Gossypol-acetic acid

• CAS: 12542-36-8
• Catalog Number: ACM12542368
• Category: Main Products
• Molecular Weight: 578.61
• Molecular Formula: C₃₂H₃₄O₁₀
• Synonyms: aceticacidgossypol;GOSSYPOL ACETATE;GOSSYPOL-ACETIC ACID;1,1,6,6,7,7-hexahydroxy-3,3-dimethyl-5,5-bis(1-methylethyl)[2,2-binaphthalene]-8,8-dicarboxaldehyde-acetic acid;Gossypolaceticacidcomplex;GOSSYPOL ACETATE 98%;GOSSYPOLMONOACETICACID;1,1,6,6,7,7-Hexahydroxy-3,3-dimethyl-5,5-bis(1-methylethyl)[2,2-binaphthalene]-8,8-dicarboxaldehyde-acetic acid
• IUPAC Name: aceticacid;7-(8-formyl-1,6,7-trihydroxy-3-methyl-5-propan-2-ylnaphthalen-2-yl)-2,3,8-trihydroxy-6-methyl-4-propan-2-ylnaphthalene-1-carbaldehyde
• Canonical SMILES: CC1=C(C(=C2C(=C1)C(=C(C(=C2C=O)O)O)C(C)C)O)C3=C(C=C4C(=C3O)C(=C(C(=C4C(C)C)O)O)C=O)C.CC(=O)O
• InChI Key: NIOHNDKHQHVLKA-UHFFFAOYSA-N
• Boiling Point: 707.9ºC at 760 mmHg
• Melting Point: 164-168°C
• Flash Point: 395.9ºC
• Appearance: Yellow crystal powder
• Exact Mass: 578.21500
• Hazard Statements: Xn
• Safety Description: 22-36
• Supplemental Hazard Statements: H302-H351
• Symbol: GHS07,GHS08

Case Study

Gossypol Acetic Acid Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis and Its Mechanism

Lin, Jian-Hong, et al. Biomolecules, 2021, 11(11), 1667.

Gossypol acetic acid (GAA) is a natural product extracted from cotton seeds that protects against oxidative stress. This study investigated the ability of GAA to attenuate myocardial I/R-induced ferroptosis and the underlying mechanism in an established rat myocardial ischemia/reperfusion (I/R) model and in isolated neonatal rat cardiomyocytes. The results suggest that GAA may play a cytoprotective role in ferroptosis-induced cardiomyocyte death and myocardial I/R-induced ferroptosis.
Mechanism of action of GAA
· H9c2 cells and cardiomyocytes were exposed to erastin, RSL3, and Fe-SP as inducers of ferroptosis.
· GAA exhibited a protective effect on H9c2 cells against cell death induced by these ferroptosis inducers by reducing malondialdehyde and reactive oxygen species levels, chelating iron content, and decreasing mRNA levels of Ptgs2.
· Furthermore, GAA could prevent cell death and lipid peroxidation in cardiomyocytes induced by oxygen-glucose deprivation/reperfusion.
· Additionally, GAA significantly reduced myocardial infarct size, lipid peroxidation, mRNA levels of ferroptosis markers Ptgs2 and Acsl4, protein levels of ACSL4 and NRF2, and increased GPX4 protein levels in ex vivo rat hearts subjected to I/R injury.

Study on the Mechanism of Gossypol Acetic Acid Inducing γH2AX in Tumor Cells

Guo, Zhong, et al. Cancer Cell International, 2014, 14, 1-9.

In vitro, gossypol acetic acid (GAA) alone can trigger the formation of γH2AX in Human mucoepidermoid carcinoma cell line (MEC-1). This work explored the possible mechanism of GAA inducing γH2AX in tumor cells. The results showed that phosphatidylinositol 3-kinase (PI3K) family members DNA-PK, ATM and ATR were involved in H2AX phosphorylation (γH2AX) in MEC-1 cells.
Experimental methods and results
· Caffeine and wortmannin, PI3K inhibitors, were utilized to determine the kinase(s) responsible for inducing γH2AX in MEC-1 cells as a result of GAA. Human glioma cell lines M059K and M059J, comprising both DNA-PK proficient and deficient cells, were also employed to identify the kinases accountable for H2AX phosphorylation induced by GAA. Immunofluorescent microscopy was used to detect γH2AX expression, while flow cytometry assay was utilized to examine γH2AX and cell cycle.
· GAA induced phosphorylation of H2AX in a manner dependent on the cell cycle, leading to a notable arrest in the G0/G1 phase of MEC-1 cells. Caffeine and wortmannin effectively hindered GAA-induced H2AX phosphorylation in MEC-1 cells. H2AX phosphorylation was observed in M059K cells following GAA treatment, but not in M059J cells. From these findings, it can be inferred that GAA treatment alone can prompt H2AX phosphorylation in a cell cycle dependent manner in MEC-1 and M059K cells, but not in M059J cells. A significant G0/G1 phase arrest was apparent in MEC-1.