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联苯胺
NMR and HPLC COA下载 MSDS下载 - Names：
Benzidine
- CAS号：
92-87-5
MDL Number： MFCD00039765 - MF(分子式)： C12H12N2 MW(分子量)： 184.24
- EINECS:202-199-1 Reaxys Number:
- Pubchem ID: Brand:BIOFOUNT
联苯胺(Benzidine,92-87-5)是一种灰红色,淡黄色或白色的粉末,结晶性芳族胺,暴露于空气和光线时会变暗.联苯胺已广泛用于血液检测和染料生产中的试剂。
| 货品编码 | 规格 | 纯度 | 价格 (¥) | 现价(¥) | 特价(¥) | 库存描述 | 数量 | 总计 (¥) |
|---|---|---|---|---|---|---|---|---|
| SS6078-25g | 25g | 95% | ¥ 4567.00 | ¥ 4567.00 | 980 | Instock | ¥ 0.00 | |
| SS6078-5g | 5g | 95% | ¥ 2080.00 | ¥ 2080.00 | 288 | Instock | ¥ 0.00 | |
| SS6078-1g | 1g | 95% | ¥ 650.00 | ¥ 650.00 | 116 | Instock | ¥ 0.00 |
| 中文别名 | 联苯胺(CAS:92-87-5);4,4'-二氨基联苯;对二氨基联苯;P,P'-聯苯胺4,4'-联苯二胺;4,4'-二氨基联苯;4,4'-联苯二胺;对二氨基联苯 |
| 英文别名 | Benzidine(CAS:92-87-5);BENZIDINE; 4,4'-Diaminobiphenyl; P-Diaminodiphenyl; [1,1'-Biphenyl]-4,4'-Diamine; 4,4'-Bianiline; 4-(4-Aminophenyl)Aniline; 4,4'-Biphenyldiamine; |
| CAS号 | 92-87-5 |
| Inchi | InChI=1S/C12H12N2/c13-11-5-1-9(2-6-11)10-3-7-12(14)8-4-10/h1-8H,13-14H2 |
| InchiKey | HFACYLZERDEVSX-UHFFFAOYSA-N |
| 分子式 Molecular Weight | C12H12N2 |
| 分子量 Formula | 184.24 |
| 溶解度Solubility | Soluble in water (0.32 mg/ml at 25 °C), DMSO, methanol, alcohol, and ether. |
| 性状 | Solid |
| 储藏条件 Storage conditions | 密封保存。 |
联苯胺(Benzidine,92-87-5)毒理性质：
|
动物 |
测试类型 |
途径 |
实验摄入量 (标准摄入量) |
影响 |
文献来源 |
|
dog |
LDLo |
oral |
200mg/kg (200mg/kg) |
|
Archiv fuer Experimentelle Pathologie und Pharmakologie. Vol. 58, Pg. 167, 1907. |
|
mouse |
LD50 |
intraperitoneal |
110mg/kg (110mg/kg) |
|
Progress in Mutation Research. Vol. 1, Pg. 682, 1981. |
|
mouse |
LD50 |
oral |
214mg/kg (214mg/kg) |
|
National Technical Information Service. Vol. PB214-270, |
|
rabbit |
LDLo |
oral |
200mg/kg (200mg/kg) |
|
Archiv fuer Experimentelle Pathologie und Pharmakologie. Vol. 58, Pg. 167, 1907. |
|
rat |
LD50 |
oral |
309mg/kg (309mg/kg) |
|
National Technical Information Service. Vol. PB214-270, |
联苯胺(Benzidine,92-87-5)物理性质：
| Physical Property | Value | Units | Temp (deg C) | Source |
|---|---|---|---|---|
| Melting Point | 120 | deg C | EXP | |
| Boiling Point | 401 | deg C | EXP | |
| pKa Dissociation Constant | 4.66 | (none) | 20 | EXP |
| log P (octanol-water) | 1.34 | (none) | EXP | |
| Water Solubility | 322 | mg/L | 25 | EXP |
| Vapor Pressure | 8.98E-07 | mm Hg | 25 | EST |
| Henry's Law Constant | 5.17E-11 | atm-m3/mole | 25 | EST |
| Atmospheric OH Rate Constant | 1.54E-10 | cm3/molecule-sec | 25 | EST |
联苯胺染液的配置：
将125mg联苯胺溶于50ml95%的甲醇中;将150mg玫瑰红B溶于50ml蒸馏水中。将上述两液混合,然后取1ml混合液,再加2滴H2O2(以0.3%为宜),即为联苯胺染液。
???????联苯胺(CAS:92-87-5;英文名:Benzidine;)实验注意事项：
1.使用92-87-5实验前需戴好防护眼镜，穿戴防护服和口罩，佩戴手套，避免与皮肤接触。
2.使用92-87-5实验过程中如遇到有毒或者刺激性物质及有害物质产生，必要时实验操作需要手套箱内完成以免对实验人员造成伤害。
3.取样品92-87-5的移液枪头需及时更换，必要时为避免交叉污染尽可能选择滤芯吸头。
4.称量药品时选用称量纸，并无风处取药和称量以免扬撒，试剂的容器使用前务必确保干净，并消毒。
5.取药品92-87-5时尽量采用多个药勺分别使用，使用后清洗干净。
6.实验后产生的废弃物需分类存储，并交于专业生物废气物处理公司处理，以免造成环境污染。
大规格定制：定制产品请将信息发送至sales@bio-fount.com。
Experimental considerations:
1. Wear protective glasses, protective clothing and masks, gloves, and avoid contact with the skin during the experiment.
2. The waste generated after the experiment needs to be stored separately, and handed over to a professional biological waste gas treatment company to avoid environmental pollution.
Tag:联苯胺蒸汽压,联苯胺合成,联苯胺标准,联苯胺应用,联苯胺合成,联苯胺沸点,联苯胺闪点,联苯胺用途,联苯胺溶解度,联苯胺价格,联苯胺作用,联苯胺结构式,联苯胺用处
| 产品说明 | 联苯胺(92-87-5)不溶于冷水,溶于热水,联苯胺易溶于乙醇,乙醚.联苯胺露置空气中或光线影响下颜色变深,联苯胺溶解度,联苯胺结构式详见主页. |
| Introduction | Benzidine is a manufactured chemical that does not occur naturally. It is a crystalline solid that may be grayish-yellow, white, or reddish-gray. |
| Application1 | 联苯胺用于硫酸盐、钨酸盐、磷酸盐和糖分的测定 |
| Application2 | 比色法测定各种氧化剂(CN-, NO2-, ClO3-, SO42-)，氧化性金属、过氧化物酶、氰化物和血液的检定 |
| Application3 |
联苯胺1g溶于5ml沸乙醇、50ml乙醚、107ml沸水、2500ml冷水，其蒸气易被皮肤吸收，中等毒，半数致死量(大鼠，经口)309mg/kg，有致癌可能性，
| 警示图 | |
| 危险性 | warning |
| 危险性警示 | Not Available |
| 安全声明 | H302,H350,H410 |
| 安全防护 | P201,P273,P308+P313,P501 |
| 备注 | 避免吸入，误食以及与皮肤接触 |
| Arlt M, Scheffler A, Suske I, Eschner M, Saragi TP, Salbeck J, Fuhrmann-Lieker T: Bipolar redox behaviour, field-effect mobility and transistor switching of the low-molecular azo glass AZOPD. Phys Che |
| Lardo MM, Diaz NB, Artaza JR, Carbia CD, Nazer R, Valdez R: [Vitamin E as protective agent against hemolysis in leprosy patients under dapsone treatment]. Medicina (B Aires). 1997;57(2):150-4. |
| Risk of Lung Cancer in Workers Exposed to Benzidine and/or Beta-Naphthylamine: A Systematic Review and Meta-Analysis PMID 26947956; Journal of epidemiology 2016 Sep; 26(9):447-58 (Review Article) Name |
| Increased risk of lung cancer associated with occupational exposure to benzidine and/or beta-naphthylamine PMID 25151432; International archives of occupational and environmental health 2015 May; 88(4 |
| Thin-layer chromatography combined with surface-enhanced Raman scattering for rapid detection of benzidine and 4-aminobiphenyl in migration from food contact materials based on gold nanoparticle doped |
1.Molecular Interactions of Carcinogenic Aromatic Amines, 4-Aminobiphenyl and 4,4'-Diaminobiphenyl, with Lactoperoxidase - Insight to Breast Cancer/PMID 29061807; Anticancer research 2017 11; 37(11):6245-6249/Name matches: lactoperoxidase 4,4'-diaminobiphenyl
Abstract:
Background/aim: Lactoperoxidase (LPO) is an antimicrobial protein present in milk, saliva, gastric secretions, tears and upper respiratory tract secretions. LPO constitutes an important enzyme of the human immune defense system. However, LPO has also been suggested to be involved in breast cancer etiology through production of reactive free radicals and activation of carcinogenic aromatic compounds. Aromatic compounds are generally highly lipophilic and thus accumulate in highly fatty breast tissues. The aromatic compounds 4-aminobiphenyl (ABP) and 4,4'-diaminobiphenyl (BZ) are known to have carcinogenic properties. LPO catalyzes their oxidation and converts them into reactive products which bind to DNA and form adducts. These DNA adducts subsequently lead to breast cancer.
Materials and methods: The crystal structure of LPO was obtained from Protein Data Bank. Structures of ABP and BZ were retrieved from PubChem database. Induced Fit Docking was performed using glide module from Schrodinger.
Results: The present study reports the structural binding of ABP and BZ with LPO using in silico approaches. The amino acid residues of LPO involved in the binding with the two aromatic ligands were characterized and binding energy values were calculated.
Conclusion: Both ABP and BZ were placed in the substrate binding site present in the distal heme cavity of LPO with good affinity. The binding mode mimicked that of the natural substrate since these compounds did not disturb the water molecule that plays an important role in the oxidation reaction. Thus, the water molecule is potentially available for facilitating the subsequent activation of the aromatic amines to reactive species which may form DNA adducts leading to breast cancer.
2.Benzidine: mechanisms of oxidative activation and mutagenesis/PMID 3091404; Federation proceedings 1986 Sep; 45(10):2465-70 (Review Article)/Name matches: peroxidase benzidine
Abstract:Benzidine oxidative activation may proceed by peroxidase-catalyzed one-electron oxidation via free radical intermediates, or by N-acetylation followed by monooxygenase-catalyzed N-hydroxylation. The peroxidase route has been examined by using horseradish peroxidase or prostaglandin H synthase in vitro. In the presence of nucleophiles such as phenols, thiols, or nucleic acids, isolable adducts are formed. The structures of these adducts have been elucidated by spectroscopic methods. The Ames test provides a useful system for studying benzidine bioactivation to mutagenic intermediates. An endogenous bacterial acetylase plays an important auxiliary role in the hepatic S9-dependent activation of benzidine. Bacterial peroxidases may also support benzidine oxidation in the Ames test.
3.Induction of erythroid differentiadon in K562 cells by different butyrate regimens/PMID 12426157; Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA 2001; 21(12):890-893/Name matches: beta-globin benzidine
Abstract:OBJECTIVE: To investigate the hemoglobinization induced by butyrate and observe the effects of different butyrate regimens on erythroid differentiation of K562 cells. METHODS: K562 cells, used as an in vitro model system, were stained with benzidine to assess hemoglobin (Hb) production in response to different treatment regimens of butyrate at varied concentrations. Comparison of the percentage of benzidine-positive cells (BZ%)in untreated and butyrate-treated K562 cells was performed. Protein absorption at 414 nm using a spectrophotometer and cellulose acetate gel electrophoresis were employed to determine the changes of Hb production in K562 cells. RESULT: The BZ% increased by 4 to 6 fold and Hb production by 9 to 14 fold 3 d after the cells were incubated with butyrate which selectively promoted fetal hemoglobin(HbF) production in K562 cells. The BZ% increased gradually and reached the peak of l9% to 28% on day 3 or 4 in cells receiving pulse treatment with butyrate for only once, followed by a subsequent rapid fall and on day 7 to 9, it decreased to the level of untreated K562 cells. The length of time for incubation with butyrate was not related to in the increment or the maintenance of the increased level of BZ%. Continuous treatment with butyrate yielded a similar result to that of a single administration of pulse treatment. In contrast, in cells with intermittent pulse treatment the BZ% reached a peak after 72 h and was maintained between 20% and 30% till 3 cycles of treatment was completed. CONCLUSION: Butyrate can induce the expression of globin genes and augment Hb producfion especially that of HbF. A sustained erythroid differentiation of K562 cells can be achieved by intermittent pulse treatment with butyrate which can be an ideal regimen for children with beta globin diseases.
Abstract:
Background/aim: Lactoperoxidase (LPO) is an antimicrobial protein present in milk, saliva, gastric secretions, tears and upper respiratory tract secretions. LPO constitutes an important enzyme of the human immune defense system. However, LPO has also been suggested to be involved in breast cancer etiology through production of reactive free radicals and activation of carcinogenic aromatic compounds. Aromatic compounds are generally highly lipophilic and thus accumulate in highly fatty breast tissues. The aromatic compounds 4-aminobiphenyl (ABP) and 4,4'-diaminobiphenyl (BZ) are known to have carcinogenic properties. LPO catalyzes their oxidation and converts them into reactive products which bind to DNA and form adducts. These DNA adducts subsequently lead to breast cancer.
Materials and methods: The crystal structure of LPO was obtained from Protein Data Bank. Structures of ABP and BZ were retrieved from PubChem database. Induced Fit Docking was performed using glide module from Schrodinger.
Results: The present study reports the structural binding of ABP and BZ with LPO using in silico approaches. The amino acid residues of LPO involved in the binding with the two aromatic ligands were characterized and binding energy values were calculated.
Conclusion: Both ABP and BZ were placed in the substrate binding site present in the distal heme cavity of LPO with good affinity. The binding mode mimicked that of the natural substrate since these compounds did not disturb the water molecule that plays an important role in the oxidation reaction. Thus, the water molecule is potentially available for facilitating the subsequent activation of the aromatic amines to reactive species which may form DNA adducts leading to breast cancer.
2.Benzidine: mechanisms of oxidative activation and mutagenesis/PMID 3091404; Federation proceedings 1986 Sep; 45(10):2465-70 (Review Article)/Name matches: peroxidase benzidine
Abstract:Benzidine oxidative activation may proceed by peroxidase-catalyzed one-electron oxidation via free radical intermediates, or by N-acetylation followed by monooxygenase-catalyzed N-hydroxylation. The peroxidase route has been examined by using horseradish peroxidase or prostaglandin H synthase in vitro. In the presence of nucleophiles such as phenols, thiols, or nucleic acids, isolable adducts are formed. The structures of these adducts have been elucidated by spectroscopic methods. The Ames test provides a useful system for studying benzidine bioactivation to mutagenic intermediates. An endogenous bacterial acetylase plays an important auxiliary role in the hepatic S9-dependent activation of benzidine. Bacterial peroxidases may also support benzidine oxidation in the Ames test.
3.Induction of erythroid differentiadon in K562 cells by different butyrate regimens/PMID 12426157; Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA 2001; 21(12):890-893/Name matches: beta-globin benzidine
Abstract:OBJECTIVE: To investigate the hemoglobinization induced by butyrate and observe the effects of different butyrate regimens on erythroid differentiation of K562 cells. METHODS: K562 cells, used as an in vitro model system, were stained with benzidine to assess hemoglobin (Hb) production in response to different treatment regimens of butyrate at varied concentrations. Comparison of the percentage of benzidine-positive cells (BZ%)in untreated and butyrate-treated K562 cells was performed. Protein absorption at 414 nm using a spectrophotometer and cellulose acetate gel electrophoresis were employed to determine the changes of Hb production in K562 cells. RESULT: The BZ% increased by 4 to 6 fold and Hb production by 9 to 14 fold 3 d after the cells were incubated with butyrate which selectively promoted fetal hemoglobin(HbF) production in K562 cells. The BZ% increased gradually and reached the peak of l9% to 28% on day 3 or 4 in cells receiving pulse treatment with butyrate for only once, followed by a subsequent rapid fall and on day 7 to 9, it decreased to the level of untreated K562 cells. The length of time for incubation with butyrate was not related to in the increment or the maintenance of the increased level of BZ%. Continuous treatment with butyrate yielded a similar result to that of a single administration of pulse treatment. In contrast, in cells with intermittent pulse treatment the BZ% reached a peak after 72 h and was maintained between 20% and 30% till 3 cycles of treatment was completed. CONCLUSION: Butyrate can induce the expression of globin genes and augment Hb producfion especially that of HbF. A sustained erythroid differentiation of K562 cells can be achieved by intermittent pulse treatment with butyrate which can be an ideal regimen for children with beta globin diseases.
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