Although some studies indicate that hesperidin has antioxidant activity in vivo , others do not demonstrate antioxidant activity in vitro.
The possible anti-inflammatory action of hesperidin is probably due to the possible anti-inflammatory action of its aglycone hesperetin. Hesperetin appears to interfere with the metabolism of arachidonic acid as well as with histamine release. Hesperetin appears to inhibit phospholipase A2, lipoxygenase and cyclo-oxygenase. There is evidence that hesperetin inhibits histamine release from mast cells, which would account for the possible anti-allergic activity of hesperidin.
Again, the possible hypolipidemic effect of hesperidin is probably due to hesperetin's possible action in lipid lowering. Hesperetin may reduce plasma cholesterol levels by inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, as well as acyl coenzyme A: cholesterol acytransferase (ACAT). Inhibition of these enzymes by hesperetin has been demonstrated in rats fed a high cholesterol diet.
The mechanism of hesperidin's possible vasoprotective action is unclear. Animal studies have shown that hesperidin decreases microvascular permeability. Hesperidin, itself or via hesperetin, may protect endothelial cells from hypoxia by stimulating certain mitochondrial enzymes, such as succinate dehydrogenase.
The mechanism of hesperidin's possible anticarcinogenic action is also unclear. One explanation may be the inhibition of polyamine synthesis. Inhibition of lipoxygenase and cyclo-oxygenase is another possibility.
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