0.05).OVA作为致敏剂,甲醛浓度为200mg/(kg·d)时,肝组织中IL-4(Interleukin-4)含量增加(P<0.01),10mg/(kg·d)褪黑素能够降低200mg/(kg·d)甲醛+OVA染毒小鼠肝脏内ROS含量(P<0.05).综上,200mg/(kg·d)甲醛灌胃染毒能使小鼠产生氧化损伤和炎症反应, ROS, MDA水平上升(P<0.05),GSH水平下降(P<0.05),肝脏中细胞因子IL-4水平上升(P<0.01), IFN-γ水平下降(P<0.05).     

碲化镉量子点对小鼠肝脏超微结构及重要生物酶活性的影响

探讨了碲化镉量子点(cadmium telluride quantum dots,CdTeQDs)对小鼠肝组织超微结构及琥珀酸脱氢酶(succinate dehydrogenase,SDH)和三磷酸腺苷酶(adenosine triphosphatase,ATPase)活性的影响。将20只雄性ICR小鼠随机分成QDs染毒组和对照组,采用尾静脉注射方式进行一次性染毒,染毒组每只小鼠注射2μmol·kg-1体重的CdTeQDs(以Cd~(2+)的摩尔浓度计算)。每5只为一组分别在染毒后的1 d、3 d和7 d处死小鼠,另外5只注射生理盐水作为对照组。取部分肝组织在透射电镜下观察其超微结构变化并使用试剂盒测定肝脏中SDH、Na~+/K~+-ATP酶、Ca~(~(2+))/Mg~(2+)-ATP酶的活性。结果显示CdTeQDs暴露后染毒组小鼠肝细胞胞浆疏松,线粒体出现肿胀、空泡、嵴减少等结构变化,表明肝细胞受到损伤且染毒1 d后损伤最严重;肝脏中染毒组SDH活性与对照组相比显著降低(P0.05);染毒1 d后,Na~+/K~+-ATP酶和Ca~(2+)/Mg~(2+)-ATP酶活性与对照组相比显著升高,随着染毒后时间的延长,其活性呈现下降的变化趋势。单次量注射CdTeQDs能够引起小鼠肝脏损伤,抑制SDH活性,引起ATP酶活性改变,这些症状在暴露时间内呈现恢复趋势。     

增塑剂邻苯二甲酸二异壬酯致小鼠肺细胞氧化损伤作用的研究

为研究增塑剂邻苯二甲酸二异壬酯(diisononyl phthalate,DINP)对小鼠肺组织的氧化损伤作用,以昆明小鼠为受试动物,随机分为5组,包括1个阴性对照组(生理盐水)和4个DINP染毒组(0.2、2、20和200 mg·kg~(-1)),灌胃14 d。光镜下发现小鼠肺组织形态随染毒剂量的增加,小鼠肺细胞的病理损伤越严重。随着DINP染毒剂量的增加,肺组织匀浆活性氧(reactive oxygen species,ROS)、丙二醛(malondialdehyde,MDA)含量和肺组织细胞DNA-蛋白质交联(DNA-protein crosslink,DPC)系数逐渐上升,还原型谷胱甘肽(glutathione,GSH)含量逐渐降低,各指标呈一定的剂量-效应关系。染毒剂量为20 mg·kg~(-1)时,ROS和MDA含量差异有统计学意义(P0.05,P0.01);染毒剂量为200 mg·kg~(-1)时,上述指标差异均有统计学意义(P0.01)。结果表明,较高剂量(≥20 mg·kg~(-1))的DINP能造成小鼠肺组织的氧化损伤和病理损伤。     

The role of thymoquinone as antioxidant protection on oxidative stress induced by imidacloprid in male and female Swiss albino mice

The aim of the present study was to evaluate the possible protective effects of thymoquinone (TQ), an antioxidant agent, against imidacloprid (IMI)-induced oxidative stress in male and female mice. In total, 48 Swiss Albino male and female mice were fed a standard rodent diet and divided into 3 equal groups: the animals in the control group (vehicle treated) were given corn oil, the second group were orally administered 15 mg/kg/day IMI alone, and the third group were orally administered 15 mg/kg/day IMI and with TQ at 10 mg/kg/day for 21 days. During the experimental period, there were no significant changes between initial body weights and final body weights of IMI treated male and female mice. IMI produced significant increase in blood, liver, kidney, and heart malondialdehyde (MDA) levels and decrease in blood and liver glutathione (GSH) levels. In addition, IMI treatment decreased erythrocyte, liver, and kidney superoxide dismutase (SOD) activity in male mice and decreased erythrocyte and liver SOD activity in female mice. Erythrocyte catalase (CAT) activities were found to be low in male and female mice. However, treatment with TQ reversed IMI-induced oxidative stress, lipid peroxidation, and activities of antioxidant enzymes. Moreover, TQ exhibited protective action against the IMI-induced histopathological changes in tissues of male and female mice. In conclusion, TQ was found to be effective in protecting mice against IMI-induced oxidative stress by enhancing antioxidant defense mechanisms.     

Antioxidant rich diet supplements (Spirulina and tamarind fruit pulp) mitigate hematological disorders in fluoride exposed mice

The effect of antioxidant rich diet supplements of Spirulina and tamarind fruit pulp at 230 mg kg^?1 body weight, separately as well as in combination, on various hematological parameters of Swiss albino mice exposed to fluoride for seven days at daily doses of 190 mg kg^?1 body weight and for 90 days at daily doses of 94 mg kg^?1 body weight is reported. Compared with controls, fluoride exposure decreased erythrocyte (12%–18%), leukocyte (16%) and platelet counts (7%, only for short-term exposure), hemoglobin (2%–17%) and packed cell volume (2%–14%) in Swiss albino mice reared on standard feed but these were altered little in the diet supplement groups. Fluoride exposure decreased lymphocytes in both standard feed (16%–21%) and diet supplement groups (5%–19%, but only after long-term exposure). Fluoride withdrawal led to recovery of the post-treated mice from long-term exposure. Spirulina alone and also in combination with tamarind fruit pulp was found more effective than tamarind alone in reducing hematological disorders in fluoride treated mice.     

苯和甲醛联合染毒对小鼠脾脏的损伤

为了探讨苯和甲醛联合染毒对小鼠脾脏的损伤以及二者是否具有一定的协同作用,选择BALB/c雄性小鼠30只,随机分为5组,每组6只,设苯组、甲醛组、苯和甲醛联合染毒组及玉米油对照组和空白对照组,对小鼠进行气态甲醛吸入染毒或/和苯玉米油溶液灌胃染毒。染毒结束后对小鼠脾脏进行组织病理学观察,并且测定脾脏的脏器系数以及脾脏组织的活性氧(ROS)和丙二醛(MDA)的含量。结果显示,苯和甲醛联合染毒组小鼠脾脏组织中ROS的含量与空白对照组相比有极显著的上升趋势(P<0.01),脾脏的脏器系数以及脾脏组织中MDA的含量与空白对照组相比有显著性差异(P<0.05)。此外,在脾脏免疫组织形态变化以及脾脏组织中MDA含量这2个生理生化指标上,苯和甲醛联合染毒对小鼠脾脏的损伤具有一定的协同作用。     

Comparative effects of five chelating agents on testicular toxicity in mice induced by acute exposure to cadmium

The aim of this study was to develop new antidotes for cadmium (Cd) since this metal is known to produce mammalian toxicity. N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD), N-benzyl-D-glucamine dithiocarbamate (BGD), diethyldithiocarbamate (DDTC), 2,3-dimercaptopropanol (BAL), and ethylenediamine-tetraacetic acid (EDTA) were studied for their ability to inhibit the adverse effects induced by Cd on mouse testes. The parameters examined included concentrations of Cd, calcium (Ca), iron (Fe), and zinc (Zn) in testes, lipid peroxidation (LPO) levels in testes, lactate dehydrogenase (LDH) activity in serum and reproductive ability of male mice. Mice injected intraperitoneally (ip) with CdCl₂ (2.5?mgCd?kg^?1) after 30?min or 24?h, were then injected ip with chelating agents (400?µmol?kg^?1). Cd increased the concentrations of testicular Ca, Cd, Fe, Zn, and LPO levels as well as the activity of LDH in serum. HBGD and BGD effectively prevented the increase in above indices, and improved the reproductive ability weakened by exposure to Cd. The results suggested that HBGD and BGD are more effective detoxificants in the case of testicular toxicity in mice induced by acute exposure to Cd.     

Toxicity of nano-anatase TiO2 to mice: Liver injury,oxidative stress

There are concerns regarding the toxicity of nano-TiO₂, but data are limited on the mechanism underlying oxidative damage to liver of mice. In order to further study these mechanisms of nano-TiO₂ particles, nano-anatase TiO₂ (5 nm) were injected into the abdominal cavity of ICR mice daily for 14 days and biochemical parameters in liver were investigated. The increase of hepatic lipids peroxide produced by nano-anatase TiO₂ suggested an oxidative attack that was activated by a reduction of antioxidative defense mechanisms as measured by analyzing the activities of superoxide dismutase, catalase, ascorbate peroxidase, and glutathione peroxidase, as well as antioxidant levels such as glutathione and ascorbic acid. The antioxidative responses of liver were reduced in mice by nano-anatase TiO₂. The oxidative stress of nano-anatase TiO₂ on liver was greater than that seen with bulk-TiO₂.     

全氟辛烷磺酸对哮喘小鼠炎症反应的影响

探讨全氟辛烷磺酸(perfluorooctane sulfonate,PFOS)暴露对哮喘小鼠Th1/Th2炎症反应的影响。选择36只雄性C57BL/6J小鼠,随机分为6组:对照组、卵清蛋白(ovalbumin,OVA)单独致敏组、PFOS染毒组(0.1、1、5、10 mg·kg~(-1)·d~(-1) PFOS+OVA致敏),每组6只。染毒和诱发哮喘后第26天收集肺泡灌洗液(BALF)进行有核细胞总数和嗜酸性粒细胞计数;用Luminex技术测定BALF中细胞因子白细胞介素-5(interleukin-5,IL-5)、白细胞介素-4(interleukin-4,IL-4)和γ干扰素(interferon-γ,IFN-γ)水平;肺组织切片染色观察其病理变化。随PFOS暴露浓度的增加,嗜酸粒细胞总数呈上升趋势(P0.05),IL-5/IFN-γ比值增加(P0.05);其中10 mg·kg~(-1)·d-1PFOS+OVA组BALF中的白细胞总数显著高于OVA单独组(P0.05),IL-4水平及IL-4/IFN-γ比值显著高于OVA单独组(P0.05),且与单独OVA组相比小鼠气道粘膜及粘膜下层厚度更厚,炎症细胞浸润更明显,PAS染色阳性的气道上皮细胞明显更高。PFOS能加重哮喘小鼠肺部的炎症反应并诱导Th2型细胞因子的表达。