Bioflavonoids: benefits, dosage, contraindications

Antioxidant

Citrus bioflavonoids, thanks to their exceptional antioxidant properties, play an important role in combating oxidative stress and cellular aging. These natural compounds act in multiple ways: they neutralize various free radicals such as hydroxyl and superoxide radicals, prevent lipid peroxidation, and chelate metals, thereby preventing metal-catalyzed oxidation. Their free-radical scavenging activity is mainly due to their ability to donate hydrogen atoms, thanks to the phenolic groups they possess, allowing stabilization of radicals on their molecular structure.nnResearch shows that orange juices rich in flavonoids and other polyphenols offer significant antioxidant capacity, suggesting that daily intake of orange juice could provide additional protection against oxidation.nn

Anti-inflammatory

Citrus bioflavonoids, notably hesperidin and nobiletin, have demonstrated a notable capacity to modulate immune and inflammatory responses. Their anti-inflammatory effects can be attributed to the inhibition of key regulatory enzymes such as protein kinase C, phosphodiesterase, phospholipase, lipoxygenase and cyclooxygenase, which play a crucial role in the formation of biological mediators that activate endothelial cells and other cells specialized in inflammation. For example, hesperidin can reduce inflammation in cases of pleurisy (a medical condition characterized by inflammation of the pleura, a thin membrane surrounding the lungs and lining the inner wall of the thoracic cavity), decreasing the fluid and the number of white blood cells involved. Nobiletin, for its part, has shown a selective effect in downregulating the expression of cyclooxygenase-2 without affecting cyclooxygenase-1, and has reduced the production of prostaglandin E2 and the expression of pro-inflammatory cytokines.

Venotonic

Bioflavonoids, including hesperidin, significantly improve venous health through several interdependent mechanisms that have been extensively documented in clinical and experimental studies. These natural compounds act mainly by strengthening venous tone and reducing venous stasis, which is crucial for preventing and managing the symptoms of chronic venous insufficiency (CVI). Hesperidin plays a vital role in modulating inflammation and in protecting venous structures from damage. It inhibits the synthesis of prostaglandins and free radicals, reduces microvascular leakage induced by bradykinin (a vasodilator peptide that helps increase blood flow), and limits leukocyte activation and migration. These actions decrease leukocyte infiltration and the tissue damage associated with CVI, thereby facilitating the healing of venous ulcers and reducing edema. In clinical practice, the use of hesperidin has shown an improvement in endothelial function, which is essential for maintaining the integrity of blood vessels and preventing vascular complications. Hesperidin supplementation could therefore represent a promising therapeutic approach for the treatment of chronic venous insufficiency.

Usages associés

Anticancer

Citrus bioflavonoids, through their antimutagenic effects, significantly inhibit tumor development and cell proliferation. They protect DNA from damage caused by UV radiation and neutralize free radicals that can induce mutations near DNA. In addition, flavonoids such as naringin and nobiletin have demonstrated the ability to inhibit enzymes involved in tumor promotion and to reduce the expression of certain pro-inflammatory genes, thereby limiting the development and progression of cancer cells. Studies have revealed that citrus flavonoids can delay tumor development, notably by positively influencing cellular metabolism and by inhibiting key metabolic pathways in tumor cells. They also exert a direct cytotoxic effect on various types of cancer cells by inducing apoptosis (programmed cell death) without affecting surrounding healthy cells.

Cardiovascular

Citrus flavonoids, including hesperidin, naringin, and nobiletin, have demonstrated a wide range of beneficial effects on cardiovascular and metabolic health, in part due to their potent antioxidant activity, their ability to improve glucose tolerance and insulin sensitivity, and their modulatory effect on lipid metabolism and adipocyte differentiation. In addition, they contribute to the suppression of inflammation and apoptosis and to the improvement of endothelial function, a key factor in the prevention of cardiovascular disease. Hesperidin, for example, acts by inhibiting phosphodiesterase and increasing intracellular cAMP, which leads to a reduction in the production of inflammatory prostaglandins and thromboxane B2. This action is crucial for its anti-inflammatory effects and for reducing platelet aggregation, helping to prevent thrombus formation. Preliminary clinical research has shown that daily intake of 500 mg of hesperidin increases flow-mediated dilation, indicating an improvement in endothelial function in patients with metabolic syndrome, in addition to reducing inflammatory biomarkers such as C-reactive protein.

Usages associés

Antimicrobial

Studies have shown that bioflavonoids possess significant antimicrobial activity, particularly against various viruses and bacteria. This activity is mainly due to non-glycosylated compounds, and the presence of a hydroxyl group at position 3 is essential for antiviral activity. 40-hydroxy-3-methoxy flavones have demonstrated efficacy against rhinoviruses and polioviruses. The structure of these flavonoids, notably multiple substitution on the A ring, is crucial for their superior antiviral activity. Quercetin and hesperidin, for example, inhibit the replication of several viruses, including herpes simplex and poliovirus. However, not all flavonoids exert this activity; grapefruit naringenin, for example, has not shown this efficacy.

Neurological

Bioflavonoids, such as hesperidin, demonstrate notable neuroprotective potential, particularly relevant for neurodegenerative disorders like Parkinson's and Alzheimer's disease. Hesperidin protects against hydrogen peroxide-induced neurotoxicity in a laboratory model. It acts by attenuating behavioral alterations, oxidative stress, and dysfunctions of mitochondrial enzyme complexes, possibly via a nitric oxide-related mechanism. In the context of Parkinson's disease, hesperidin improves vascular tone and reduces stasis, contributing to the normalization of capillary permeability and lymphatic drainage, which is crucial for modulating inflammatory responses in the brain. It also inhibits phosphodiesterase, thereby increasing intracellular cAMP, which reduces the production of inflammatory prostaglandins and thromboxane, key molecules in the inflammatory and coagulation processes associated with neurodegeneration. Furthermore, hesperidin has shown positive effects on endothelial function, which is essential for preventing cardiovascular complications often associated with neurodegenerative diseases. It also helps modulate leukocyte gene expression, which could contribute to its anti-atherogenic and cardioprotective effects, thereby reducing the risk of progression of neurodegenerative diseases. By regulating glutathione (GSH) levels, glutathione peroxidase (GPx) and catalase activities, and preventing the formation of reactive oxygen species, hesperidin could help prevent the depletion of dopamine and its metabolites, which is critical in diseases such as Parkinson's.