Catalogue Number
BF-A4014
Analysis Method
HPLC,NMR,MS
Specification
98%(HPLC)
Storage
2-8°C
Molecular Weight
293.27
Appearance
Yellow crystalline powder
Botanical Source
herbs of Aristolochia debilis Sieb. et Zucc
Structure Type
Alkaloids
Category
Standards;Natural Pytochemical;API
SMILES
COC1=CC=CC2=C3C4=C(C=C21)NC(=O)C4=CC5=C3OCO5
Synonyms
1,3-Benzodioxolo[6,5,4-cd]benz[f]indol-5(6H)-one, 8-methoxy-/Aristololactam/8-Methoxy[1,3]benzodioxolo[6,5,4-cd]benzo[f]indol-5(6H)-one
IUPAC Name
14-methoxy-3,5-dioxa-10-azapentacyclo[9.7.1.02,6.08,19.013,18]nonadeca-1(18),2(6),7,11(19),12,14,16-heptaen-9-one
Density
1.5±0.1 g/cm3
Solubility
DMF
Flash Point
234.4±25.7 °C
Boiling Point
463.9±34.0 °C at 760 mmHg
Melting Point
InChl
InChI=1S/C17H11NO4/c1-20-12-4-2-3-8-9(12)5-11-14-10(17(19)18-11)6-13-16(15(8)14)22-7-21-13/h2-6H,7H2,1H3,(H,18,19)
InChl Key
MXOKGWUJNGEKBH-UHFFFAOYSA-N
WGK Germany
RID/ADR
HS Code Reference
3822000000
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:13395-02-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
MSDS
27352112
Background: Exposure to aristolochic acid (AA) can cause AA nephropathy, which is characterized by extensive proximal tubular damage and polyuria.
Methods: To test the hypothesis that polyuria might be induced by altered regulation of aquaporins (AQPs) in the kidney, different doses of AA-I or aristolactam I (AL-I) were administered intraperitoneally to Sprague-Dawley rats, and urine, blood, and kidney samples were analyzed. In addition, AQP1, AQP2, AQP4 and AQP6 expression in the kidney were determined.
Results: The results showed dose-dependent proximal tubular damage and polyuria in the AA-I- and AL-I-treated groups, and the nephrotoxicity of AL-I was higher than that of AA-I. The expression of renal AQP1, AQP2 and AQP4, but not AQP6 were significantly inhibited by AA-I and AL-I. Comparison of the inhibition potencies of AA-I and AL-I showed that AL-I was a stronger inhibitor of AQP1 expression than AA-I, while there was no difference in their effects on AQP2 and AQP4.
Conclusion: These results suggested that AA induced renal damage and polyuria were associated with a specific decrease in the expression of renal AQP1 AQP2 and AQP4, and AL-I showed higher nephrotoxicity than AA-I, which might be attributable to the differences in their inhibition of AQP1.
© 2016 S. Karger AG, Basel.
Expression of Renal Aquaporins in Aristolochic Acid I and Aristolactam I-Induced Nephrotoxicity
Ji Li 1 , Liang Zhang, ZhenZhou Jiang, XiuQin He, LuYong Zhang, Ming Xu
2016
10445409
Aristolochic acid (AA) a naturally occuring nephrotoxin and carcinogen is implicated in a unique type of renal fibrosis, designated Chinese herbs nephropathy (CHN). We identified AA-specific DNA adducts in kidneys and in a ureter obtained from CHN patients after renal transplantation. AA is a plant extract of aristolochia species containing AA I as the major component. Aristolactams are the principal detoxication metabolites of AA, which were detected in urine and faeces from animals and humans. They are activated by cytochrome P450 (P450) and peroxidase to form DNA adducts. Using the 32P-postlabelling assay we investigated the formation of DNA adducts by aristolactam I in these two activation systems. A combination of two independent chromatographic systems (ion-exchange chromatography TLC and reversed-phase HPLC) with reference compounds was used for the identification of adducts. Aristolactam I activated by peroxidase led to the formation of several adducts. Two major adducts were identical to adducts previously observed in vivo. 7-(deoxyguanosin-N2-yl)aristolactam I (dG-AAI) and 7-(deoxyadenosin-N6-yl)aristolactam I (dA-AAI) were formed in DNA during the peroxidase-mediated one-electron oxidation of aristolactam I. Aristolactam I activated by P450 led to one major adduct and four minor ones. Beside the principal AA-DNA adducts identified recently in the ureter of one patient with CHN, an additional minor adduct was detected, which was found to have indistinguishable chromatographic properties on TLC and HPLC from the major adduct formed from aristolactam I by P450 activation. Thus, this minor AA-adduct might be evolved from the AAI detoxication metabolite (aristolactam I) by P450 activation. These results indicate a potential carcinogenic effect of aristolactam I in humans.
Aristolactam I a Metabolite of Aristolochic Acid I Upon Activation Forms an Adduct Found in DNA of Patients With Chinese Herbs Nephropathy
M Stiborova 1 , E Frei, A Breuer, C A Bieler, H H Schmeiser
1999 Jul
3673113
1. After oral administration of aristolochic acid I (AAI) and aristolochic acid II (AAII) to rats, the following metabolites were isolated from the urine and their structures elucidated: aristolactam I, aristolactam Ia, aristolochic acid Ia, aristolic acid I and 3,4-methylenedioxy-8-hydroxy-1-phenanthrenecarboxylic acid (metabolites of AAI); or aristolactam Ia, aristolactam II and 3,4-methylenedioxy-1-phenanthrenecarboxylic acid (metabolites of AAII). A further metabolite of AAII having a lactam structure has not yet been isolated in pure form. 2. The metabolic pathways have been elucidated by administration of various metabolites. 3. The principal metabolite of AAI in rats was aristolactam Ia; 46% of the dose was excreted in the urine in form of this metabolite and 37% in the faeces. The other substances were minor metabolites. Those metabolites of AAII whose structures have been elucidated were minor metabolites; the largest proportion consisted of aristolactam II, which accounted for 4.6% in the urine and 8.9% in the faeces. 4. The mouse was the only animal which had the same metabolite patterns of AAI and AAII as those found in the rat. Not all the metabolites listed above were found in urine from guinea pigs, rabbits, dogs and man.
Studies on the Metabolism of Aristolochic Acids I and II
G Krumbiegel 1 , J Hallensleben, W H Mennicke, N Rittmann, H J Roth
1987 Aug
Description :
Aristololactam I (AL-I), is the main metabolite of aristolochic acid I (AA-I), participates in the processes that lead to renal damage.Aristololactam I (AL-I) directly injures renal proximal tubule cells, the cytotoxic potency of AL-I is higher than that of AA-I and that the cytotoxic effects of these molecules are mediated through the induction of apoptosis in a caspase-3-dependent pathway[1].
