Table 3 Antioxidant activities of myricetin

Density functional theory

in silico

The bond dissociation enthalpy computed and the compound showed ionization potentials 161.4 kcal/mol.

[64]

Antioxidant response element (ARE) activation

in vitro

Activates Nrf2 antioxidant response element pathways and is involved in myricetin-induced expression profiling in hepatic cells.

[65]

Deoxyribose degradation

in vitro

Significant antioxidant activity (complex with iron) in the presence of ascorbic acid.

[8]

DPPH

in vitro

Myricetin/HP-β-CD inclusion complex formation enhances antioxidant activity of drugs.

[66]

DPPH

in vitro

Significant RSA dose-dependently

[50]

DPPH, ABTS

in vitro

Inhibition activity from 13.3 to 99.8% at doses of 0.03 to 1 mg/ml during 5 to 20 min.

[67]

DPPH, FRAP

in vitro

High RSA in DPPH assay, and intermediate ferric reducing ability in FRAP assay.

[68]

DPPH, FRAP, ABTS

in vitro

Mean activity for FRAP (27.2, 26.7) mmol Fe²⁺/L, DPPH (7.9, 9.3) mmol TEAC/L, and ABTS (9.3, 11.5) mmol TEAC/L.

[69]

DPPH, FRAP, ORAC

in vitro

EC₅₀ value of DPPH, FRAP and ORAC assays were recorded as 7.60 μg, 8.86 and 12.99 mmol Trolox equivalents per gram.

[70]

DPPH, TPTZ, superoxide

in vitro

Myricetin and its derivatives showed IC₅₀ value from 1.82 to 3.27 μg/mL in DPPH assay and 1.86 to 3.83 μg/mL in superoxide assay however, 1.38 to 2.89 μM equivalent to Fe²⁺ /mL for TPTZ assay.

[71]

H₂O₂

in vitro

Increases hydrogen peroxide resistance in Saccharomyces cerevisiae.

[72]

DPPH, ROS

in vitro

21–54% scavenging activity in DPPH assay (5–10 μg/mL) and 35–73% intracellular ROS scavenging activity (1–10 μg/mL). Significantly inhibits H₂O₂-induced cell death and activated antioxidant enzymes.

[73]

NO

in vitro

Mean scavenging activity compared to hydrophilic antioxidants.

[74]

ROS

in vitro

Inhibits peroxynitrite-mediated DNA damage in primary astrocytes at 5 μM.

[75]

ROS

in vitro

The IC₃₀ value for inhibitory effect on triglyceride and ROS were recorded as > 150 μM and 122.7 μM.

[76]

ROS

in vitro

Inhibits H₂O₂-induced cell death and increases cell survival (65%).

[77]

DCFH-DA

in vivo

Inhibits ROS production in normal individuals and in patients with sickle cell anemia.

[78]