苯甲醇
货号:
IB1550
品牌:
Jinpan
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产品简介
有效期 | 2年 |
描述 | 密度:1.045 g/mL |
EC | EINECS 202-859-9 |
MDL | MFCD00004599 |
InChIKey | WVDDGKGOMKODPV-UHFFFAOYSA-N |
InChI | InChI=1S/C7H8O/c8-6-7-4-2-1-3-5-7/h1-5,8H,6H2 |
PubChem CID | 244 |
别名 | 苄醇 |
英文名称 | Benzyl Alcohol |
CAS | 100-51-6 |
分子式 | C7H8O |
分子量 | 108.14 |
储存条件 | 2-8℃ |
纯度 | ≥98% |
外观(性状) | Colourless Liquid |
单位 | 瓶 |
生物活性 | Benzyl alcohol, a bacteriostatic agent found in many parenteral preparations, has been implicated as the agent responsible for precipitating the gasping syndrome in premature neonates. [1] |
In Vivo | Benzyl alcohol was administered intraperitoneally to adult (23-28 g) and neonatal (2-7 g) CD-1 male mice. Gross behavioral changes were monitored. Low doses (400 mglkg) produced minimal toxic effects within an initial 4-h observation period. At the end of this time, the LDso was determined to be lo00 mg/kg for both age groups. When mortality in the adult group was observed after 7 d following a single treatment with benzyl alcohol, the LDso on day 7 was determined to be 650 mg/kg. Rapid absorption and conversion of benzyl alcohol to its primary metabolite, benzaldehyde, occurred within both experimental groups; the plasma levels of each were comparable in both neonatal and mature animals when determined by GC. In an attempt to alter the toxicity of benzyl alcohol, pyrazole and disulfiram were used to inhibit the activities of alcohol dehydrogenase and aldehyde dehydrogenase, respectively. Treatment with pyrazole, before benzyl alcohol exposure, resulted in an increase in benzyl alcohol levels to 203% of control values and a marked increase in toxicity. These data imply that the acute toxicity of benzyl alcohol, which includes sedation, dyspnea, and loss of motor function, is due to the alcohol itself and not to its metabolite, benzaldehyde.[1] |
SMILES | OCC1=CC=CC=C1 |
靶点 | Others |
细胞实验 | Taking into account the lack of mortality among animals receiving 500 mgkg of benzyl alcohol or bezaldehyde, additional groups were injected with the test compounds at doses from 500 to 1500 mgkg and observed. Animals that survived the observation period of 4 h were monitored daily for lethal effects for up to two weeks. Duplicate experimenta were carried out on consecutive days and cumulative data were used in determining the LD,,’s.Additional groups of mice were used for the measurement of the concentrations of benzyl alcohol and benzaldehyde in blood speci- mens. Levels of both substances obtained from adult animals receiving benzyl alcohol (1000 mgkg) or benzaldehyde (1150 mgkg) alone served as controls. Neonatal mice were given similar doses of both substances for comparison. Adult mice were then pretreated with pyrazole (500 mg/kg), a known inhibitor of alcohol dehydrogenase,e 15 min prior to the administration of benzyl alcohol (1000 mg/kg) or benzaldehyde (1150 mg/kg). Although no report of pyrazole inhibi_x005ftion of benzyl alcohol metabolism in the mouse can be found in the literature, it was felt that pyrazole would be a useful probe in evaluating the metabolism of benzyl alcohol in this species. Other adult experimental animals were given disulfiram (125 mg/kg), an inhibitor of aldehyde dehydrogenase,’ 24 h prior to the administration of either benzyl alcohol (1000 mg/kg) or benzaldehyde (1150 mg/ kg). In all cases, plasma levels of both substances were monitored over a 75-min period. Blood specimens were obtained under ether anesthesia via cardiac puncture. Plasma was obtained from whole blood drawn into EDTA-treated tubes. The samples were centrifuged at 3300 x g for 10 min, and the resultant supernatant plasma was used for gas chromatographic analysis. [1] |
数据来源文献 | [1] McCloskey SE, et al. J Pharm Sci. 1986, 75(7):702-705. |
规格 | 500mg 1g |