甲醛和苯联合染毒对小鼠肝脏DPC的影响

甲醛、苯、氨等是室内主要的空气污染物,这些有机化合物具有挥发性,这些污染物中污染最为普遍以是甲醛、苯。由于甲醛和苯的挥发性,两者常常在多种污染源共存,是我国室内空气污染的主要物质,这两种物质由于挥发性大污染扩散很快,而且具有很大的生物毒性,对基因具有致突变性,这两种污染物对健康的危害越来越受到科研人员的关注。     

甲醛对DNA损伤的彗星实验研究

甲醛是一种遗传毒性物质。国内外学者的大量研究证实,甲醛可以引起DNA-DNA、DNA-蛋白质分子交联,但对于甲醛是否能够引起DNA分子的断裂,学界却存在分歧。本实验以颊黏膜细胞作为实验材料,通过彗星实验对甲醛的遗传毒性——尤其是DNA分子断裂作用进行了系统的研究。结果显示甲醛在较低浓度(5μmol／L,7,5μmol／L,10μmol／L)时具有断裂作用,在较高浓度(15μmol／L,30μmol／L,50μmol／L)时则具有交联作用。根据本实验的结果,本文还首次论证了甲醛断裂作用的断裂峰值(7．5μmol／L)。     

甲醛对DNA损伤的彗星实验研究

甲醛是一种遗传毒性物质。国内外学者的大量研究证实,甲醛可以引起DNA-DNA、DNA-蛋白质分子交联,但对于甲醛是否能够引起DNA 分子的断裂,学界却存在分歧。本实验以颊黏膜细胞作为实验材料,通过彗星实验对甲醛的遗传毒性——尤其是DNA 分子断裂作用进行了系统的研究。结果显示甲醛在较低浓度(5μmol/L,7.5μmol/L,10μmol/L)时具有断裂作用,在较高浓度(15μmol/L,30μmol/L,50μmol/L)时则具有交联作用。根据本实验的结果,本文还首次论证了甲醛断裂作用的断裂峰值(7.5μmol/L)。     

4种常用水产药物对青虾幼虾的毒性研究

采用静水法研究了4种常用水产药物对青虾幼虾的毒性。结果表明：水温29℃~30℃时,溴氯海因对青虾幼虾24 h、48 h和72 h的LC50分别为19.05 mg/L、11.75 mg/L、11.75 mg/L,安全浓度为1.24 mg/L;聚维酮碘对青虾幼虾的24 h、48 h和72 h的LC50分别为49.27 mg/L、44.61 mg/L、43.68 mg/L,安全浓度为10.52 mg/L;甲醛对青虾幼虾的24 h、48 h和72 h的LC50分别为72.47 mg/L、66.41 mg/L、53.71 mg/L,安全浓度为10.93 mg/L;高锰酸钾对青虾幼虾的24 h、48 h和72 h的半致死浓度（LC50）分别为6.06 mg/L、4.07 mg/L、3.79 mg/L,安全浓度为0.48 mg/L。4种药物对青虾幼虾的毒性依次为高锰酸钾〉溴氯海因〉聚维酮碘〉甲醛。     

利用酶清除室内甲醛气体的新方法

甲醛脱氢酶是一种可以将甲醛进行转换的氧化还原酶,利用改质甲醛脱氢酶对于甲醛的专一反应性可达到去除甲醛气体的效果.根据密闭空间测试甲醛去除效率,在10min 内可去除空间中85% 的甲醛气体.经过现场测试后发现,将甲醛去除器置放在含有福尔马林的储藏室中可在一周内降低70% 的甲醛浓度,两周后可将甲醛浓度降至安全标准以下.结果显示甲醛去除器不仅能够去除实验室中密闭空间内的甲醛气体,在一般布满甲醛气体的空间中依然可以在短时间内去除空间中的甲醛气体,避免人体受到甲醛的危害.     

氧化应激对溶酶体储存与转运甲醛的影响

内源甲醛代谢失调被认为是导致阿尔茨海默病的危险因素之一,甲醛蓄积会引起神经细胞的死亡和认知功能的降低.研究表明,细胞内甲醛分布于溶酶体内,而溶酶体功能异常与神经退行性疾病密切相关.本文采用甲醛特异荧光探针,在氧化应激条件下,检测到小鼠脑微血管内皮细胞株bEnd.3和小鼠神经瘤母细胞株N2a溶酶体内甲醛明显升高;在慢性脑低灌注大鼠动物模型中,其脑神经细胞的溶酶体内甲醛也升高(P0.01);LeuLeuOMe处理bEnd.3细胞,使其溶酶体膜通透性增加,导致细胞内甲醛蓄积,而胞外甲醛降低.以上结果证明,溶酶体具有储存和转运甲醛的功能,如果溶酶体出现结构与功能的异常,会导致甲醛代谢失调,造成认知损害.     

常见“食品非法添加物”的科学解读

甲醛是什么？ 甲醛是一种具有高反应活性的小分子有机物。在常温下,甲醛可以以很高的浓度挥发到空气中,具有强烈的刺激性气味。甲醛易溶于水、醇和醚。通常,市场销售的甲醛多以水溶液形式出现。甲醛是一种用途广泛、生产工艺简单、原料供应充足的大众化工原料,世界年产量在2500万吨左右。     

室内观赏植物对甲醛的吸收及抗逆效果研究

该研究采用密封舱法模拟室内甲醛污染环境(熏蒸箱内甲醛浓度设置为0.1~0.5 mg·m~(-3),熏气时间12 h),对6种常见室内观赏植物进行甲醛熏蒸实验,测定了植物对甲醛的吸收效率、叶面伤害指数及过氧化物酶(POD)等指标。结果表明:这6种常见观赏植物对甲醛均具较好的净化效果,甲醛熏蒸浓度为0.1~0.3 mg·m~(-3),白鹤芋对甲醛的净化效果最好;熏蒸浓度0.5 mg·m~(-3),绿萝和吊兰具有较好的净化和抗逆性能;铁线蕨对甲醛的耐受力较弱,适合作为室内甲醛污染的指示性植物。几种受试植物的POD酶与甲醛吸收率呈显著正相关关系(P0.05),表明植物POD活力变化是受甲醛胁迫后的主要抗逆应答机制之一。     

专家教你如何防治甲醛污染

北京市质监局日前通过官网公布了北京生产的木制家具质量抽检结果,32种不合格家具中12种含有超标甲醛,且多为摆放在卧室床边的床头柜。由此,人们为甲醛污染牵动的神经再度紧绷。据专家介绍,甲醛是许多建材及家具中不可缺少的成分,其实只要产品甲醛含量不超标就无须恐慌。关键是消费者要避免一些认识和消费中的误区,科学合理地预防甲醛超标造成的危害。容易忽视的甲醛污染源人们往往误以为甲醛只来自于大型家具、大面积铺设的地板等家居物品。其实,家居中有很多我们注意不到的地方,也在悄悄地散发出甲醛。而且由于消费者在选购中往往忽视对某些家居产品甲醛含     

微生物对甲醛的净化效应与作用机制

甲醛是一种无色、强刺激性、危害人体嗅觉及免疫功能的有毒气体。目前工业的快速发展和室内装修的盛兴使得甲醛成为工业废气和室内空气污染的重要来源之一,也是当前威胁人类健康的主要杀手之一。开发高效净化甲醛的新技术是解决空气污染的重要途径。生物因能动态、持续地吸收利用甲醛,使得生物净化成为一种新兴、高效、绿色的甲醛污染防治技术。甲基营养菌等微生物可特异地吸收、同化甲醛等一碳化合物,逐渐成为生物净化甲醛的新宠。本文在分析甲醛的危害及其净化技术现状的基础上,从种群多样性、作用机理和应用等方面综述了微生物净化甲醛的研究进展。     

Dose–Response Effects of Diphenylhydantoin on Pregnant Dams and Embryo‐Fetal Development in Rats

Despite the widespread use of diphenylhydantoin (DPH), there is a lack of reliable information on the teratogenic effects, correlation with maternal and developmental toxicity, and dose–response relationship of DPH. This study investigated the dose–response effects of DPH on pregnant dams and embryo‐fetal development as well as the relationship between maternal and developmental toxicity. DPHwas orally administered to pregnant rats from gestational days 6 through 15 at 0, 50, 150, and 300 mg/kg/day. At 300 mg/kg, maternal toxicity including increased clinical signs, suppressed body weight, decreased food intake, and increased weights of adrenal glands, liver, kidneys, and brain were observed in dams. Developmental toxicity, including a decrease in fetal and placental weights, increased incidence of morphological alterations, and a delay in fetal ossification delay also occurred. At 150 mg/kg, maternal toxicity manifested as an increased incidence of clinical signs, reduced body weight gain and food intake, and increased weights of adrenal glands and brain. Only minimal developmental toxicity, including decreased placental weight and an increased incidence of visceral and skeletal variations, was observed. No treatment‐related maternal or developmental effects were observed at 50 mg/kg. These results show that DPH is minimally embryotoxic at a minimal maternotoxic dose (150 mg/kg/day) but is embryotoxic and teratogenic at an overt maternotoxic dose (300 mg/kg/day). Under these experimental conditions, the no‐observed‐adverse‐effect level of DPH for pregnant dams and embryo‐fetal development is considered to be 50 mg/kg/day. These data indicate that DPH is not a selective developmental toxicant in the rat.     

三株光合细菌的毒性试验研究

以昆明小白鼠为实验动物,对类球红细菌Z1、沼泽红假单胞菌Z2及光合细菌分离株C2采用急性毒性试验、骨髓细胞微核试验和精子畸形试验进行安全性评定。结果表明,急性毒性试验:实验组小白鼠的一般状况、器官含水量、器官系数及血常规检查,与对照组差异均无显著性(P>0.05);骨髓细胞微核试验和精子畸形试验实验组与阴性对照组(生理盐水)差异均无显著性(P>0.05),与阳性对照组(环磷酰胺40 mg/kg)比较,骨髓细胞微核试验差异有极显著性(P<0.01),精子畸形率试验差异有显著性(P<0.05)。以上结果说明,三株光合细菌均不具有毒性。     

Embryo‐Fetal Developmental Toxicity Studies with Pregabalin in Mice and Rabbits

Pregabalin was evaluated for potential developmental toxicity in mice and rabbits. Pregabalin was administered once daily by oral gavage to female albino mice (500, 1250, or 2500 mg/kg) and New Zealand White rabbits (250, 500, or 1250 mg/kg) during organogenesis (gestation day 6 through 15 [mice] or 6 through 20 [rabbits]). Fetuses were evaluated for viability, growth, and morphological development. Pregabalin administration to mice did not induce maternal or developmental toxicity at doses up to 2500 mg/kg, which was associated with a maternal plasma exposure (AUC_0–24) of 3790 μg?hr/ml, ≥30 times the expected human exposure at the maximum recommended daily dose (MRD; 600 mg/day). In rabbits, treatment‐related clinical signs occurred at all doses (AUC_0–24 of 1397, 2023, and 4803 μg?hr/ml at 250, 500, and 1250 mg/kg, respectively). Maternal toxicity was evident at all doses and included ataxia, hypoactivity, and cool to touch. In addition, abortion and females euthanized moribund with total resorption occurred at 1250 mg/kg. There were no treatment‐related malformations at any dose. At 1250 mg/kg, compared with study and historical controls, the percentage of fetuses with retarded ossification was significantly increased and the mean number of ossification sites was decreased, which correlated with decreased fetal and placental weights, consistent with in utero growth retardation. Therefore, the no‐effect dose for developmental toxicity in rabbits was 500 mg/kg, which produced systemic exposure approximately 16‐times human exposure at the MRD. These findings indicate that pregabalin, at the highest dose tested, was not teratogenic in mice or rabbits     

Effects of Melamine and Cyanuric Acid on Embryo‐Fetal Development in Rats

After the outbreak of acute renal failure associated with melamine‐contaminated pet food, melamine and melamine‐related compounds have become of great interest from a toxicologic perspective. We investigated the potential effects of melamine in combination with cyanuric acid (M + CA, 1:1) on pregnant dams and embryo‐fetal development in rats. M + CA was orally administered to pregnant rats from gestational days 6 through 19 at doses of 0, 3, 10, and 30 mg/kg/day of both melamine and cyanuric acid. Maternal toxicity of rats administered 30 mg/kg/day M + CA was manifested as increased incidences of clinical signs and death; gross pathologic findings; higher blood urea nitrogen and creatinine levels; lower body weight gain and food intake; decreased thymus weight; and increased heart, lung, and kidney weights. Histopathological examinations revealed an increase in the incidence of congestion, tubular necrosis/degeneration, crystals, casts, mineralization, inflammatory cells in tubules, tubular dilation, and atrophy of glomeruli in maternal kidneys, whereas fetal kidneys did not show any histopathological changes. Developmental toxicity included a decrease in fetal (28%) and placental weights and a delay in fetal ossification (n = 7). Increased incidence of gross and histopathological changes in the maternal kidney was also found in the middle dose group (n = 12). No treatment‐related maternal or developmental effects were observed in the low dose group (n = 12). Under these experimental conditions, M + CA is embryotoxic at an overt maternotoxic dose in rats and the no‐observed‐adverse‐effect level of M + CA is considered to be 3 mg/kg/day for pregnant dams and 10 mg/kg/day for embryo‐fetal development.     

Exposure of pregnant mice to chromium picolinate results in skeletal defects in their offspring

BACKGROUND: Chromium(III) picolinate, [Cr(pic)(3)], is a widely marketed dietary supplement. However, Cr(pic)(3) has been associated with oxidative damage to DNA in rats and mutations and DNA fragmentation in cell cultures. In isolated case reports, Cr(pic)(3) supplementation has been said to cause adverse effects, such as anemia, renal failure, liver dysfunction, and neuronal impairment. To date, no studies have been published regarding the safety of chromium picolinate supplementation to a developing fetus, although Cr(pic)(3) has been recommended for pregnant women who are diagnosed with gestational diabetes. METHODS: From gestation days (GD) 6-17, pregnant CD-1 mice were fed diets containing either 200 mg/kg Cr(pic)(3), 200 mg/kg CrCl(3), 174 mg/kg picolinic acid, or the diet only to determine if Cr(pic)(3), CrCl(3), or picolinic acid could cause developmental toxicity. Dams were sacrificed on GD 17, and their litters were examined for adverse effects. RESULTS: The incidence of bifurcated cervical arches was significantly increased in fetuses from the Cr(pic)(3) group as compared to the diet-only group. Fetuses in the picolinic acid-treated group had an incidence double that of the control group; however, this increase was not statistically significant. Fetuses in the CrCl(3) group did not differ from the controls in any variable examined. No maternal toxicity was observed in any of the treatment groups. CONCLUSIONS: High maternal oral exposures to chromium picolinate can cause morphological defects in developing offspring of mice.     

Effects of tert-butyl acetate on maternal toxicity and embryo-fetal development in Sprague-Dawley rats

This study investigated the potential adverse effects of tert-butyl acetate (TBAc) on maternal toxicity and embryo-fetal development after maternal exposure of pregnant rats from gestational days 6 through 19. TBAc was administered to pregnant rats by gavage at 0, 400, 800, and 1,600 mg/kg/day. All dams were subjected to a Caesarean section on day 20 of gestation, and their fetuses were examined for any morphological abnormalities. At 1,600 mg/kg, maternal toxicity manifested as increases in the incidence of clinical signs and death, lower body weight gain and food intake, increases in the weights of adrenal glands and liver, and a decrease in thymus weight. Developmental toxicity included a decrease in fetal weight, an increase in the incidence of skeletal variation, and a delay in fetal ossification. At 800 mg/kg, only a minimal developmental toxicity, including an increase in the incidence of skeletal variation and a delay in fetal ossification, were observed. In contrast, no adverse maternal or developmental effects were observed at 400 mg/kg. These results show that a 14-day repeated oral dose of TBAc is embryotoxic at a maternally toxic dose (i.e., 1,600 mg/kg/day) and is minimally embryotoxic at a nonmaternally toxic dose (i.e., 800 mg/kg/day) in rats. However, no evidence for the teratogenicity of TBAc was noted in rats. It is concluded that the developmental findings observed in the present study are secondary effects to maternal toxicity. Under these experimental conditions, the no-observed-adverse-effect level of TBAc is considered to be 800 mg/kg/day for dams and 400 mg/kg/day for embryo-fetal development.     

The role of maternal toxicity in lovastatin-induced developmental toxicity

The role of maternal toxicity in lovastatin-induced developmental toxicity in rats was examined in a series of studies. The first study administered lovastatin at 100, 200, 400, or 800 mg/kg/day (mkd) orally to mated rats from Gestation Day (GD) 6 through 20. Maternal toxicity was observed as transient dose-related body weight losses at the initiation of dosing; there were also deaths and/or morbidity at 400 and 800 mkd. These toxicities occurred in conjunction with forestomach lesions. Mean fetal weights were decreased in all groups (-5 to -16%), and the incidence of skeletal malformations, variations, and incomplete ossifications was increased. The 2 highest doses produced the most severe maternal and developmental effects. Using the same dosages, the second study avoided gestational maternal weight losses and morbidity by starting treatment 14 days before mating with dosing continued to GD 20. There were transient dose-related body weight losses after the start of dosing and deaths in the 400- and 800-mkd groups; however, there was no evidence of maternal toxicity during gestation. Developmental toxicity was evident only as slight, but generally significant (p< or =0.05) decreases in mean fetal weights in groups given > or =200 mkd (-2 to -5%). Significantly, no skeletal abnormalities were observed. A third study administered the pharmacologically active metabolite of lovastatin subcutaneously at dose levels that matched oral maternal drug exposures. In the high-dose group, maternal weight gain and mean fetal weight were slightly decreased but there were no treatment-related skeletal abnormalities. Finally, a series of toxicokinetic studies assessed whether the 2 different developmental toxicity profiles were due to differences in drug exposure between the developmentally toxic and non-toxic dosing regimes. The data showed that groups with no skeletal abnormalities had maternal and embryonic/fetal drug concentrations similar to or even greater than the groups with fetal abnormalities. These results indicate that fetal skeletal abnormalities observed at lovastatin dose levels > or =100 mkd are not due to a direct teratogenic effect, but are the result of excessive maternal toxicity, which most likely involves a nutritional deficiency associated with forestomach lesions and reduced maternal food intake.     

Developmental Toxicity Studies with Pregabalin in Rats: Significance of Alterations in Skull Bone Morphology

Pregabalin was administered to pregnant Wistar rats during organogenesis to evaluate potential developmental toxicity. In an embryo‐fetal development study, compared with controls, fetuses from pregabalin‐treated rats exhibited increased incidence of jugal fused to maxilla (pregabalin 1250 and 2500 mg/kg) and fusion of the nasal sutures (pregabalin 2500 mg/kg). The alterations in skull development occurred in the presence of maternal toxicity (reduced body weight gain) and developmental toxicity (reduced fetal body weight and increased skeletal variations), and were initially classified as malformations. Subsequent investigative studies in pregnant rats treated with pregabalin during organogenesis confirmed the advanced jugal fused to maxilla, and fusion of the nasal sutures at cesarean section (gestation day/postmating day [PMD] 21) in pregabalin‐treated groups. In a study designed to evaluate progression of skull development, advanced jugal fused to maxilla and fusion of the nasal sutures was observed on PMD 20–25 and PMD 21–23, respectively (birth occurs approximately on PMD 22). On postnatal day (PND) 21, complete jugal fused to maxilla was observed in the majority of control and 2500 mg/kg offspring. No treatment‐related differences in the incidence of skull bone fusions occurred on PND 21, indicating no permanent adverse outcome. Based on the results of the investigative studies, and a review of historical data and scientific literature, the advanced skull bone fusions were reclassified as anatomic variations. Pregabalin was not teratogenic in rats under the conditions of these studies     

Metabolomic evaluation of di-n-butyl phthalate-induced teratogenesis in mice

Di-n-butyl phthalate (DBP) has been linked to the neural, reproductive and developmental toxicity. We present here a metabolomic study that characterized the metabolic variations associated with the DBP-induced teratogenesis in maternal and fetal mice. DBP at 50 and 300?mg/kg were administrated to pregnant C57 mice, via gastric intubation on gestation day 7?C9, respectively. Maternal mice were euthanized on gestation day 16 and examined for fetal development and malformations. Metabolomic study of maternal serum, placenta and fetal brain tissues was performed using gas chromatography time-of-flight mass spectrometry combined with multivariate data analysis (MVDA). The results showed that a 50?mg/kg dose of DBP had no significant effect on fetal development and a 300?mg/kg dose caused embryo resorption and fetal malformations (primarily eye abnormalities and encephalocele). MVDA indicated that DBP at two doses gave rise to disruption of maternal and fetal metabolic profiles characterized by significantly altered tricarboxylic acid cycle, amino acid, purine and lipid metabolism.