Myricetin is a member of the flavonoid class of polyphenolic compounds, with antioxidant properties. Common dietary sources include vegetables (including tomatoes), fruits (including oranges), nuts, berries, tea, and red wine.

Myricetin is structurally similar to fisetin, luteolin, and quercetin and is reported to have many of the same functions as these other members of the flavonol class of flavonoids. Reported average intake of myricetin per day varies depending on diet, but has been shown in the Netherlands to average 23 mg/day.

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. Dihydromyricetin is frequently sold as a supplement and has controversial function as a partial GABA_A receptor potentiator and treatment in Alcohol Use Disorder (AUD). Myricetin can alternatively be produced directly from kaempferol, which is another flavonol.

Antioxidants are molecules present in fruits and vegetables that have been demonstrated to protect against some forms of cancer and cardiovascular disease. Biomolecules and cell structures can experience oxidative stress due to the presence and activity of reactive oxygen species (ROS). ROS like •OH, •O₂⁻, and H₂O₂ are produced during cellular metabolism processes (aerobic respiration). ROS can damage lipids, DNA, and proteins.

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. Flavonoids including myricetin are able to scavenge for ROS and can chelate intracellular transition metal ions that ultimately produce ROS.

Myricetin also enhances the effects of other antioxidants. Myricetin can induce the enzyme glutathione S-transferase (GST). GST has been suggested to protect cells against oxidative stress by protecting cells against free-radicals. In vitro studies have shown that myricetin significantly increased GST activity.

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]}. It has been seen that when in the presence of cyanide, autoxidation is favored, resulting in superoxide, a byproduct characteristic of causing cellular damage ^{[citation needed]}. However, sodium azide, superoxide dismutase, and catalase have been seen to inhibit the autoxidation of myricetin.

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.