呋喃丹对雄性大鼠急性生殖损伤的研究

目的：探讨农药呋喃丹对雄性大鼠生殖系统急性损害作用。方法：以0．3，1．5，3．0mg/kg剂量经口染毒7d，检测大鼠血清及睾丸组织匀浆中脂质过氧化指标超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px)、丙二醛（MDA）、活性氧，睾丸组织标志酶β－葡萄糖醛酸苷酶（β-G）、葡萄糖－6磷酸脱氢酶（G－6－PD）、乳酸脱氢酶同工酶X（LDHx）及一氧化氮（NO）、一氧化氮合酶（NOS）的含量或活力。结果：染毒7d大鼠血清GSH－Px、β-G、NOS活力下降，睾丸组织匀浆中MDA、活氧含量及β－G、NOS活力升高（P＜0．05），GSH－Px、SOD活力下降（P＜0．05）。结论：短时间接触呋喃丹可对大鼠睾丸组织产生脂质过氧化作用，对睾丸组织有损害。     

呋喃丹对大鼠睾丸组织标志酶活性影响的动态观察

为探讨农药呋喃丹对雄性大鼠睾丸组织的损害作用 ,以低、中、高剂量 (0 3、1 5和 3 0mg kgBW)经口连续染毒 77天 ,分别于染毒第 7、35和 77天检测大鼠血清及睾丸组织匀浆中 β-葡萄糖苷酶 (β-G)、葡萄糖 - 6 -磷酸脱氢酶 (G - 6 -PD)、乳酸脱氢酶同工酶X(LDHx、)的活性。结果显示 ,染毒第 7天大鼠 3个染毒组血清中 β -G活性显著低于对照组 (P <0 0 5) ,低剂量组睾丸组织匀浆中 β -G活性高于对照组、而高剂量组低于对照组 (P <0 0 5) ;染毒第 77天中高剂量组血清中G - 6 -PD活性 ,高剂量组睾丸组织匀浆中LDHx活性均低于对照组 (P <0 0 5) ,其它指标及时段未见明显改变。提示呋喃丹对大鼠睾丸组织有一定损害作用。     

二氯苯胺对小鼠睾丸中某些酶的影响

以150、300、600 mg/kg剂量小鼠灌胃染毒2,3-二氯苯胺,测定小鼠睾丸匀浆上清液中还原性谷胱甘肽(GSH)的含量、超氧化物歧化酶(SOD)以及乳酸脱氢酶x(LDHx)的活性。与对照组比较,低剂量的2,3-二氯苯胺对小鼠睾丸GSH含量以及SOD酶活性有一定的抑制作用,随着2,3-二氯苯胺染毒剂量增加,GSH含量和SOD酶活性显著升高,LDHx酶活性显著降低。提示2,3-二氯苯胺对小鼠睾丸组织中的某些酶活性有一定的影响。     

壬基酚对大鼠睾丸和血清中某些生化指标的影响

目的研究环境类激素壬基酚对大鼠睾丸和血清中某些生化指标的影响.方法以壬基酚50、100、200 mg/kg剂量对Wistar雄性大鼠连续经口染毒35 d,检测大鼠睾丸组织匀浆及血清中β-葡萄糖醛酸苷酶(β- G )、乳酸脱氢酶同工酶(LDHx)、超氧化物歧化酶(SOD)的活性及谷胱甘肽(GSH)、丙二醛(MDA) 含量,血中睾酮(T)、雌二醇(E2)水平.结果 50 mg/kg处理组睾丸组织中β-G和200 mg/kg处理组血清中LDHx活性显著高于对照组(P＜0.05);200 mg/kg处理组睾丸组织中SOD活性及血中T含量显著低于对照组(P＜0.05).结论壬基酚可能会诱发大鼠睾丸和血清某些生化指标的改变,表明对睾丸有损伤.     

三硝基甲苯对大鼠睾丸某些生化功能的影响

本研究采用急性染毒方式，观察三硝基甲苯（ＴＮＴ）对大鼠睾丸某些生化功能的影响。结果表明，２０００ｍｇ／ｋｇＴＮＴ染毒组睾丸葡萄糖－６－磷酸脱氢酶（Ｇ－６－ＰＤ）、乳酸脱氢酶（ＬＤＨ）、山梨醇脱氢酶（ＳＤＨ）和酸性磷酸酶（ＡＣＰ）活性下降，睾丸锌含量下降，而血清锌含量上升。１０００ｍｇ／ｋｇＴＮＴ染毒组睾丸Ｇ－６－ＰＤ和ＡＣＰ活性也下降，而血清锌含量升高。表明睾丸中Ｇ－６－ＰＤ和ＡＣＰ活性以及血清锌含量变化较为敏感。     

二甲基甲酰胺对小鼠睾丸组织结构和睾丸酶的影响

目的探讨二甲基甲酰胺（DMF）对睾丸组织结构及睾丸酶活力的影响。方法将40只SPF级健康成年雄性昆明种小鼠随机分为空白对照组（0g／kg）、低（0．5g／kg）、中（1g／kg）、高（2g／蝇）剂量染毒组。每天灌胃染毒DMF一次，空白对照组以蒸馏水灌胃，连续灌胃30d。于染毒前1d称重小鼠，以后每3d称重1次。于第31日摘除眼球取血并颈椎脱臼处死小鼠。每组随机抽取两只小鼠的一侧睾丸，制备病理切片。采用试剂盒测定其余睾丸琥珀酸脱氢酶（SDH）、乳酸脱氢酶（LDH）、酸性磷酸酶（ACP）活力。结果与空白对照组（0g／kg）比较，染毒第9天后各染毒组小鼠体重下降（P〈0．05）。随染毒剂量增高，睾丸组织中ACP活力有增高趋势，各染毒组ACP活力显著高于空白对照组（P〈0．01）。中、高剂量染毒组SDH活力显著低于空白对照组（P〈0．01）。各染毒组LDH活力显著低于空白对照组（P〈0.01）。结论在本实验染毒时间和剂量范围内，DMF能引起小鼠睾丸组织病理学改变并且抑制睾丸酶的活力。     

氯化锰对雄性大鼠亚急性生殖毒性机制研究

选取健康性成熟雄性Wistar大鼠灌胃染毒 10mg/kg、 2 0mg/kg和 40mg/kg氯化锰 ,每日 1次 ,连续染毒3 0d ,应用分光光度法测定血清和睾丸匀浆中MDA、ROS、NO、SOD、GSH Px、LDH、LDHx、G 6 PD、β G和NOS的水平和活力。结果显示 ,染毒氯化锰 2 0mg/kg组仅睾丸匀浆中ROS、SOD、LDHx和G 6 PD活力与阴性对照组比较差异有显著性 (P <0 0 5 )。在 40mg/kg组 ,血清中LDHx和G 6 PD下降 ,睾丸匀浆中的MDA、ROS升高 ,SOD、GSH Px、LDHx和 β G活力下降 ,与对照组比较差异有显著性或高度显著性 (P <0 0 5或P <0 0 1) ,并且SOD、ROS、LDHx和G 6 PD有明确剂量 效应关系 ,r值为 0 5 782、 -0 5 3 47、 -0 5 814和 -0 4972 (均P <0 0 5 )。各染毒剂量组睾丸匀浆中NOS活力均明显高于对照组 ,差异有显著性 (均P <0 0 5 )。说明亚急性染毒氯化锰可使大鼠睾丸组织产生脂质过氧化作用 ,使睾丸标志酶活力降低 ,睾丸匀浆中NOS活力升高 ,使间质细胞、支持细胞和生精细胞受损 ,并形成一个损伤链 ,这些可能是锰致雄性生殖功能受损的部分机制     

醋酸铅对雄性小鼠生殖功能的影响

给雄性小鼠灌胃染毒醋酸铅 10mg/kg、 2 0mg/kg和 40mg/kg ,每天 1次连续 3 5d。应用分光光度法测定血清和睾丸中酶活性 ,按标准方法测定小鼠生育力 ,并对睾丸、附睾进行组织病理学检查。结果表明 ,雄鼠受精率、雌鼠妊娠率、平均每窝活胎率及睾丸匀浆中的 β G和LDHx随染毒剂量增加而降低 ,死胎率和吸收胎率随染毒剂量增加而升高 ,与阴性对照组比较差异均有显著性 (P <0 0 5 ) ,并呈现明确的剂量 反应关系 ,r值依次为 -0 412、 -0 42 0、-0 5 3 7、 -0 5 3 8、 -0 617、 0 5 42和 0 5 3 5。雄鼠交配率 ,血清和睾丸匀浆中G 6 PD、ACP、LDH仅在 40mg/kg组与阴性对照组比较差异有高度显著性和显著性 (P <0 0 1或P <0 0 5 )。说明染毒醋酸铅≥ 2 0mg/kg剂量可损害雄性小鼠生殖功能。     

氧乐果对小鼠睾丸特征性酶的影响及茶多酚的拮抗作用

目的研究有机磷农药——氧乐果对小鼠睾丸特征性酶的影响以及茶多酚对它的拮抗作用。方法将80只昆明雄性小鼠随机分成8组，即3个氧乐果染毒组，1个对照组，1个茶多酚组和茶多酚＋低、中、高剂量氧乐果染毒组。染毒组分别灌胃1、2、4mg／kg氧乐果；茶多酚组灌胃180mg／kg茶多酚；茶多酚＋低、中、高剂量染毒组小鼠提前灌胃茶多酚180mg／kg，2h以后分别灌胃1、2、4mg／kg氧乐果，对照组灌胃生理盐水，共灌胃6d。用比色法检测睾丸组织中睾丸特征性酶——碱性磷酸酶（AKP）、酸性磷酸酶（ACP）、乳酸脱氢酶（LDH）及乳酸脱氢酶X酶（LDH—X）的活力。结果随着氧乐果染毒剂量的增加，小鼠体重和睾丸重下降（P〈0，01或P〈0．05），睾丸AKP、ACP和LDH活力均升高（P〈0，05或P〈0，01）。预先灌胃茶多酚，2h后灌胃氧乐果，小鼠体重和酶活力有所变化，但与对照组比较，差异均无统计学意义（P〉0．05）。结论茶多酚对氧乐果所造成的小鼠睾丸特征性酶的影响有拮抗作用。     

甲醛对小鼠肺组织形态及肺泡灌洗液成分的影响

为探讨甲醛对小鼠肺组织形态及肺泡灌洗液成分的影响,取48只小鼠静式吸入甲醛染毒,每日2h,连续2个月。染毒浓度分别为21、42和84mg／m^3,光镜下观察小鼠肺组织形态变化,并测定肺泡灌洗液（BALF）中乳酸脱氢酶（LDH）、酸性磷酸酶（ACP）、碱性磷酸酶（AKP）含量。与对照组相比,光镜下可见吸入甲醛的小鼠肺毛细血管充血,肺泡间隔增宽,有炎细胞浸润,随着染毒剂量增加病理改变加重;小鼠BALF中不同剂量组的LDH、ACP和AKP含量均有所增加（P〈0．05）,但组间差异无统计学意义（P〉0．05）。提示吸入一定浓度的甲醛可以造成肺组织的细胞损伤。     

转基因雄性小鼠不育原因分析

目的研究转基因雄性小鼠不育的主要原因。方法以野生型C57BL／6J作为对照，比较检测健康性成熟雄性转基因小鼠的睾丸、附睾、前列腺、提肛肌的脏器系数和精子数、精子活动度、活精率、精子畸形率；观察睾丸组织病理学变化及睾丸组织葡萄-6-磷酸脱氢酶（G-6-PD）、乳酸脱氢酶（LDH）、乳酸脱氢酶同工酶（LDH-X）及琥珀酸脱氢酶（SDH）的活性。结果与正常非转基因对照鼠相比，转基因鼠睾丸的脏器系数与正常对照鼠相接近，附睾、提肛肌的脏器系数显著降低。精子数、直线运动精子数显著降低（P〈0．01）；转基因鼠睾丸组织曲细精管变薄，生精细胞排列不整齐，层次减少（2层），上皮部分有变性，精原细胞、初级精母细胞分裂异常，精子形成减少；G-6-PD、LDH、LDH-X及SDH的活性均显著低于对照鼠。结论外源基因整合后，引起睾丸组织酶活性下降，影响各细胞的生理、生化功能，进而引起睾丸发育严重障碍，精子减少和活动能力降低而导致不育。     

Effect of 2-phenyl-3-p-(beta-pyrrolidinoethoxy) phenyl-beta-methoxy benzofuran hydrochloride (DBF) on the biochemistry of the fallopian tube and uterus of rhesus monkey (Macaca mulatta).

The effects of the nonsteroidal title compound (DBF) on the biochemical composition of the Fallopian tube and uterus were studied in the rhesus monkey. Monkeys received 2 mg/kg daily by mouth, which is the antifertility dose. The weight of the pituitary was significantly decreased (p less than .05) due to treatment, but the weights of the Fallopian tube, uterus, ovary and adrenal were unaltered. In both the Fallopian tube and uterus, DBF induced a significant increase (p less than .01) in the concentration of glycogen, protein and nonprotein nitrogen, and a significant decrease (p less than .01) in the concentration of lactic acid. The total phospholipid level in the uterus showed an increase (p less than .01) in the activities of adenasine triphosphatase (ATPase), malic dehydrogenase, acid and alkaline phosphatases, and glucose-6-phosphate dehydrogenase (G-6-PD) was seen. Lactic dehydrogenase activity fell (p less than .01) and the activity of beta-glucuronidase was unchanged. In the uterus, ATPase, malic dehydrogenase, alkaline phosphatase and lactic dehydrogenase activities increased significantly (p less than .01), beta-glucuronidase and acid phosphatase activities fell (p less than .01) and G-6-PD activity was unaltered. The antifertility effect of DBF may be due to its ability to elicit many biochemical effects similar to those induced by a typical estrogen.     

Effect of malathion and endosulfan on brain acetylcholinesterase and ovarian steroidogenesis of Channa punctatus (Bloch)

The effect of sublethal concentrations of malathion (organophosphorus insecticide) and endosulfan (organochlorine insecticide) was investigated in Channa punctatus. Brain acetylcholinesterase (AchE) and ovarian delta 5,3 beta-hydroxysteroid dehydrogenase (delta 5,3 beta-HSD) and glucose-6-phosphate dehydrogenase (G-6-PD) activities were studied. Apart from the loss of stage II and III oocytes, the absence of delta 5,3 beta-HSD and G-6-PD activity indicating the inhibition of steroidogenesis was seen in the malathion- and endosulfan-treated fish ovaries. Malathion demonstrated a dose-dependent inhibition of brain AchE activity, whereas endosulfan caused no significant reduction of AchE activity.     

广东粤北地区新生儿疾病筛查及防治对策研究

目的 分析2009-2012年广东省粤北地区新生儿疾病筛查现状和先天性甲状腺功能减低症（CH）、葡萄糖-6-磷酸脱氢酶缺乏症（G-6-PD）和苯丙酮尿症（PKU）的发病率情况.方法 对粤北地区2009-2012年新生儿疾病筛查资料进行回顾性分析.结果粤北地区2009-2012年的新生儿疾病平均筛查率为88.84％,并且逐年升高.CH发病率为0.56‰（1：1789）,高于广东其他城市;G-6-PD 7 759例,检出率为4.93％（1：20）; PKU 2例,检出率为0.013‰（1：78 707）.结论 总结分析粤北地区新生儿疾病筛查现状,为今后筛查工作的进展提供科学依据,对提高粤北地区出生人口素质,减少出生缺陷率,保障耍幼儿健康发展起着关键作用.     

甲醛对雄性小鼠睾丸中酶活力的影响

目的探讨甲醛对雄性小鼠睾丸中酶活力的影响。方法28只昆明种雄性小鼠随机分为4组,每组7只。设低、中、高剂量组分别以0.2、2.0、20.0mg/kg甲醛腹腔注射染毒,每天1次,连续7d,测定睾丸中乳酸脱氢酶(LDH)、葡萄糖-6-磷酸脱氢酶(G-6-PD)、山梨醇脱氢酶(SDH)活力。同时设对照组,腹腔注射生理盐水。结果小鼠睾丸G-6-PD、SDH活力随染毒剂量增大而降低,低、中、高剂量组SDH活力与对照组比较,差异均有统计学意义(P<0.05或P<0.01),低、中、高剂量组LDH和G-6-PD活力与对照组比较,差异无统计学意义(P>0.05)。结论甲醛对雄性小鼠睾丸中的酶具有不良影响,从而产生一定的生殖毒性。     

Biochemical changes in the fallopian tube and uterus of the rhesus monkey (Macaca mulatta) under the influence of progestational contraceptive steroids.

The effect of oral administration of progestational contraceptive steroids such as megestrol acetate (MGA), norethynodrel (NE) and ethynodiol dliacetate (EDA), on the reproductive organs of rhesus monkeys has been studied. The ovarian weight was raduced by MGA whereas, NE enhanced the weight of the Fallopian tube, uterus, ovary, adrenal and pituitary and EDA that of the Fallopian tube only.Treatment with MGA caused a rise in the levels of lactic acid and non-protein nitrogen (NPN), fall in the levels of glycogen and no alteration of the protein concentration of the Fallopian tube and uterus. Further, a marked Inhibition of the activities of β -glucuronidase, adenosine triphosphatase (ATPase), alkaline phosphatase, malic dehydrogenase (MDH) and enhancement of those of acid phosphatase, lactic dehydrogenase (LDH) and glucose-6-phosphate dehydrogenase (G-6-PD) were observed in both tissues.As a result of the treatment with NE, the Fallopian tube and uterus recorded a significant increase in the concentrations of protein and glycogen; however, the NPN level of the tube was diminished and that of the uterus was enhanced. On the other hand, depression of the activities of β -glucuronidase and LDH and stimulation of those of ATPase, MDH and alkaline phosphatase were observed in both tissues. However, acid phosphatase activity of the uterus and G-6-PD activity of the tube were reduced markedly.     

Activities of Pentose Shunt and Glycolytic Enzymes in Lungs of Ozone-Exposed Rats

After seven days of exposure of rats to 0.8 ppm ozone, the activities of pentose shunt and glycolytic enzymes of the lungs were significantly increased, α-Tocopherol partially retarded the elevation of glucose-6-phosphate dehydrogenase (G-6-PD), 6-phosphogluconate dehydrogenase (6-P-GD), and malic enzyme, but not of others. In a separate exposure of rats to 0.75 ppm ozone, the activities of glutathione (GSH) peroxidase, GSH reductase, G-6-PD, 6-P-GD, and pyruvate kinase decreased initially and then increased above their respective controls. The results can be partially attributed to increased needs of reductive detoxification of lipid peroxide. Increased activities may be related to the development of adaptation by the animals.     

Association between glucose-6-phosphate dehydrogenase deficiency and neonatal jaundice: interaction with multiple risk factors.

This nonconcurrent cohort study was carried out to evaluate the association of neonatal jaundice with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency and its interactions with other risk factors. The G-6-PD enzyme activity of 12,379 neonates was screened by a semi-quantitative fluorometric assay and double-checked by a quantitative method to identify a G-6-PD deficient cohort of 333 neonates. Matched with these on birth date, sex and delivery hospital were a G-6-PD normal cohort of 653 neonates. Neonatal jaundice was defined by a peak serum bilirubin (PSB) level of > or = 15 mg/dl. A significant association between G-6-PD deficiency and neonatal jaundice was observed in male but not female neonates. There was an inverse dose-response relation between G-6-PD activity and neonatal jaundice among male neonates. Both hypoxia/asphyxia and maternal hepatitis B surface antigen (HBsAg) carrier status were associated with an increased risk of neonatal jaundice among G-6-PD deficient but not G-6-PD normal male neonates. Based on multiple regression analyses, an additively synergistic effect on PSB level and severe jaundice (PSB > or = 20 mg/dl) was observed for G-6-PD deficiency and maternal HBsAg carrier status.