Isoflavones prevent oxidative stress and inhibit the activity of the enzyme monoamine oxidase in vitro
Oxidative stress occurs due to an imbalance between antioxidant defenses and pro-oxidant agents in brain. This condition has been associated to the pathogenesis of several brain diseases; therefore, increasing the use of compounds that exert antioxidant activity. Thus, the objective of this study was to evaluate, in vitro, the effect of isoflavones in: (1) lipid peroxidation, catalase activity and thiol groups in the presence of pro-oxidants: sodium nitroprusside or Fe2+/EDTA complex in rat brain homogenates; (2) the activity of the enzyme monoamine oxidase (MAO). As a result, the isoflavones reduced lipid peroxidation in a manner dependent on the concentration and protected against the reduction of catalase activity as well as the induced thiol oxidation in brain tissue. In addition, isoflavones inhibited MAO activity (MAO-A and MAO-B). Taken together, our results showed that isoflavones avoided oxidative stress and decreased the MAO activity, suggesting a promissory use in the treatment of neurodegenerative diseases.
KeywordsOxidative stress Isoflavones Antioxidant Monoamine oxidase
We acknowledge fellowships from CNPq (R.F.) and CAPES (L.F.S., A.B., C.M.F, L.R.P).
This study was financed in part by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil (CAPES) - Finance Code 001, and CAPES/PROEX (23038.005848/2018-31; support number: 0737/2018). Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul – FAPERGS/Brazil (2080–2551/13-5-PqG-001/2013) and Conselho Nacional de Desenvolvimento Científico e Tecnológico – CNPq/Brazil (475210/2013-1).
Compliance with ethical standards
Conflict of interest
Authors declare that they do not hold any conflict of interest.
All applicable international, national, and/or institutional guidelines for the care and use of animals were followed.
- 6.Silva JP, Coutinho OP (2010) Free radicals in the regulation of damage and cell death—basic mechanisms and prevention. Drug Discov Ther 4:144–167Google Scholar
- 7.Cohen G (1988) Oxygen radicals and Parkinson’s disease. In: Halliwell B (ed) Oxygen Radicals and Tissue Injury. FASEB, Bethesda, pp 130–135Google Scholar
- 12.Pereira RP, Fachinetto R, Souza AP, Puntel RL, Santos GNS, Heinzmann BM, Boschetti TK, Athayde ML, Burger ME, Morel AF, Morsch VM, Rocha JB (2008) Antioxidant effects of different extracts from Melissa officinalis, Matricaria recutita and Cymbopogon citrates. Neurochem Res 34:973–983CrossRefGoogle Scholar
- 21.Takimoto CH, Glover K, Huang X, Hayes SA, Gallot L, Quinn M, Jovanovic BD, Shapiro A, Hernandez L, Goetz A, Llorens V, Lieberman R, Crowell JA, Poisson BA, Bergan RC (2003) Phase I pharmacokinetic and pharmacodynamic analysis of unconjugated soy isoflavones administered to individuals with cancer. Cancer Epidemiol Biomark Prev 12:1213–1221Google Scholar
- 23.Aebi H (1984) Catalase in vitro methods enzymol. Academic Press 105:121–126Google Scholar
- 37.Graf E, Mahoney JR, Bryant RG, Eaton JW (1984) Iron catalyzed hydroxyl radical formation: stringent requirement for free iron coordination site. J Biol Chem 259:3620–3624Google Scholar
- 39.Halliwell B, Gutteridge JMC (1989) Lipid peroxidation: a radical chain reaction. Free Radic Biol Med. 2nd Edition Clarendon Press, OxfordGoogle Scholar
- 47.Boadi WY, Thaire L, Kerem D, Yannai S (1991) Effects of dietary factors on antioxidant enzymes in rats exposed to hyperbaric oxygen. Vet Hum Toxicol 33:105–109Google Scholar
- 51.Seif-El-Nasr M, Amina SA, Rania MA (2008) Effect of MAO-B inhibition against ischemia-induced oxidative stress in the rat brain. Drug Res 58:160–167Google Scholar