丙烯酰胺作业工人的脊髓及大脑诱发电位

本文对30名具有周围神经症状或体征的丙烯酰胺作业工人进行脊髓及大脑体感诱发电位研究,结果发现脊髓传导速度减慢,脊髓传导时间延长,但脊髓以上中枢传导时间未见改变,提示脊髓上行传导神经纤维受损,而脊髓以上的脑干皮层感觉传导纤维未受影响,脊髓体感神经传导束的损害与接触丙烯酰胺程度有关。听觉诱发电位各指标未见改变,提示听觉神经传导系统未受损害。     

二硫化碳作业工人的神经肌电图及大脑诱发电位研究

本文对96名二硫化碳作业工人进行了神经肌电图测定,并对其中部分工人作了胫后神经体感诱发电位、视觉诱发电位和脑干听觉诱发电位检查。结果发现,二硫化碳作业工人的神经肌电图改变,符合周围神经远端轴索病之特点。胫后神经体感诱发电位结果显示,脊髓传导时间延长,脊髓传导速度减慢,颈髓以上中枢传导时间与对照组相比,无显著差异。视觉诱发电位和脑干听觉诱发电位无明显改变。     

溴氰菊脂对家兔体感诱发电位及周围神经传导功能的影响

目的 研究溴氰菊酯对家兔体感诱发电位（SEP）及周围神经传导功能的影响。方法利用丹麦产Neurom atic-2000C型神经-肌电描记仪,对不同溴氰菊酯染毒剂量家兔进行染毒前后体感诱发电位、感觉神经传导速度（SCV）、运动神经传导速度（MCV）进行测定。结果 与染毒前及对照组比较,高、中剂量染毒组染毒后SEP的N1、P1、N2波潜伏时明显延长（P〈0.05,P〈0.01）。与染毒前及对照组比较,高剂量染毒组染毒后SCV潜伏时明显延长,高、中剂量染毒组染毒后传导速度明显减慢（P〈0.05,P〈0.01）。与染毒前及对照组比较,高、中剂量染毒组染毒后MCV远端潜伏时明显延长、传导速度明显减慢（P〈0.05,P〈0.01）。结论 溴氰菊酯可对家兔造成神经电生理的异常,体感诱发电位及周围神经传导功能的测定可用于评价溴氰菊酯对家兔神经功能的影响。     

大鼠亚慢性丙烯酰胺中毒神经行为功能及电生理的改变

目的 观察丙烯酰胺亚慢性染毒对大鼠神经行为功能及电生理变化的影响.方法 30只雄性SD大鼠随机分为3组(对照组、低和高剂量组)每组10只,分别以生理氯化钠、丙烯酰胺20、40 mg/kg剂量腹腔注射,每周3次,共10周,测量大鼠体重、热板仪、甩尾、后肢撑力及神经传导速度等指标.结果 中毒后大鼠体重减轻,从第4周开始高剂量组与对照组比较有统计学意义(P＜0.05),第6周高剂量组与低剂量组比较有统计学意义(P＜0.01),热板仪实验异常(高剂量组时间延长57%,低剂量组时间延长44%),甩尾实验时间延长(高剂量组延长38%),后肢展开距离明显加宽(高剂量组增加102%,低剂量组增加61%),胫神经和腓肠神经传导速度降低(感觉神经传导速度降低32%,运动神经传导速度降低33%).结论 丙烯酰胺可引起大鼠的热觉传导异常,运动神经损伤,传导速度降低.     

溴氰菊酯经皮染毒对家兔神经系统的急性影响

[目的]探讨溴氰菊酯对家兔神经系统功能的影响。[方法]利用丹麦产Keypiont神经肌电描记仪,对家兔进行溴氰菊酯25mg/kg染毒前后体感诱发电位(SEP)及运动神经传导速度(MCV)的测定,并对数据进行统计分析。[结果]与染毒前比较,染毒后SEP的P1、P2、N1波潜伏时明显延长(P<0.05),远端潜伏时无显著差异(P>0.05),家兔后肢近端潜伏时染毒前后差异有显著性(P<0.05),运动神经传导速度显著减慢(P<0.01)。[结论]在此剂量染毒下,溴氰菊酯对家兔神经系统有明显的损害作用。     

二硫化碳对实验大鼠神经系统神经营养因子的影响

目的探讨二硫化碳染毒对大鼠神经生长因子(NGF)和脑源性神经营养因子(BDNF)蛋白表达的影响。方法健康雄性Wistar大鼠20只随机分成对照组和二硫化碳组,每组10只。二硫化碳组大鼠腹腔注射二硫化碳玉米油溶液,开始4周染毒剂量为150mg/kg,1次/d,6次/周,后4周染毒剂量为300mg/kg,1次/d,6次/周。对照组腹腔注射等剂量的玉米油溶液。染毒结束后对周围神经损伤体征进行评分,同时检测胫神经运动神经传导速度和腓肠神经感觉神经传导速度;并应用免疫组化方法检测NGF、BDNF在海马及坐骨神经中的蛋白表达情况。结果二硫化碳染毒8周后染毒组大鼠周围神经体征评分明显升高;与对照组比较,神经电生理测定结果显示二硫化碳染毒组胫神经运动神经和腓肠神经感觉神经传导速度明显减慢,潜伏期延长,波幅减低。染毒组大鼠海马及坐骨神经中NGF和BDNF表达较对照组显著降低。结论二硫化碳染毒导致的神经组织NGF、BDNF蛋白表达下降可能参与了其神经毒作用。     

丙烯酰胺的毒性研究

本文AAM的急性毒性试验,昆明小鼠经口LD_(50)为154mg/kg。动物慢性中毒以后肢瘫痪、坐骨运动神经传导速度减慢和周围神经病理损伤为主,并有剂量—反应关系。AAM对皮肤粘膜有一定的刺激作用。Amse试验、染色体畸变和微核试验皆为阴性。     

丙烯酰胺染毒后胫神经及腓肠神经电生理指标的变化

目的观察丙烯酰胺亚慢性染毒对大鼠胫神经及腓肠神经电生理指标的影响。方法 36只健康雄性Wistar大鼠随机分为0、2、4、6、8、10周6组,以0周为对照组。染毒组给予丙烯酰胺(生理盐水溶液)40 mg/kg腹腔注射,每周3次。对照组同样方式注射生理盐水。分别于第0、2、4、6、10周测定胫神经运动神经传导速度(MNCV)和腓肠神经感觉神经传导速度(SNCV)。结果实验第4周时,染毒大鼠的MNCV减慢,波幅(AMP)降低(P<0.05);实验第6周开始,染毒组大鼠的潜伏期(LAT)延长(P<0.05),且各电生理指标持续改变至第10周。实验第4周时,染毒大鼠的SNCV减慢,潜伏期延长(P<0.05),且各电生理指标持续改变至第10周;其中,波幅改变无统计学意义。结论丙烯酰胺可致染毒大鼠胫神经及腓肠神经各电生理指标改变,并随染毒时间增加进行性加剧。     

人参三醇组皂苷对大鼠坐骨神经急性损伤后修复的研究

目的探讨人参三醇组皂苷(PTS)对大鼠坐骨神经急性损伤后的保护作用。方法建立大鼠坐骨神经挤压伤模型,随机分为PTS 100、50、25 mg/kg剂量组(每组10只),坐骨神经损伤后每日腹腔注射PTS;模型对照组(10只),坐骨神经损伤后每日给予同样剂量的生理盐水;空白对照组(10只),不损伤坐骨神经,每日给予同样剂量的生理盐水。坐骨神经损伤术后1、2、3、4 w观察坐骨神经功能指数(SFI)、运动神经传导速度(MNCV)。结果坐骨神经损伤术后21、30 d PTS 100 mg/kg bw剂量组的SFI分别为-30.2±10.4及-20.0±6.9明显优于模型对照组-52.1±11.0及-46.2±7.8(P0.05),术后30 d PTS 100 mg/kg bw剂量组的MNCV为14.72±4.34明显优于模型对照组8.27±2.53(P0.05)。结论人参三醇组皂苷对大鼠坐骨神经急性损伤后有一定的保护作用。     

锌 硒对汞致大鼠听力损伤影响的研究

目的:探讨汞中毒对大鼠听力功能的损伤以及锌、硒对大鼠听力功能的保护作用。方法:将40只雌雄各半Wistar大鼠随机分成对照组(A)、汞中毒组(B)、锌保护组(C)和硒保护组(D)四组。B、C、D三组分别用氯化汞(4 mg/kg)、氯化汞(4 mg/kg)和硫酸锌(4 mg/kg)、氯化汞(4 mg/kg)和亚硒酸钠(2 mg/kg)连续灌胃30 d,正常饲料和去离子水喂养,对照组正常饲料和生理盐水喂养,30 d后脑干电诱发电位测定大鼠听力功能。结果:B组大鼠脑干电诱发电位Ⅰ、Ⅱ波潜伏期明显长于A组,波峰明显低于A组,C、D组大鼠脑干诱发电位Ⅰ、Ⅱ波潜伏期没有延长或是延长不明显,波峰有所下降或是下降不明显。结论:B组大鼠听力明显下降,锌、硒对汞致大鼠听力功能的损伤有保护作用,且具有较强的保护雄性大鼠的作用。     

细胞周期依赖性蛋白激酶5/p35在2,5-己二酮中毒大鼠神经组织中的表达

目的 探讨细胞周期依赖性蛋白激酶5(CDK5)在2,5-己二酮(HD)中毒性周围神经病发病过程中的作用.方法 30只雄性Wistar大鼠,随即分为对照组、200mg/kg HD染毒组和400mg/kg HD染毒组,每组10只.染毒途径为腹腔注射,每周5次,连续8周,建立HD中毒性神经病模型.利用Western blotting方法检测大脑、脊髓和坐骨神经胞浆蛋白和膜蛋白中CDK5、p35和p25的相对含量.结果 与对照组相比,P35蛋白含量在200、400mg/kg HD染毒大鼠大脑和脊髓胞浆蛋白组分中明显降低,而在脊髓和坐骨神经膜蛋白组分中含量明显升高,差异均有统计学意义(P＜0.01);p25变化趋势与p35基本一致.CDK5在200、400mg/kg HD染毒大鼠大脑胞浆和膜蛋白中均明显下降;除坐骨神经膜蛋白组分中未检出外,在脊髓和坐骨神经中CDK5含量明显升高,与对照组比较,差异有统计学意义(P＜0.01).结论 HD中毒后大鼠神经组织中CDK5及其激活因子p35和p25发生明显改变,这种改变可能与HD中毒性周围同神经病的发病机制有关.     

Prenatal and perinatal acrylamide disrupts the development of cerebellum in rat: Biochemical and morphological studies

Acrylamide is known to cause neurotoxicity in the experimental animals and humans. The literature on its neurotoxic effect in the adult animals is huge, but the effect of acrylamide on the embryonic and postnatal development is relatively less understood. The present study examined its effects on the development of external features and cerebellum in albino rats. Acrylamide was orally administered to non-anesthetized pregnant females by gastric intubation 10 mg/kg/day. The animals were divided into three groups as follows. (1) Group A, newborn from control animals; (2) Group B; newborns from mothers treated with acrylamide from day 7 (D7) of gestation till birth (prenatal intoxicated group); (3) Group C; newborns from mothers treated with acrylamide from D7 of gestation till D28 after birth (perinatally intoxicated group). Acrylamide administered either prenatally or perinatally has been shown to induce significant retardation in the newborns' body weights development, increase of thiobarbituric acid-reactive substances (TBARS) and oxidative stress (significant reductions in glutathione reduced [GSH], total thiols, superoxide dismutase [SOD] and peroxidase activities) in the developing cerebellum. Acrylamide treatment delayed the proliferation in the granular layer and delayed both cell migration and differentiation. Purkinje cell loss was also seen in acrylamide-treated animals. Ultrastructural studies of Purkinje cells in the perinatal group showed microvacuolations and cell loss. The results of this study show that prenatal and perinatal acrylamide or its metabolites disrupts the biochemical machinery, cause oxidative stress and induce structural changes in the developing rat cerebellum.     

Somatosensory evoked potentials in workers exposed to toluene and styrene.

Somatosensory evoked potentials (SEPs) were used to evaluate possible subclinical impairment of the nervous system due to occupational exposure to toluene and styrene. A group of 36 rotogravure printers with severe exposure to toluene, 20 workers with severe exposure to styrene in a glass laminate manufacturing plant, and a comparison group of healthy subjects were studied. The severity of exposure was documented by measurements of toluene and styrene concentrations in breathing zone air, by hippuric acid concentration in urine in the group exposed to toluene, and by urinary mandelic acid concentration in the group exposed to styrene. Somatosensory evoked potentials were measured by stimulation of the median nerve at the wrist and the tibial nerve at the ankle. Peripheral conduction velocities (CVs) in both extremities and central conduction time (CCT) after tibial nerve stimulation were significantly decreased in both exposed groups. Significantly prolonged latencies of peripheral and cortical SEPs to median nerve stimulation as well as cortical SEPs to tibial nerve stimulation were found in workers exposed to styrene. Some abnormalities in SEPs at peripheral or spinal and cortical levels were found in eight workers exposed to toluene and six workers exposed to styrene. Of these, in three workers exposed to toluene and two to styrene increased CCT and delayed latencies of cortical responses at normal conduction values in the periphery were found. A trend for increased frequency of abnormal SEPs with duration of exposure to toluene and styrene and alcohol abuse was found. Abnormalities in SEPs in the exposed groups are most probably of multifactorial origin. Central SEP abnormalities in both exposed groups could indicate early signs of subclinical dysfunction at spinal and cortical levels and could be due to toluene or styrene exposure probably potentiated by alcohol consumption in the group exposed to toluene.     

Acrylamide does not cause apparent changes in genetic expression of creatine kinase in rat cerebellum

Acrylamide inhibits creatine kinase (CK) activities in the brain of rats or mice. However, its effects on genetic expression of CK have not yet been studied. CK mRNA and protein level were examined by RT-PCR and Western blotting, respectively. Neither cytosolic CK (B subunit) and mitochondrial CK (ubiquitous form) mRNA nor B subunit protein was clearly changed in the cerebellum from rats intoxicated with acrylamide (50 mg/kg/day i.p. for 8 days) and showing clinical neurotoxic signs.     

Infant rats respond differently to alcohol after nursing from an alcohol-intoxicated dam.

Our previous studies indicate that rat pups are able to detect the low levels of ethanol (175 mg %) found in the milk of a moderately intoxicated dam. The present study tested the effect of infantile interactions (including suckling) with ethanol-treated mothers on later behavioral responsiveness to ethanol's sensory properties. In Experiment 1, pups suckled from dams subjected to a 2.5 g/kg ethanol dose (i.g.) or water-treated females during postnatal days (PDs) 3, 5, 7, 9, 11, and 13. During PD 15, these pups were exposed to procedures to induce a conditioned aversion to the low level of ethanol (175 mg % in water), with lithium chloride as the unconditioned stimulus. Conditioning was more effective for pups with the prior ethanol experience within the nursing context. Greater responsiveness to ethanol in milk also was found for conditioning control pups that had interacted with intoxicated dams than for those that had interacted with water-treated dams. Experiment 2 determined that interaction with an intoxicated dam was sufficient for altered responsiveness to ethanol, in that the additional conditioning procedures of Experiment 1 were not needed for the effect. Generally, a relatively brief history of infantile interaction with ethanol-intoxicated dams increased later responsiveness to ethanol's orosensory properties. The results suggest that moderately intoxicated dams within the nursing context provide information to the progeny that may lead to the establishment of ethanol-related memories.     

Creatine kinase activities in brain and blood:possible neurotoxic indicator of acrylamide intoxication.

OBJECTIVES--To examine whether the activities of creatine kinase (CK) correlate with neurological disturbances caused by acrylamide. METHODS--The activities of CK and other enzymes reported to be inhibited by acrylamide in the brain and plasma, and landing foot spread (LFS) were measured in mice and rats intoxicated with acrylamide. RESULTS--Activity of CK was suppressed by acrylamide in the brain of mice in parallel with the neurological dysfunction measured by LFS. No clear alterations were found in glyceraldehyde-3-phosphate dehydrogenase, neuron-specific enolase, and lactate dehydrogenase activities over the experimental period (eight days for the exposure and 43 days for the recovery). In rats, among the plasma enzymes examined, suppression of CK activity was most notable, but thyroid activity was not affected. CONCLUSIONS--Among the enzymes so far examined, the CK activities in the brain and blood seem to be the most sensitive indicators of acrylamide intoxication.     

大鼠亚慢性丙烯酰胺中毒神经行为功能的改变

目的　观察丙烯酰胺亚慢性染毒对大鼠神经行为功能的影响。方法　选用雄性Wistar大鼠分别以 2 0和 4 0mg/kg剂量腹腔注射 ,每周 3次 ,连续 2个月 ,每周测量大鼠体重、热觉传导、压痛阈值、后肢撑力、转棒等指标。结果　中毒后大鼠体重减轻 ,但与对照组相比无显著性差异 (P >0 0 5 ) ,热觉传导异常 (高剂量组时间延长 5 5 % ,低剂量组缩短 39% ) ,压痛阈值变小 (第 4周高剂量组降低 4 5 % ,第 7周低剂量组降低 4 5 % ) ,后肢展开距离明显加宽 (高剂量组增加 10 9% ,低剂量组增加 5 9% ) ,在转捧上停留的时间缩短 (第 4周高剂量组缩短 98% ,第 6周低剂量组缩短81% ) ,与对照组相比 ,均有显著性差异 (P <0 0 5 )。结论　丙烯酰胺可引起大鼠的热觉传导异常 ,痛觉传导加快 ,运动神经损伤 ,运动协调能力降低。