补肾健脾方对小鼠急性毒性影响试验

目的 观察补肾健脾方灌胃给药的急性毒性反应.方法 以含生药4g/ml浸膏的补肾健脾方药为供试品,依40ml/kg的给药量（最大给药量）灌胃给药;小鼠每天2次灌胃给药,最大给药量为按生药量计320g/kg.观察小鼠异常或不良反应、死亡及主要脏器异常病变.结果 灌胃给药后未见其他异常或不良反应,无小鼠死亡.处死解剖未见主要脏器异常病变.结论 小鼠灌胃给药最大给药量为按生药量计320g/kg,此剂量相当于拟临床人用药的106.7倍,除给药后有短时间的不适外,未见明显的毒性反应.     

兔眼结膜中阿奇霉素的浓度测定及其药动学

目的建立兔眼结膜中阿奇霉素的LC-MS/MS检测方法,研究阿奇霉素滴眼液在兔眼结膜中的药动学特征。方法 184只新西兰白兔进行单次以及多次给阿奇霉素滴眼液后,于不同时间点取眼结膜样本匀浆处理后以沉淀法去除匀浆液中蛋白基质,采用LC-MS/MS法测定兔眼结膜中的阿奇霉素。以克拉霉素为内标,采用Ultimate XB-Phenyl(100 mm×3.0 mm,3μm)色谱柱,流动相为乙腈-0.01 mol.L-1乙酸铵水溶液(含0.1%乙酸)(75∶25,V/V),电喷雾离子源,正离子SRM扫描分析,内标和阿奇霉素离子对分别为:m/z 748→m/z 590和m/z 749→m/z 591。结果阿奇霉素结膜浓度在10.128～8 102.4μg.L-1范围内线性关系良好(r=0.998 7);最低定量限为10.128μg.L-1;批内和批间RSD均小于10%;方法准确度在85%～115%之间。单次给药后参比制剂和受试制剂的药动学参数tmax分别为2 h和2 h,ρmax分别为22.29μg.g-1和21.80μg.g-1,AUC1-192分别为528.0μg.h.g-1和536.5μg.h.g-1,t1/2分别为25.5 h和24.1 h。多次给药后参比制剂和受试制剂的药动学参数tmax分别为8 h和8 h,ρmax分别为53.10μg.g-1和51.62μg.g-1,AUC1-192分别为1 584.9μg.h.g-1和1 379.4μg.h.g-1,t1/2分别为28.8 h和23.7 h。受试制剂和参比制剂药动学行为基本一致。结论建立的检测方法简便、灵敏。多次给药后在兔眼结膜内存在蓄积现象。     

力达霉素抗肝癌作用的实验研究

目的观察力达霉素(LDM)在体外、体内对肝癌的抑制作用。方法用四甲基偶氮唑蓝(MTT)方法测定力达霉素和丝裂霉素C对人肝癌BEL-7402细胞及小鼠肝癌22细胞的增生抑制作用。以小鼠移植性肝癌22模型观察不同剂量力达霉素的治疗效果。结果力达霉素和丝裂霉素对人肝癌BEL-7402细胞的半数抑制浓度(IC50)分别为(0.0030±0.0006)nmol/L和(150±27)nmol/L。力达霉素对小鼠肝癌22细胞的IC50为0.025nmol/L。体内试验:力达霉素静脉给药1次及延迟静脉给药3次对小鼠移植性肝癌22细胞的生长均有显著抑制作用。当通过静脉给予1次力达霉素剂量为0.025、0.05和0.1mg/kg时对肝癌22细胞抑瘤率分别为62%、72%和85%。结论力达霉素在体外对肝癌细胞增生有强烈的抑制作用,动物试验有显著疗效     

应用蒙特卡罗模拟评价和优化大肠埃希菌感染时的抗菌药物给药方案

目的根据药动/药效(PK/PD)理论应用蒙特卡罗模拟评价和优化大肠埃希菌(Escherichia coli,E.coli)感染者的给药方案。方法调查笔者所在医院E.coli感染时的应用抗菌药物的情况,将出现频率较高的静脉滴注头孢曲松、阿米卡星、哌拉西林他唑巴坦和美罗培南各给药方案进行蒙特卡罗模拟,以获最佳治疗方案。结果对目标MIC大肠埃希菌的CFR均达标的方案有:头孢曲松3种给药方案2.0 g、1次/d,3.0 g、1次/d和2.0 g、1次/12 h;阿米卡星3种给药方案5.0 mg/kg、10.0 mg/kg、18.0 mg/kg(成人每日总量不超过1.5 g);哌拉西林他唑巴坦2种给药方案4.5 g、1次/8 h,4.5 g、1次/6 h;美罗培南4种给药方案0.5 g、1次/6 h,1.0 g、1次/8 h,0.5 g、1次/6 h,2.0 g、1次/6 h。结论对时间依赖性抗菌药物采用增加给药频次或对浓度依赖型抗菌药物采用增加给药剂量是对耐药菌的优选用药方案。     

高效液相色谱法测定小诺霉素的血药浓度

用CLC-ODS.C18柱作高效液相色谱测定小诺霉素血药浓度并做兔静注后的药代动力学研究。这一方法检测限0.2ng,最小检测血药浓度达0.1μg/ml,线性范围1～20μg/ml。小诺霉素和内标氯氮平的保留时间分别为6.8min和8.3min。方法准确、灵敏、快速,适用于小诺霉素药代动力学研究和血药浓度监测。3只新西兰兔单次静注小诺霉素10mg后,药时曲线经计算机自动拟合,符合二室开放模型。主要药动学参数为t1/2α=0.536±0.01h,t1/2β=2.59±0.98h,Vc=0.204±0.051L/kg,CL=0.18±0.026L/kg。     

白蛋白融合干扰素α-2b猕猴长期毒性试验

用人血清白蛋白(HSA)对干扰素进行修饰,制成的新型白蛋白-干扰素融合蛋白(Albumin-Interferon fusion protein,A-IFN,Woferon),不仅保留了干扰素的生物学功能,而且使用时更加安全。为了确定Woferon的安全性,开展了猕猴皮下给药长期毒性试验,观察动物重复给药后的一般生活状态及心电图、血液学、血液生化和尿液等指标的变化。结果猕猴皮下注射高剂量(800μg/kg)白蛋白融合干扰素α-2b会引起可逆性白细胞(WBC)、血小板(PLT)下降和天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)的升高;猕猴对200μg/kg剂量有较好的耐受性;50μg/kg为无毒性反应剂量。TK研究表明:50μg/kg剂量,Cmax为(434.8±38.0)ng/ml,临床拟用剂量下血浆药物浓度为8ng/ml,安全倍数超过50倍。     

力达霉素烯二炔发色团对肝癌的实验治疗

目的研究力达霉素发色团对肝癌的实验治疗。方法采用体内接种肿瘤法研究力达霉素发色团对小鼠肝癌22或裸鼠人肝癌Bel-7402的抗肿瘤作用。结果力达霉素发色团在肿瘤接种24h后1次静脉给药能明显抑制小鼠肝癌22的生长，当剂量达4．6、9．2、18．3μg／kg时，抑制率分别为59％、81％、85％。力达霉素发色团在接种肿瘤后72h给药的抑瘤效果不如接种后24h的效果强。力达霉素发色团（LDC）和力达霉素（LDM）均能抑制裸鼠肝癌Bel-7402肿瘤的生长。接种后d27。具有相同克分子数的LDC（18．5μg／kg）和LDM（250μg／kg）的抑瘤率分别为51．1％和45．9％，抑瘤效果相当。LDC对肿瘤生长的抑制作用存在剂量．效应关系。结论力达霉素发色团在动物体内能抑制小鼠肝癌和人裸鼠肝癌的生长，是力达霉素产生生物学作用的主要活性部分。     

重组集成干扰素α在不同动物长期毒性实验血清中中和抗体的产生及活性研究

目的研究重组集成干扰素α在金黄地鼠和猕猴长期毒性实验血清中中和抗体的产生及抗体活性的强弱。方法将金黄地鼠与猕猴分别分为10、30、100μg/kg与1、10、100μg/kg3个剂量组,均每日皮下注射重组集成干扰素α1次,各连续用药60、30d,取给药期和恢复期不同时间的血清,采用细胞病变抑制法进行检测。结果金黄地鼠的30、100μg/kg剂量组与猕猴的3个剂量组从给药第3wk起,在血清中检测到具有中和活性的抗体,抗体滴度在给药第4wk或恢复期第1wk达最高峰,并持续到恢复期结束。其中,猕猴10、100μg/kg剂量组的中和活性高于同期1μg/kg剂量组,10、100μg/kg剂量组之间则无显著性差异(P>0.05),1μg/kg剂量组在恢复期结束时已检测不到中和活性。结论金黄地鼠和猕猴重复注射重组集成干扰素α,血清中均能检测到中和抗体(低剂量组除外),抗体滴度和持续时间与注射剂量呈正相关。     

Exendin-4对自发性Ⅱ型糖尿病KKAy小鼠的治疗作用

研究Exendin-4对自发性Ⅱ型糖尿病KKAY小鼠的治疗作用.以胰岛素为阳性对照,给自发性Ⅱ型糖尿病KKAy小鼠皮下注射Exendin-4(0.2,0.6,1.8μg/kg),每天给药1次,连续给药4周,分别于首次给药后0,1,2,3,4 h及1,2,3,4周取血,测定小鼠空腹血糖浓度;末次给药后1 h取血,测定空腹血清胰岛素、甘油三酯、总胆固醇浓度.给自发性Ⅱ型糖尿病KKAy小鼠皮下注射1.0 IU/kg剂量胰岛素,在给药后1,2,3 h及1,2,3,4周,其空腹血糖浓度与空白对照组比,均显著降低.自发性Ⅱ型糖尿病KKAy小鼠给Exendin-4后1,2,3 h及1,2,3,4周,空腹血糖浓度显著降低(P<0.05 VS对照);连续给药4周后,其血清胰岛素浓度显著增加,0.6 μg/kg组和1.8 big/kg组血清甘油三酯浓度下降(P<0.05 VS对照).Exendin-4对自发性Ⅱ型糖尿病KKAy小鼠有治疗作用.     

高山红景天提取物的药理研究

红景天提取物皮下注射100mg/kg,一次给药或连续三天给药均有抗游泳疲劳作用,100mg/kg一次给药具有抗抓棒疲劳作用,100—200mg/kg 均无增强或拮抗戊巴比妥钠催眠作用,90mg/kg 无抗常压缺氧作用,45—200mg/kg一次或多次给药均无抗低压缺氧作用,10mg/kg 无抗肾上腺素高血糖作用。红景天浸膏灌胃给药1.25—10.0g/kg 一次给药,或5g/kg 连续六天给药均无抗抓棒疲劳作用。红景天提取物给小鼠灌胃给药 LD_(50)为45.01±7.37g/kg,给小鼠腹腔注射 LD_(50)为2.68±0.67g/kg。     

A conscious rat model involving bradycardia and hypotension after oral administration: a toxicokinetical study of aconitine

1.?A model of aconitine-induced bradycardia and hypotension, which is similar to aconitine poisoning in humans, was constructed in conscious rats by oral administration.

2.?Blood pressure (BP) and heart rate (HR) of Sprague-Dawley rats were measured using a volume pressure recording (VPR) system. The pharmacokinetics of toxic doses of aconitine and its metabolites were analyzed using UPLC-MS/MS.

3.?The HR was significantly decreased by 29% at 2?h after oral administration of 200?μg/kg aconitine. When the dose was increased to 400?μg/kg, systolic BP and diastolic BP were significantly decreased by 11% and 12% at 2?h after the administration, except when bradycardia occurred at 2?h and 4?h. The drug concentration-time curve showed a double-peak phenomenon in rats administered a 400?μg/kg dose. The AUC_0–12?h value in the 400?μg/kg group significantly increased 0.8-fold compared to the 200?μg/kg group. Moreover, a high plasma concentration of 16-O-demethyaconitine was found in the rats that received two toxic doses.

4.?In conclusion, bradycardia and hypotension are induced in conscious rats by a toxic dose of aconitine (400?μg/kg), and there was no significant difference in dose-normalized AUC_0–12?h values between oral administrations of 200?μg/kg and that of 400?μg/kg. However, the dose-normalized C_max and AUC_0–12?h values in 200?μg/kg and 400?μg/kg groups were significantly smaller than those in 100?μg/kg group. The metabolites of aconitine, 16-O-demethyaconitine, and benzoylaconitine may also contribute to the hypotensive response.     

EFFECTS OF SUBACUTE OPIOID ADMINISTRATION DURING LATE PREGNANCY IN THE RAT ON THE INITIATION, DURATION AND OUTCOME OF PARTURITION AND MATERNAL LEVELS OF OXYTOCIN AND ARGININE VASOPRESSIN

1. The effects, on parturition in the rat, of subacute and acute opioid administration were studied. Further experiments investigated the role of modulation of maternal plasma and pituitary oxytocin (OXY) and arginine vasopressin (AVP) levels in these effects. 2. Subacute opioid (M320, buprenorphine or bremazocine) administration prolonged the gestation of rats. This was accompanied by toxic effects on the offspring. Acute subcutaneous (s.c.) M320 (10 micrograms/kg) administration was accompanied by prolonged gestation without toxic effects. 3. Subacute M320 (10 micrograms/kg, s.c., twice daily) treatment was accompanied by increased interbirth intervals in parturient rats. 4. Maternal OXY but not AVP release, as assessed by measurement of plasma and pituitary immunoreactivity, was elevated during and up to 1 h after the completion of parturition. Subacute M320 treatment did not inhibit this elevated OXY release.     

Safety assessment of N-acetyl-l-threonine

N-acetyl-l-threonine (NAT) is a dietary constituent that has been identified at low concentrations (<1 μg/g fresh weight) in numerous foods. The current paper reports the outcome of toxicology studies conducted to assess the effects of NAT. No evidence of mutagenicity or genotoxicity was observed in in vitro bacterial or in vivo mammalian studies. No mortalities or evidence of adverse effects were observed in Sprague–Dawley (SD) rats following acute oral administration of 2000 mg of NAT/kg of body weight (kg of bw). A 28-day repeated dose toxicity study was conducted in SD rats by incorporating NAT into diets at concentrations targeting up to 1000 mg of NAT/kg of bw/day. All rats survived until scheduled sacrifice and no biologically significant differences were observed in any of the NAT treatment groups for body weights, feed consumption, clinical signs, behavioral, ophthalmology, hematology, coagulation, clinical chemistry, organ weights, or gross or microscopic changes. Based on these results, NAT does not represent a risk for mutagenicity or genotoxicity, is not acutely toxic, and the no-observed-adverse-effect-level (NOAEL) for systemic toxicity from repeated dose dietary exposure to NAT is 848.5 and 913.6 mg/kg of bw/day for male and female SD rats, respectively.     

Nitric oxide signalling is involved in diarylheptanoid‐induced increases in femoral arterial blood flow in ovariectomized rats

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The No-Observed-Adverse-Effect Level (NOAEL) of Baby Aloe Powder (BAP) for Nutraceutical Application Based Upon Toxicological Evaluation

Aloe has been used in versatile herbal medications and nutraceuticals throughout history. Aloe is widely considered to be generally safe for humans and used globally. The effectiveness and pharmacological properties of aloe are dependent upon when the plant is collected. However, little is known about the toxicology of whole-body aloe collected within less than 1 yr. Based upon widespread exposure to aloe, it is important to determine a daily intake level of this chemical to ensure its safety for humans. To determine the no-observed-adverse-effect level (NOAEL) of baby aloe powder (BAP) for clinical application, Sprague-Dawley (SD) rats were treated orally for 4 wk with 4 different concentrations: 0, 0.125, 0.5, and 2 g/kg body weight (bw). In this study, no significant or dose-dependent toxicological effects of BAP were observed in biochemical or hematological parameters, urinalysis, clinical signs, body weight, and food and water consumption. There were changes in some biomarkers in certain treated groups compared to controls; however, all values were within their reference ranges and not dose-dependent. Based on these results, the NOAEL of BAP was estimated to be greater than 2 g/kg bw in male and 2 g/kg bw in female SD rats. Collectively, these data suggest that BAP used in this study did not produce any marked subacute toxic effects up to a maximum concentration of 2 g/kg bw, and thus use in nutraceuticals and in pharmaceutical and cosmetic applications at a concentration of >2 g/kg is warranted.     

Reproductive toxicity of cabergoline in mice, rats, and rabbits

Cabergoline, a new dopaminergic ergot derivative with potent long-lasting prolactin (PRL)-lowering properties, was assessed using standard reproductive studies in the mouse, rat, and rabbit with oral administration. Because of the compound's pharmacologic activity, several aspects remain incompletely explored in the rat, in which prolactin is the luteotrophic hormone. A fertility study in female rats was possible only at very low doses (0.5, 1, and 2 μg/kg/d) because higher doses completely inhibited implantation. In male rats no adverse effects were seen on male reproductive performance or on the offspring at doses up to 320 μg/kg/d given for 10 weeks prior to mating with untreated females. In a developmental toxicity study in rats treated from day 6 to day 15 of gestation at doses (6.25, 12.5, and 25 μg/kg/d) not exceeding the active dose for inhibition of egg nidation (ED₅₀ = 25 μg/kg), a high incidence of total litter loss occurred as a reflection of inhibition of egg nidation at the highest dose, but embryofetal development was not impaired in litters reaching term. An exploratory study at 30 or 1000 μg/kg/d with treatment from day 5 of gestation or later demonstrated that cabergoline did not affect the maintenance of pregnancy at 30 μg/kg/d given from day 7 or later, or at 1000 μg/kg/d given from day 9. Doses of 500, 2000, and 8000 μg/kg/d (treatment from day 6 to day 15 of gestation) did not inhibit egg nidation in mice and showed no adverse effects on intrauterine development Doses ranging from 5 to 8000 μg/kg/d administered from day 6 to day 18 of gestation in the rabbit were associated with maternal effects, including a reduction in body weight gain and food and water intake starting from 500 μg/kg/d and increased reactivity at the highest doses (4000 and 8000 μg/kg/d). Effects on intrauterine development were restricted to a reduction in mean fetal and placental weights at 4000 and 8000 μg/kg/d. In peri- and postnatal studies in rats (treatment from day 15 or 17 of gestation to weaning) cabergoline did not affect fetal development and parturition up to 100 μg/kg/d, but strongly inhibited milk secretion starting from 10 μg/kg/d, thus leaving unexplored the postnatal phase at higher doses. When neonatal rats (born from untreated dams) were treated directly with cabergoline at 10, 30, and 90 μg/kg/d from day 7 to 13 after birth, treatment was well tolerated up to the highest dose tested (90 μg/kg/d). It was concluded that cabergoline did not impair fertility in the male rat, was not teratogenic in mice and rabbits, did not affect the latter phase of gestation or parturition in the rat, and was not toxic when administered directly to neonatal rats.     

Toxicity evaluation of hydroalcoholic extract of Ferula gummosa root

Traditionally, people use harvested Ferula gummosa for medicinal purposes. However, no information about its safety and toxicity is available. In the present study, the toxicological profile of sub-chronic oral administration of hydroalcoholic extract of F. gummosa radix is evaluated in rats. The extract was orally administrated at 100 and 600 mg/kg to male rats for 28 days. After 28 days, clinical signs, mortality, body weights, food and water consumption, organ weights, hematology, serum biochemistry, as well as histopathological and neurobehavioral changes were examined. Also, the sedative effect of this extract was evaluated in mice at the doses of 100, 600, and 800 mg/kg. Its cytotoxicity against human stroma-vascular cells and human renal epithelial cells were also evaluated. No lethality or adverse toxic signs were seen during the experimental period. There were no significant changes in body and organ weights, hematology, serum biochemistry, and histopathological examination. The extract decreased the rotarod performance, but did not increase pentobarbital-induced hypnosis. Also, F. gummosa extract significantly decreased cell viability at the concentrations of higher than 400 μg/mL. In conclusion, the sub-chronic toxicity study of F. gummosa hydroalcoholic extract demonstrated the extract to be safe for the tested dosage and route of administration.     

Comparative study of toxicity of 4-nitrophenol and 2,4-dinitrophenol in newborn and young rats

The toxicities of 4-nitrophenol and 2,4-dinitrophenol in newborn and young rats was examined and the susceptibility of newborn rats was analyzed in terms of presumed unequivocally toxic and no observed adverse effect levels (NOAELs). In the 18-day repeated dose newborn rat study, 4-nitrophenol was orally given from Day 4 to Day 21 after birth but did not induce any toxicity up to 160 mg/kg in the main study, although it induced death in one of six males at 160 mg/kg, and three of six males and one of six females at 230 mg/kg in a prior dose-finding study. In the 28-day repeated dose oral toxicity study starting at 6 weeks of age, 4-nitrophenol caused the death of most males and females at 1,000 mg/kg but was not toxic at 400 mg/kg except for male rat-specific renal toxicity. As unequivocally toxic levels were considered to be 230 mg/kg/day in newborn rats and 600 to 800 mg/kg/day in young rats, and NOAELs were 110 mg/kg/day in newborn rats and 400 mg/kg/day in young rats, the susceptibility of the newborn to 4-nitrophenol appears to be 2.5 to 4 times higher than that of young animals. In the newborn rat study of 2,4-dinitrophenol, animals died at 30 mg/kg in the dose-finding study and significant lowering of body and organ weights was observed at 20 mg/kg in the main study. In the 28-day young rat study, clear toxic signs followed by death occurred at 80 mg/kg but there was no definitive toxicity at 20 mg/kg. As unequivocally toxic levels and NOAELs were considered to be 30 and 10 mg/kg/day in newborn rats and 80 and 20 mg/kg/day in young rats, respectively, the toxicity of 2,4-dinitrophenol in newborns again seems to be 2 to 3 times stronger than in young rats. Abnormalities of external development and reflex ontogeny in the newborn were not observed with either chemical. Based on these results, it can be concluded that the toxic response in newborn rats is at most 4 times higher than that in young rats, at least in the cases of 4-nitrophenol and 2,4-dinitrophenol.     

Testicular toxicity of dietarily or parenterally administered bisphenol A in rats and mice.

Male Crj:Wistar rats, HsdHot:Holtzman SD rats, Crj:CD-1(ICR) mice and C57BL/6CrSlc mice were administered bisphenol A (BPA) in the diet at a level of 0 (control) and 0.25% for 8 weeks. Daily BPA intake was about 200 and 400 mg/kg for rats and mice, respectively. No conspicuous signs of general or reproductive toxicity were observed after administration in any strain of these animals. Serum testosterone concentrations were not decreased in BPA-fed rats and mice. Successive subcutaneous administration of BPA at a dose of 200 mg/kg/day for 4 weeks significantly decreased the testis, epididymis, prostate and seminal vesicle weights, and the testicular daily sperm production in Jcl:Wistar rats. Successive intraperitoneal administration of BPA at a dose of 20 mg/kg/day for 4 weeks decreased the prostate and seminal vesicle weights but not the testis or epididymis weights. An intraperitoneal dose of 2 mg BPA/kg/day did not cause any toxicity. These results indicate that dietarily administered BPA is less toxic to most strains of rats and mice, and the maximum non-toxic dose and/or minimum toxic dose may be about 200 mg/kg/day. Subcutaneous or intraperitoneal BPA is much more toxic on male reproductive and sex accessory organs than dietary.     

天麻细粉片毒性及安全性的实验研究

目的观察天麻细粉片在实验动物中的毒性和安全性。方法急性毒性试验采用昆明种小鼠和SD大鼠各20只,雌雄各半,天麻细粉片剂量为15．0异,kg体重,观察14d,记录中毒表现。Ames试验采用了菌株TA97、TA98、TA100和TA102,在加S9与不加S9的条件下加入天麻细粉片,剂量分别为8、40、200、1000、5000μg／皿。小鼠骨髓细胞微核试验和精子畸变试验均采用昆明种小鼠,天麻细粉片剂量为1．25、2．50、5．00g／kg体重,用环磷酰胺40mg/kg体重为阳性对照。30d喂养试验采用SD大鼠,雌、雄各40只,天麻细粉片剂量为2．81、5．62、11．25g/kg体重,连续给予30d,观察动物一般状况和体重,测定血液学及血液生化学指标、脏器系数。并进行组织病理学检查。结果急性毒性试验结果显示天麻细粉片在小鼠和大鼠中的最大耐受剂量（MTD）均〉15．0g／kg体重,属无毒级。天麻细粉片的Ames试验、小鼠骨髓细胞微核试验和精子畸变试验结果均为阴性。30d喂养试验显示动物一般状况良好,各剂量天麻细粉片对动物的体重、进食量、食物利用率以及脏器重量和脏器系数均无明显影响．对动物的血常规和血清生化指标也无明显影响。病理检查显示高剂量天麻细粉片对动物的肝、肾、胃肠、脾、卵巢（睾丸）等组织无明显毒性。结论本实验条件下天麻细粉片未见明显毒性或致畸和致突变作用。