Effects of whole-body microwave exposure on the plasma corticosterone, glucose, uric acid and allantoin levels in rats

To investigate the effects of whole-body microwave exposure on plasma corticosterone, glucose, uric acid and allantoin levels, rats weighing 245-300 g (light group) and 440-510 g (heavy group) were exposed to microwaves with a frequency of 2,450 MHz at the power density of 10 mW/cm2 under an ambient temperature of 21 to 23 degrees C for one hour. Rectal temperatures were increased by 3.4 degrees C in the light group and 1.4 degrees C in the heavy group after microwave exposure. Plasma levels of corticosterone, glucose and uric acid did not change in both groups after microwave exposure. Plasma levels of allantoin increased significantly only in the heavy group after microwave exposure. These results suggest that the plasma levels of allantoin, a metabolite of uric acid, may be useful as a biological variable for assessment of the effects of whole-body microwave exposure in rats. The increase of plasma allantoin level after microwave exposure could not be explained only by the degree of increased rectal temperature caused by hyperthermic effects of microwaves.     

Effects of whole-body vibration exposure on DOPAC and VIP-like immunoreactivity in the rat brain]

In order to clarify the involvement of cerebral 3,4-dihydroxyphenylacetic acid (DOPAC) and vasoactive intestinal polypeptide (VIP) in whole-body vibration stress, DOPAC and VIP-like immunoreactivity (VIP-LI) in various discrete brain regions of rats exposed to whole-body vibration (4G, 20 Hz, 90 min) were assayed. The results showed that the whole-body vibration increased the DOPAC level in the frontal cortex and nucleus accumbens, but did not induce a concurrent change of VIP-LI in these regions. VIP-LI was significantly increased in the amygdala, and decreased in the hippocampus, accompanied by no significant change of DOPAC. These results show that whole-body vibration affects cerebral VIP neuron systems in addition to its nonspecific action, i.e. the activation of mesofrontal and mesoaccumbens dopamine neuron systems. It is assumed that the amygdalofugal VIP neuronal system is involved in the regulation of hypothalamic and pituitary hormone secretions, and that VIP in the hippocampus plays a part in modulating the blood circulation in the cortex in whole-body vibration stress.     

适量运动和甲状腺激素对大鼠血液氧化应激反应的影响

目的 观察适量运动和甲状腺激素对大鼠血液H2O2含量和抗氧化能力的影响.方法 将64只Wistar大鼠随机分为8组:对照组(C)、轻度甲亢组(T1)、重度甲亢组(T2)、甲减组(J)、运动组(E)、轻度甲亢运动组(ET1)、重度甲亢运动组(ET2)、甲减运动组(EJ).C组生理盐水灌胃,T1和T2组分别给予左旋甲状腺素片100和200 μg/d灌胃,J组给予甲巯咪唑10 mg/d灌胃,运动为负重(6％体重)游泳训练30 min/d.喂养14d后,检测全血中的H2O2含量、谷胱甘肽过氧化酶(GPx)活力、红细胞超氧化物歧化酶(SOD)活力以及血浆丙二醛(MDA)含量.结果 与对照组比较,甲亢组H2O2含量、GPx活力、SOD活力和MDA含量均升高,差异有统计学意义(P＜0.05);甲减组H2O2含量、GPx活力、SOD活力和MDA含量均降低,差异有统计学意义(P＜0.05);与相应非运动组比较,运动组H2O2含量和GPx活力增高,SOD活力和MDA含量降低,差异有统计学意义(P＜0.05).结论 运动和甲亢均可诱发全血H2O2含量和抗氧化酶GPx活力增高,而且甲亢会诱发氧化损伤,但适量运动可减轻氧化损伤.大鼠血液对运动氧应激反应代偿作用强于甲亢时.     

适量运动和甲状腺激素对大鼠心脏氧化应激反应的影响

目的 观察适量运动和甲状腺激素对大鼠心脏H2O2含量和抗氧化能力的影响.方法 将64只Wistar大鼠随机分为8组:对照组(C)、轻度甲亢非运动组(T1)、重度甲亢非运动组(T2)、甲减非运动组(J)、运动组(E)、轻度甲亢运动组(ET1)、重度甲亢运动组(ET2)、甲减运动组(EJ).C组生理盐水灌胃,T1和T2组分别给予左旋甲状腺素片100和200 μg/d灌胃,J组给予甲巯咪唑10 mg/d灌胃,运动为负重6％体重游泳训练30 min/d.喂养14d后,检测心脏组织匀浆中的H2O2含量、谷胱甘肽过氧化酶(GPx)活力、超氧化物歧化酶(SOD)活力以及丙二醛(MDA)含量.结果 甲亢组和甲亢运动组与相应对照组比较,H2O2有升高趋势而GPx有降低趋势(P＞0.05),MDA含量增高,差异有统计学意义(P＜0.05).甲减非运动组和甲减运动组与相应对照组比较,GPx和SOD活力均升高,差异有统计学意义(P＜0.05).与相应对照组比较,甲减非运动组MDA含量降低,而甲减运动组MDA含量升高,差异有统计学意义(P＜0.05).甲状腺激素水平异常的运动组与对应非运动组比较,心肌组织的H2O2含量、GPx活力和MDA含量均升高,但SOD活力降低,差异有统计学意义(P＜0.05).结论 甲亢非运动、甲亢运动和甲减运动均会诱发失代偿性氧化损伤,适量运动不会诱发氧化损伤.     

硒碘对大鼠谷胱甘肽过氧化物酶活力及甲状腺激素代谢的影响──Ⅱ．硒碘营养状态对大鼠甲状腺激素代谢的影响

用四种硒水平饲料和两种碘含量饮水饲养大鼠观察了其甲状腺激素（ＴＨ）代谢。硒组间肝脏、肾脏Ⅰ型脱碘酶（ＩＤⅠ）活力、血清Ｔａ含量差异显著；两碘组间甲状腺重量、甲状腺过氧化物酶（ＴＰＯ）活力。甲状腺碘含量、肾脏ＩＤⅠ及大脑Ⅱ型脱碘酶（ＩＤⅡ）活力差异明显；Ⅰ－（不加碘）组中甲状腺ＩＤⅠ活力与血清三碘甲腺原氨酸（Ｔａ）含量呈显著正相关。提示硒缺乏通过ＩＤⅠ影响ＴＨ代谢继而影响大脑ＩＤⅡ活力并可加重碘缺乏的效应；低碘时甲状腺ＩＤⅠ在维持循环Ｔａ含量中起重要作用；碘缺乏有可能增加硒缺乏的效应；硒、碘对ＴＨ代谢的影响可能在一定程度上取决于自身和对方的营养状态。     

Effects of pre- and postnatal polychlorinated biphenyl exposure on metabolic rate and thyroid hormones of white-footed mice

Energy budgets have proven to be a valuable tool for predicting life history from physiological data in terrestrial vertebrates, yet these concepts have not been applied to the physiological effects of contaminants. Contaminants might affect energy budgets by imposing an additional metabolic cost or by reducing the overall amount of energy taken in; either process will reduce the energy available for production (i.e., growth or reproduction). This study examined whole animal energetic effects of polychlorinated biphenyl (PCB) exposure in white-footed mice (Peromyscus leucopus). Exposure to PCBs is known to reduce concentrations of plasma thyroid hormones, and thyroid hormones exert strong control over the rate of energy metabolism in mammals. Peromyscus leucopus that were proven breeders were fed PCBs in their food at 0, 10, and 25 ppm. Through lactation, offspring were exposed to PCB from conception and were maintained on the maternal diet to adulthood. No effects were seen on energy metabolism (O2 consumption, measured in adulthood) or on growth, but there were large dose-dependent decreases in thyroid hormone concentrations, particularly T4. The apparent disparity in our data between unchanged metabolic rates and 50% reductions in T4 concentrations can be rationalized by noting that free T3 (the fraction not bound to plasma protein) in treated mice was not significantly different from controls and that metabolism is most strongly influenced by free T3. Overall, this study did not demonstrate any energetic consequences of PCB exposure in P. leucopus at dietary concentrations up to 25 ppm.     

The regulation of the thyroid-stimulating hormone of the anterior pituitary gland by thyroid hormone and by 9-cis-retinoic acid

Thyroid-stimulating hormone, TSH, of the anterior pituitary gland is regulated by the binding of the thyroid hormone-activated thyroid receptor to the TSH gene at the same time as the binding of the 9-cis-retinoic acid-activated retinoid X receptor to the same gene. Both interactions, separately or simultaneously, can suppress and thus regulate the expression of the TSH gene.     

The effect of particle size of whole-grain flour on plasma glucose, insulin, glucagon and thyroid-stimulating hormone in humans

OBJECTIVE: Although it is well known that consumption of whole-grain foods with higher fiber content results in beneficial health effects, most Americans usually prefer bread made with white flour. Changes in bread texture and undesirable intestinal responses have been reported as reasons for avoiding consumption of whole-grain foods or high-fiber menus. The purpose of this study was to determine whether consumption of bread made with ultra-fine-ground whole-grain wheat flour retained beneficial effects while reducing undesirable effects. METHODS: Twenty-six men and women, 31 to 55 years of age, consumed glucose solutions or bread made with traditional white, conventional whole-grain wheat (WWF), or ultra-fine whole-grain wheat (UFWF) flour (1 g carbohydrate/kg body weight) in a Latin square design after two days of controlled diet. The effect on glycemic response was determined by comparing blood variables, after a tolerance test with white bread, WWF bread, and UFWF bread, with those after a glucose tolerance test. RESULTS: Men and women had similar responses to all tolerances except postprandial TSH. Glucose and insulin levels one half hour after the glucose load were significantly higher than after any of the bread tolerances. Glucose, but not insulin, areas under the curve were significantly higher after the glucose load than areas after the three breads. Consumption of UFWF resulted in glucose and insulin responses, as well as areas under the curve, similar to those after consumption of conventional whole-wheat bread. CONCLUSION: The particle size of whole grain wheat flour did not substantially affect glycemic responses.     

围生期接触磺胺二甲嘧啶对子代大鼠甲状腺功能的影响

目的研究围生期母体接触磺胺二甲嘧啶对子代大鼠甲状腺功能的影响。方法受孕母鼠在受孕第7日起至哺乳期结束每天分别给予磺胺二甲嘧啶0、50、100和200mg/kg,HE染色观察20日龄子代大鼠甲状腺的组织病理学变化,并用免疫组织化学染色观察甲状腺内核增殖抗原的表达。结果各染毒剂量组子代大鼠甲状腺滤泡细胞出现不同程度的增生表现,核增殖抗原表达阳性细胞数显著高于对照组(P0.05)。结论磺胺二甲嘧啶可通过母体干扰子代大鼠甲状腺功能。     

微波全身照射对带肿瘤和非带肿瘤大鼠免疫反应的影响

雌性Fisher344大鼠照射2450MHz微波（10、20和40mW/cm^2;SAR=3.4、6.8和13.6MwW/g）两周，每周天，每天3小时，还植入乳腺腺癌R－3230AC动物，照射后脾脏有核细胞密度和血清IgG含量与照射功率密度呈负的剂量－－效应关系；外 因非PHA刺激的淋巴细胞转化与功率密度呈正的剂量－－效应关系。非带肿瘤动物无上述剂量－－效应关系出现，说明带肿瘤动物的免疫系统对微波照射反应的敏感性高于非带肿瘤动物，前者的细胞和体液免疫反应均出现变化，意义有待查明。     

黑木耳多糖对高功率微波辐射大鼠卵巢和子宫形态结构的影响

目的:探讨黑木耳多糖对高功率微波辐射大鼠卵巢和子宫形态结构的影响。方法:Wistar大鼠30只,随机分为正常对照组、辐射模型组和治疗组,每组10只。辐射模型组和治疗组给予表面功率200 mW/cm2,10 min的微波辐射。正常对照组和辐射模型组蒸馏水1.5 ml灌胃,治疗组1%木耳多糖1.5 ml灌胃,连续10天。第11天取卵巢和子宫,制备组织学标本,光学显微镜观察。结果:治疗组与辐射模型组相比,卵巢皮质增厚,卵泡数量增多,各级卵泡形态结构基本正常,黄体形态规则;子宫内膜增厚,上皮细胞排列较紧密,固有层内子宫腺增多,腺腔扩大,组织细胞结构基本正常。结论:木耳多糖在高功率微波辐射时,对卵巢和子宫具有保护修复作用。     

Effects of short-term exposure to whole-body vibration on wakefulness level

To investigate the relationships between whole-body vibration and changes in wakefulness, We measured the change of a subjective wakefulness level and electroencephalogram (EEG). Subjects are ten healthy male university students. The subjects were exposed to whole-body vibration with frequency (10 Hz) and acceleration level (0.6 ms(-2) r.m.s.) for 12 min in the seated position. Subjective wakefulness level was evaluated using the questionnaire of VASS (Visual Analog Sleepiness Scale) and KSS (The Kwansei Gakuin Sleepiness Scale). For the electroencephalogram (EEG) measurement, AAT (Alpha Attenuation Test) which repeats three times each opened and closed eye for 1 min was conducted. Wakefulness levels were defined as the ratio of mean alpha-wave power during eyes closed versus eyes opened. VASS and KSS increased and subjective level of wakefulness decreased from pre- to post exposure in all subjects, regardless of vibration exposure. The objective wakefulness levels of AAT were reduced at the post-exposure test in all subjects. In the case with exposure to whole-body vibration was a significant difference from the case without exposure to whole-body vibration. It is suggested that a short-term exposure to whole-body vibration may cause a reduction of wakefulness level.     

Dibutyl-phthalate exposure from mesalamine medications and serum thyroid hormones in men

Background

Dibutyl phthalate (DBP) is an endocrine disruptor and used in some medication coatings, such as mesalamine for treatment inflammatory bowel disease (IBD).

Prenatal exposure to polybrominated diphenyl ether flame retardants and neonatal thyroid-stimulating hormone levels in the CHAMACOS study

Studies published in the last 3 decades have demonstrated global human exposure to polybrominated diphenyl ether (PBDE) flame retardants. A growing body of literature suggests that PBDEs may disrupt thyroid hormone homeostasis. Although thyroid hormones play an essential role in brain development, few studies have investigated relations between prenatal exposure to PBDEs and neonatal thyroid hormone levels, and none have measured thyroid-stimulating hormone (TSH) levels in neonates. The authors measured 10 PBDE congeners in serum collected between October 1999 and October 2000 from 289 pregnant women living in California's Salinas Valley and abstracted TSH levels from their children's medical records. Individual PBDE congeners showed null or weak nonsignificant inverse relations with neonatal TSH. Total serum PBDE was not associated with neonatal TSH (β = 0.00, 95% confidence interval: -0.06, 0.06). Except for brominated diphenyl ether 153, a higher serum PBDE level was related to elevated odds of high TSH (≥80th percentile), but associations were not statistically significant. Associations were not modified by infant sex, age at TSH measurement, maternal serum polychlorinated biphenyl concentration, or mode of delivery. Results were robust to sensitivity analysis. The authors found no conclusive evidence that prenatal exposure to PBDEs at levels similar to those of the general US population is related to neonatal TSH.     

Associations between prenatal exposure to polychlorinated biphenyls and neonatal thyroid-stimulating hormone levels in a Mexican-American population, Salinas Valley, California

BACKGROUND: Studies have reported that prenatal exposure to polychlorinated biphenyls (PCBs) may alter neurodevelopment in both humans and animals. Furthermore, prenatal exposure to some PCB congeners and commercial mixtures has been shown to decrease free and total thyroxine (T(4)) blood levels in animals. Because thyroid hormones (TH) are essential for normal neurologic development, it has been suggested that the deleterious neurodevelopmental effect of PCBs may occur through TH disruption. PCBs may in turn affect TH levels by inducing the microsomal enzyme uridinediphosphate glucuronosyltransferase (UDP-GT), which is involved in TH elimination. OBJECTIVES: Our goals were to group PCB congeners based on their potential to induce microsomal enzymes in animals, and to examine the relationship between neonatal TSH levels and prenatal exposure to PCB congeners grouped according to their structure and potential mechanisms of action. METHODS: We measured the concentration of 34 PCB congeners in serum samples collected from 285 pregnant women and the thyroid-stimulating hormone (TSH) levels in their children's blood collected shortly after birth. RESULTS: We found no association between the sum of PCB congeners, the toxic equivalents, or structure-based groupings (mono- or di-ortho substituted congeners), and TSH blood concentration. However, we found a positive association between the sum of congeners suspected to be UDP-GT inducers (more specifically cytochrome P450 2B inducers) in animals and neonatal TSH levels. In individual congener analyses, PCBs 99, 138, 153, 180, 183, 187, 194, and 199 were positively associated with neonatal TSH levels after adjustment for covariates. PCBs 194 and 199 remained significant after adjustment for multiple hypothesis testing. CONCLUSIONS: Our results support grouping PCB congeners based on their potential mechanism of action of enzyme induction when investigating associations with TH. Findings also suggest that PCBs affect TH homeostasis even at the low background level of exposure found in the CHAMA-COS (Center for the Health Assessment of Mothers and Children of Salinas) population.