Adaeva OI et al. (2026), Apiol from Parsley Seeds as a Source for the Sy...

ECB-ART-55017

ACS Omega 2026 Apr 12;1118:26195-26205. doi: 10.1021/acsomega.5c09328.

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Apiol from Parsley Seeds as a Source for the Synthesis of Coenzyme Q0 Propanoic Acid Conjugates with Amines Featuring Antioxidant Activity.

Adaeva OI, Demchuk DV, Shevchenko OG, Semenova MN, Semenov VV.

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Quinone-containing compounds are known for their free-radical scavenging activity and pronounced antioxidant properties. They could be promising for the alleviation of progressive neuronal damage in neurodegenerative diseases, caused in particular by oxidative stress. In this study, coenzyme Q0 derivatives featuring the fragment of natural quinone propanoic acid conjugated with dopamine, 5-methoxytryptamine, β-alanine, and γ-aminobutyric acid were synthesized. Apiol, the main metabolite of parsley seed extract, was used as a starting material. The aim of this study was to explore antioxidant activity of the targeted compounds in vitro using several assays, including determination of free radical scavenging capacity, inhibition of lipid peroxidation in mouse brain homogenate, and evaluation of toxicity and membrane-protective effects in mouse red blood cells (RBCs). All conjugates of the quinone propanoic acid fragment demonstrated significant antioxidant activity. The free radical scavenging capacity of the compounds in DPPH and ABTS tests was associated with the presence and amount of unsubstituted OH groups in the aromatic ring. The dopamine derivative was identified as the most potent inhibitor of both oxidative mouse RBC hemolysis and intracellular generation of reactive oxygen species. The 5-methoxytryptamine quinone derivative considerably suppressed Fe2+/ascorbate-initiated lipid peroxidation in the mouse brain homogenate. All compounds showed no toxicity on a sea urchin embryo model and could be considered potential neuroprotective agents due to the antioxidant properties of the quinone fragment and facile cleavage of the labile amide bond, thereby providing the targeted delivery of biogenic amines into the desired location.

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	1. Coenzyme Q0 derivatives.
	1. Oxidative Transformation of Lactone (7) with Methylamine
	2. Synthesis of CoQ0 Propanoic Acid Derivatives Conjugated with Biogenic Amines and Amino Acids
	2. Effect of compounds 2, 3, 6a–e, and 16 at 100 μM concentration on TBARS accumulation in mouse brain homogenate. TBARS concentration was measured at 1 h after the initiation of lipid peroxidation by Fe2+/ascorbate. Control: sample without test compounds. Intact: sample without initiation of Fe2+/ascorbate peroxidation. Vertical bars: mean ± SE (n = 4–20).
	3. Hemolytic activity (erythrotoxicity) of quinone derivatives 2, 3, 6a–e, and 16 (10 μM) after 1, 3, and 5 h of incubation. Control: RBC without test compounds. Vertical bars: mean ± SE (n = 3–9).
	4. Effect of quinones 2 and 3 (20 μM) on ROS generation, metHb/oxyHb ratio, and ferrylHb/oxyHb ratio in mouse RBC after 1 h incubation. Vertical bars: mean ± SE (n = 6–12).
	5. Effect of quinone derivatives 6a–e and 16 (10 μM) on mouse RBC hemolysis under oxidative stress induced by H2O2 (A) and AAPH (B) after 1–5 h incubation. Control: RBC without test compounds. Vertical bars: mean ± SE (n = 4–5).
	6. Effect of quinone derivatives 6a–e and 16 (10 μM) on metHb/oxyHb and ferrylHb/oxyHb ratio in mouse RBC under AAPH-induced hemolysis after 5 h incubation. Control: RBC without test compounds. Vertical bars: mean ± SE (n = 10–12).
	7. Effect of compounds 6a–e and 16 (20 μM) on AAPH-induced intracellular ROS generation in mouse RBC (CAA-RBC assay). Intact: RBC without compounds and ROS initiator. The results were calculated as % of control (ROS production in AAPH-treated RBC without test compounds). Vertical bars: mean ± SE (n = 12–24).