[5] Myricetin is produced from the parent compound taxifolin through the (+)-dihydromyricetin intermediate and can be further processed to form laricitrin and then syringetin, both members of the flavonol class of flavonoids.

[6] Dihydromyricetin is frequently sold as a supplement and has controversial function as a partial GABAA receptor potentiator and treatment in Alcohol Use Disorder (AUD).

Gradual but steady accretion of such damage can lead to the development of many diseases and conditions including thrombosis, diabetes, persistent inflammation, cancer, and atherosclerosis.

[3] Multiple studies have demonstrated that myricetin also has the potential to act as a pro-oxidant due to its tendency to undergo autoxidation depending upon its environment [citation needed].

[1] Myricetin may also act as a pro-oxidant in its ability to increase the production of hydroxy radicals through reactions with Fe2+ or Fe3+−EDTA and hydrogen peroxide[citation needed].

The resulting hydroxy radicals are often linked to DNA degradation, however, there are doubts as to whether or not this damage would be significant when analyzed in vivo since in vitro studies with both bovine and human serum albumin exhibited extensive protection against it.

Myricetin reduces the risk of skin tumorigenicity that is caused by polycyclic aromatic hydrocarbons like benzo(a)pyrene, a highly carcinogenic compound.

On a more biochemical level, it was shown that topical application of myricetin to mice inhibited the binding of benzo(a)pyrenes to DNA and protein native to epidermal skin cells.

[1] This data shows that myricetin is not unilaterally able to reduce the carcinogenic activity of all polycyclic aromatic hydrocarbons or even the more specific subclass of benzo(a)pyrenes.

The antioxidants catalase, superoxide dismutase, mannitol, and sodium azide in combination with Cu2+ increased the DNA degradation activity of myricetin.

[8] Structural analysis of myricetin and other flavonoids with observed antiviral effects indicate that the 3,4’ free hydroxyl groups likely are responsible for inhibition.

The flavonoid has been demonstrated to have a hypoglycemic effect by increasing the ability of adipocytes, as well as cells of the soleus muscle and liver of rats, to uptake glucose.

In the mouse myoblast cell line known as C2C12, treatment with myricetin not only increased glucose uptake, but also enhanced lipogenesis, a result not seen from any of the other bioflavonoids tested.

[10] There is also evidence indicating that other characteristics of myricetin, such as its effect against inflammation, oxidative stress, and hyperlipidemia, may be helpful to reduce or even prevent other clinical issues which arise from diabetes mellitus.

[11] It is also proposed that myricetin may have the ability as a potent flavonoid antioxidant to prevent LDL oxidation, thus slowing the body's local inflammatory response and delaying the appearance of the first fatty streak and onset of atherosclerosis.

[15] Myricetin, along with other lipoxygenase- and cyclooxygenase-blocker flavonoids are seen to have significant anti-inflammatory characteristics, demonstrated by their ability to reduce edemas caused by carrageenan and croton oil.

[10] Other studies suggest that myricetin's anti-inflammatory nature could also potentially be dependent upon interfering in inflammatory signal pathways by inhibiting various kinases and, consequently, the function of tumor necrosis factor alpha.

Through the inhibition of NF-B binding activity, these natural compounds were reported to significantly reduce the lipopolysaccharide (LPS)-induced interleukin (IL)-12 production in mouse main macrophages as well as the RAW264.7 monocytic cell-line.

[19] Myricetin produced epithelial layer contractile reflexes in separate rat aortic rings at a concentration of 50 M.[20] This substance induces the synthesis of cytosolic unbound calcium in cultured bovine endothelial cells.