A4626
1-乙酰基-2-苯肼
≥98%
别名:
N-Acetyl-N′-phenylhydrazine, acetylphenylhydrazine
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关于此项目
线性分子式:
CH3CONHNHC6H5
化学文摘社编号:
分子量:
150.18
NACRES:
NA.25
PubChem Substance ID:
UNSPSC Code:
12352127
EC Number:
204-055-3
MDL number:
Application
用于造血系统研究的 1-乙酰基-2-苯肼 (AcPhHZ) 可与氧合血红蛋白反应形成自由基，可用于诱导溶血性贫血。
Biochem/physiol Actions
乙酰苯肼（1-Acetyl-2-phenylhydrazine，AcPhHZ) 是一种用于实验动物模型的血管肿瘤引发剂。
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 3 Oral
存储类别
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
wgk
WGK 3
ppe
dust mask type N95 (US), Eyeshields, Faceshields, Gloves
Y Fujii et al.
Journal of electron microscopy, 46(6), 477-484 (1997-01-01)
A new 'tissue-stamp culture' method was developed for stamping proliferating erythroblasts of mouse spleens on collagen-coated coverslips after inducing haemolytic anaemia by administration of 1-acetyl-2-phenylhydrazine, and then adherent splenic cells were cultured for a few days. We could obtain many
H Ohno et al.
Fundamental and applied toxicology : official journal of the Society of Toxicology, 20(2), 141-146 (1993-02-01)
DQ-2511, a new anti-ulcer drug, was administered to beagle dogs for 4 weeks to investigate the mechanism whereby this drug induced hemolytic anemia and its reversibility in comparison with beta-acetylphenylhydrazine. Hemolytic anemia accompanied by an increase in the number of
R Olinescu et al.
Research communications in chemical pathology and pharmacology, 84(1), 27-34 (1994-04-01)
Following the administration of phenylhydrazine, cadmium chloride and ethanol to rats there was a marked increase in the concentration of liver lipid peroxides and a sharp decline in GSH levels. The oxidative stress generated by the action of these toxic
T M Fischer
Biochimica et biophysica acta, 985(2), 218-228 (1989-10-16)
Cross bonding and stiffening of the human red cell membrane was studied using treatments with SH, amino, and carboxyl reagents, oxidizing and denaturing treatments and acidification. Membrane cross bonding was initiated when, after red cell treatment, opposite areas of the
P Caprari et al.
Biochemical medicine and metabolic biology, 45(1), 16-27 (1991-02-01)
After in vitro treatment of normal, glucose-6-phosphate dehydrogenase-deficient or pyruvate kinase-deficient human erythrocytes with three different oxidizing agents, the extent of lipid peroxidative degradation and the alterations of membrane proteins were evaluated. Exposure to tert-butylhydroperoxide induced, most markedly in G6PD-
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