Stereochemistry | ABSOLUTE |
Molecular Formula | C40H52O4 |
Molecular Weight | 596.8385 |
Optical Activity | UNSPECIFIED |
Defined Stereocenters | 2 / 2 |
E/Z Centers | 9 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CC(\C=C\C=C(C)\C=C\C1=C(C)C(=O)[C@@H](O)CC1(C)C)=C/C=C/C=C(C)/C=C/C=C(C)/C=C/C2=C(C)C(=O)[C@@H](O)CC2(C)C
InChI
InChIKey=MQZIGYBFDRPAKN-UWFIBFSHSA-N
InChI=1S/C40H52O4/c1-27(17-13-19-29(3)21-23-33-31(5)37(43)35(41)25-39(33,7)8)15-11-12-16-28(2)18-14-20-30(4)22-24-34-32(6)38(44)36(42)26-40(34,9)10/h11-24,35-36,41-42H,25-26H2,1-10H3/b12-11+,17-13+,18-14+,23-21+,24-22+,27-15+,28-16+,29-19+,30-20+/t35-,36-/m0/s1
Astaxanthin (ATX), a red-orange carotenoid that originates the pink or red color of salmon, trout, lobster, shrimp, and other sea organisms, exhibits antioxidant, anti-inflammatory, and antiapoptotic effects. Recently, ATX was shown to protect neurons in experimental models of acute injuries, chronic neurodegenerative disorders, and neurological diseases and was proposed as a beneficial strategy to treat neurological diseases. In addition, ATX chelates several metal ions, preventing metal ion-induced oxidative stress, it has anti-inflammatory properties and it acts as a damper of singlet oxygen levels. Being a part of naturally derived supplements Oncotris™ in genitourinary cancer patients was revealed, that astaxanthin could support the body to overcome the treatment-related toxicities - and the relative oxidative stress in cancer patients.
CNS Activity
Originator
Approval Year
PubMed
Patents
Sample Use Guides
astaxanthin (Oncotris™) used as supplementary management in genitourinary cancer patients who had undergone oncological therapy
Route of Administration:
Oral
There were investigated whether the antioxidant agent astaxanthin (ATX) protects neurons from AβOs-induced excessive mitochondrial ROS generation, NFATc4 activation, and RyR2 mRNA downregulation. Primary hippocampal cultures were incubated with 0.1 μM ATX for 1.5 h prior to AβOs addition (500 nM). It was found that incubation with ATX (≤10 μM) for ≤24 h was nontoxic to neurons, evaluated by the live/dead assay. Preincubation with 0.1 μM ATX also prevented the neuronal mitochondrial H2O2 generation induced within minutes of AβOs addition. Longer exposures to AβOs (6 h) promoted NFATc4-eGFP nuclear translocation and decreased RyR2 mRNA levels, evaluated by detection of the eGFP-tagged fluorescent plasmid and qPCR, respectively. Preincubation with 0.1 μM ATX prevented both effects. These results indicate that ATX protects neurons from the noxious effects of AβOs on mitochondrial ROS production, NFATc4 activation, and RyR2 gene expression downregulation.