High impact information on NSC77009

• With IC50 values ranging from 1.0 to 18.7 muM, hamamelitannin and the galloylated proanthocyanidins isolated from Hamamelis virginiana L. were found to be most potent inhibitors of 5-LOX [1].
• The effects of hamamelitannin, gallic acid and dl-alpha-tocopherol were evaluated on murine fibroblasts exposed to t-butylhydroperoxide (BHP) in terms of the cell survivals [2].
• On peroxidation of lipid bilayers induced by 2,2'-azobis-(2-amidinopropane) dihydrochloride (AAPH) in terms of inhibition period (tinh), hamamelitannin showed the longest tinh time (1107.0 +/- 38.18 sec), followed by those of dl-alpha-tocopherol (877.5 +/- 31.8 sec) and gallic acid (771.0 +/- 4.2 sec) [2].
• The kinetic chain length, defined as the propagation numbers of a lipid peroxyl radical, and calculated from the ratio (Rp/Ri) of the rate of lipid peroxidation to that of inhibition by dl-alpha-tocopherol, hamamelitannin and gallic acid were 27.23, 7.86 and 7.09, respectively [2].
• Tannins from Hamamelis virginiana: Identification of Proanthocyanidins and Hamamelitannin Quantification in Leaf, Bark, and Stem Extracts [3].

Biological context of NSC77009

• When estimating by the direct method, IC50 values of hamamelitannin, gallic acid and dl-alpha-tocopherol were 93.5 +/- 2.1 microM, 141.6 +/- 2.0 microM and 1590.0 +/- 330.0 microM, respectively [2].
• One hundred % protection against TNF-induced DNA fragmentation and cytotoxicity was obtained for hamamelitannin concentrations higher than 10 microM [4].
• Treatment of the cells with the test compounds in a dose-range of 2-166 microg/ml prior to the exposure to benzo(a)pyrene (B(a)P, 10 microM, 2.5 microg/ml) led to a significant reduction of induced DNA damage which was dose-dependent for all test compounds, except for hamamelitannin [5].
• Thus, hamamelitannin inhibits the TNF-mediated endothelial cell death without altering the TNF-induced upregulation of endothelial adhesiveness [4].
• Concentrations (1-100 microM) of hamamelitannin that inhibited the TNF-mediated cell death and DNA fragmentation, however, failed to inhibit the TNF-induced ICAM-1 expression and EAhy926 cell adhesiveness to U937 cells [4].

Anatomical context of NSC77009

• Hamamelitannin from Hamamelis virginiana inhibits the tumour necrosis factor-alpha (TNF)-induced endothelial cell death in vitro [4].

Associations of NSC77009 with other chemical compounds

• Catechin and a low-molecular weight proanthocyandin fraction (W(M)) caused only slight increases of OTM up to concentrations of 166 microg/ml whereas hamamelitannin and the proanthocyandin fraction with higher molecular weight (W(A)) led to a two-fold enhancement of OTM at the same concentrations [5].
• Previously we demonstrated that hamamelitannin (2',5-di-O-galloyl hamamelose) in Hamamelis virginiana L. exhibits potent superoxide-anion scavenging activity [6].

Gene context of NSC77009

• The observed anti-TNF activity of hamamelitannin may explain the antihamorrhaegic use of H. virginiana in traditional medicine and its claimed use as a protective agent for UV radiation [4].
• (4) When hamamelitannin was treated with superoxide anions generated by a KO2-crown ether system, HPLC analysis showed the disappearance of hamamelitannin and the concomitant formation of hamamelitannin-derived radicals (g = 2.005, delta H1 = 2.16 G, delta H2 = 4.69 G) was detected by ESR spectrometry.(ABSTRACT TRUNCATED AT 250 WORDS)[6]

Analytical, diagnostic and therapeutic context of NSC77009

• An HPLC method for the determination of hamamelitannin, catechins and gallic acid in witch hazel bark, twig and leaf has been developed [7].

References