1. 1,2,3-trihydroxybenzene
2. Acid, Pyrogallic
3. Pyrogallic Acid
1. Benzene-1,2,3-triol
2. 87-66-1
3. 1,2,3-trihydroxybenzene
4. Pyrogallic Acid
5. 1,2,3-benzenetriol
6. Fourrine Pg
7. Fouramine Brown Ap
8. Fourrine 85
9. Pyro
10. Piral
11. C.i. Oxidation Base 32
12. Benzenetriol
13. Fouramine Base Ap
14. C.i. 76515
15. 1,2,3-trihydroxybenzen
16. Benzene, 1,2,3-trihydroxy-
17. Nsc 5035
18. 2,3-dihydroxyphenol
19. 1,2,3-trihydroxybenzen [czech]
20. 1,2,3-trihydroxy-benzene
21. Nsc-5035
22. 01y4a2qxy0
23. Chembl307145
24. 35296-77-6
25. Chebi:16164
26. 1,2,3-benzenetriol, Homopolymer
27. Benzene-1,2,3-triol (pyrogallol)
28. Mfcd00002192
29. Ncgc00091507-01
30. 1, 2, 3-benzenetriol
31. Dsstox_cid_5983
32. Dsstox_rid_77980
33. Dsstox_gsid_25983
34. 30813-84-4
35. 1,2,3-trihydroxybenzen (czech)
36. Ci Oxidation Base 32
37. Cas-87-66-1
38. Pyrogallol [nf]
39. Pyg
40. Ccris 1940
41. Hsdb 794
42. Pyrogallol, Acs
43. Einecs 201-762-9
44. Brn 0907431
45. Unii-01y4a2qxy0
46. Ci 76515
47. Pyrogallol;
48. Trihydroxybenzene
49. Ai3-00709
50. Pyrogallol Polymer
51. Pyrogallol Solution
52. Pyrogallol-[d6]
53. 1,3-benzenetriol
54. Pyrogallol, 98%
55. Pyrop
56. Pyrogallol Acs Grade
57. 1,3-trihydroxybenzen
58. 1216684-97-7
59. Pyrogallic Acid,(s)
60. 1,3-trihydroxybenzene
61. Benzene-1,2-3-triol
62. Pyrogallol [mi]
63. Pyrogallol, Acs Reagent
64. Pyrogallol [hsdb]
65. Pyrogallol [inci]
66. Benzene,2,3-trihydroxy-
67. Wln: Qr Bq Cq
68. Pyrogallol [vandf]
69. Pyrogallol [mart.]
70. Schembl3532
71. Pyrogallol [who-dd]
72. C.i. Oxidation Base 32
73. 4-06-00-07327 (beilstein Handbook Reference)
74. Mls001066376
75. Pyrogallol, Analytical Standard
76. 1,2,3-trihydroxybenzene, Xiv
77. Dtxsid6025983
78. Pyrogallol, >=98% (hplc)
79. Pyrogallol, P.a., Acs Reagent
80. Nsc5035
81. Zinc330141
82. Bcp15871
83. Hy-n1579
84. Pyrogallol, Acs Reagent, >=99%
85. Str08708
86. Tox21_111143
87. Tox21_202373
88. Bbl011607
89. Bdbm50031472
90. Pyrogallol, Vetec(tm) Reagent Grade
91. S3885
92. Stl163335
93. Akos000120163
94. Am10660
95. Ccg-266100
96. Cs-w019928
97. 1,2,3-benzenetriol (acd/name 4.0)
98. Ncgc00091507-02
99. Ncgc00091507-03
100. Ncgc00259922-01
101. Pyrogallol, Purum, >=98.0% (hplc)
102. Ac-11384
103. Bp-12538
104. Da-40956
105. Gmn
106. Pyrogallol, Saj First Grade, >=98.0%
107. Smr000471842
108. Pyrogallol, Jis Special Grade, >=99.0%
109. Ft-0606230
110. P0570
111. C01108
112. Ab-131/40221933
113. Q388692
114. W-104009
115. 2,3-dihydroxyphenol; Benzene-1,2,3-triol; Nsc 5035
116. F0001-2163
| Molecular Weight | 126.11 g/mol |
|---|---|
| Molecular Formula | C6H6O3 |
| XLogP3 | 0.5 |
| Hydrogen Bond Donor Count | 3 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 0 |
| Exact Mass | 126.031694049 g/mol |
| Monoisotopic Mass | 126.031694049 g/mol |
| Topological Polar Surface Area | 60.7 Ų |
| Heavy Atom Count | 9 |
| Formal Charge | 0 |
| Complexity | 84.3 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
/Experimental Therapy/ ... Pyrogallol had highly cytotoxic effect on human lung cancer cell lines and less effect on human bronchial epithelium cell line. This study was performed to investigate the beneficial effect of pyrogallol on human lung cancer cell lines - H441 (lung adenocarcinoma) and H520 (lung squamous cell carcinoma). The MTT (cytotoxic) data showed the inhibition growth of lung cancer cells followed pyrogallol treatment. The cell cycle of lung cancer cells was arrested in G2/M phase using flow cytometry. Using Western blot analysis, the cell cycle related proteins - cyclin B1 and Cdc25c were decreased in a time-dependent manner and the phosphorylated Cdc2 (Thr14) was increased within 4h pyrogallol treatment. Moreover, the higher cleavage of poly (ADP)-ribose polymerase (PARP), the increased of Bax concurrent with the decreased of Bcl-2 indicated that pyrogallol treatment resulted in apoptosis of lung cancer cells. The cell apoptosis was also directly demonstrated using Annexin V-FITC and TUNEL stain. Additionally, the tumoricidal effect of pyrogallol was measured using a xenograft nude mice model. After 5 weeks of pyrogallol treatment could cause the regression of tumor. Taking in vitro and in vivo studies together, these results suggest that pyrogallol can be developed as a promising anti-lung cancer drug particular for the non-small cell lung cancer (NSCLC).
PMID:19233505 Yang CJ et al; Lung Cancer 66 (2): 162-8 (2009)
4. 4 = Very toxic: Probable oral lethal dose (human) 50-500 mg/kg, between 1 teaspoon and 1 ounce for 80 kg person (150 lb).
Gosselin, R.E., H.C. Hodge, R.P. Smith, and M.N. Gleason. Clinical Toxicology of Commercial Products. 4th ed. Baltimore: Williams and Wilkins, 1976., p. II-128
Antioxidants
Naturally occurring or synthetic substances that inhibit or retard oxidation reactions. They counteract the damaging effects of oxidation in animal tissues. (See all compounds classified as Antioxidants.)
The substance can be absorbed into the body by ingestion.
International Program on Chemical Safety/Commission of the European Communities; International Chemical Safety Card on Pyrogallic acid (April 2006). Available from, as of May 20, 2010: https://www.inchem.org/pages/icsc.html
Readily absorbed via skin.
Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996., p. 2842
...Readily absorbed from gastroenteric tract & from parenteral sites of injection. Little is absorbed through intact skin. ...readily conjugated with hexuronic, sulfuric, or other acids & excreted within 24 hr via kidneys. A fraction is excreted unchanged.
Clayton, G.D., F.E. Clayton (eds.) Patty's Industrial Hygiene and Toxicology. Volumes 2A, 2B, 2C, 2D, 2E, 2F: Toxicology. 4th ed. New York, NY: John Wiley & Sons Inc., 1993-1994., p. 1596
...Pyrogallol /is a metabolite of tannic acid...
Clarke, M. L., D. G. Harvey and D. J. Humphreys. Veterinary Toxicology. 2nd ed. London: Bailliere Tindall, 1981., p. 123
With pyrogallol derivatives...the middle phenolic group is methylated, with catechol derivatives methylation may be meta or para, dependent on the other substituents present. Pyrogallol /is methylated by catechol o-methyl transferase to form/ 2-methyl pyrogallol.
Parke, D. V. The Biochemistry of Foreign Compounds. Oxford: Pergamon Press, 1968., p. 86
Pyrogallol in rats yields 3-methoxycatechol & 2-methoxyresorcinol. In grass yields 2-methoxyresorcinol. /From table/
Goodwin, B.L. Handbook of Intermediary Metabolism of Aromatic Compounds. New York: Wiley, 1976., p. 46
Pyrogallol in beef yields purpurogallin. In tea yields purpurogallin. /From table/
Goodwin, B.L. Handbook of Intermediary Metabolism of Aromatic Compounds. New York: Wiley, 1976., p. 46
For more Metabolism/Metabolites (Complete) data for Pyrogallic acid (7 total), please visit the HSDB record page.
Pyrogallol (PG) as a polyphenol induces apoptosis in cells. The effects of PG on the growth and death of endothelial cells (ECs) /were examined/. PG dose-dependently inhibited the growth of calf pulmonary artery endothelial cells (CPAEC) and human umbilical vein endothelial cells (HUVEC). PG also induced apoptosis in both cells accompanied by the loss of mitochondrial membrane potential (DeltaPsi(m)). CPAEC were more sensitive to PG than HUVEC concerning cell growth and death. Caspase inhibitors (pan-caspase, caspase-3, -8 or -9 inhibitor) did not affect the growth inhibition of CPAEC by PG. However, pan-caspase inhibitor (Z-VAD) significantly reduced apoptosis and the loss of DeltaPsi(m) in PG-treated CPAEC. PG reduced ROS level and increased GSH depleted cell numbers in CPAEC. While Z-VAD increased ROS levels in PG-treated CPAEC, it decreased GSH depleted cell numbers. In conclusion, PG inhibited the growth of ECs, especially CPAEC via caspase-dependent apoptosis and GSH depletion.
PMID:19913593 Han YH et al; Food Chem Toxicol 48 (2): 558-63 (2010)
Pyrogallol (PG) as a polyphenol compound induces apoptosis in several types of cells. Here, we evaluated the effects of PG on endothelial cells (ECs), especially calf pulmonary artery endothelial cells (CPAEC) in relation to the cell growth, ROS and glutathione (GSH) levels. PG dose-dependently inhibited the growth of CPAEC and human umbilical vein endothelial cells (HUVEC) at 24 h. PG also induced apoptosis in CPAEC, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsim). PG decreased ROS level including O2*- and PG dose-dependently increased GSH depleted cell number in both EC types. N-acetyl-cysteine (NAC; a well-known antioxidant) increased ROS levels in PG-treated CPAEC with the prevention of cell death and GSH depletion. In conclusion, PG inhibited the growth of ECs, especially CPAEC via apoptosis. PG-induced EC death was related to GSH depletion rather than ROS level changes.
PMID:19956894 Han YH et al; Oncol Rep 23 (1): 287-92 (2010)
Treatment with 50 or 100 uM pyrogallol (PG) significantly inhibited the cell growth of human pulmonary A549 cells for 72 hr. DNA flow cytometric analysis indicated that PG slightly induced a G1 phase arrest of the cell cycle at 24 or 48 hr, but did not induce the specific cell cycle arrest at 72 hr. Intracellular GSH depletion was observed in PG-treated cells. PG induced apoptosis in A549 cells, as evidenced by sub-G1 cells, annexin V staining cells, and the loss of mitochondrial membrane potential (DeltaPsi(m)). The intracellular ROS (reactive oxygen species) level including O(2)(*-) increased in PG-treated A549 cells at 24 and 48 hr, and persisted at 72 hr. The changes in GSH as well as ROS levels by PG affected the cell viability in A549 cells. In conclusion, PG inhibited the growth of human pulmonary A549 cells by inducing cell cycle arrest as well as triggering apoptosis.
PMID:19202562 Han YH et al; J Biochem Mol Toxicol 23 (1): 36-42 (2009)
Pyrogallol (PG) decreased the viability of human pulmonary adenocarcinoma Calu-6 cells in a dose- and time-dependent manner. The induction of apoptosis by PG was accompanied by the loss of mitochondrial membrane potential (DeltaPsi(m)), cytochrome c release from mitochondria and activation of caspase-3 and caspase-8. All tested caspase inhibitors, especially the pan-caspase inhibitor (Z-VAD), markedly rescued Calu-6 cells from PG-induced cell death. Rescue was accompanied by inhibition of caspase-3 activation and PARP cleavage. Treatment with Z-VAD also prevented the loss of mitochondrial membrane potential (DeltaPsi(m)). In conclusion, PG inhibits the growth of Calu-6 cells via caspase-dependent apoptosis.
PMID:19000662 Han YH et al; Chem Biol Interact 177 (2): 107-14 (2009)
For more Mechanism of Action (Complete) data for Pyrogallic acid (7 total), please visit the HSDB record page.
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