Gossypitrin, a naturally occurring flavonoid, attenuates iron-induced neuronal and mitochondrial damage
| dc.contributor.author | Bécquer Viart, María Ángeles | |
| dc.contributor.author | Armentero López, Adonis | |
| dc.contributor.author | Alvarez Almiñaque, Daniel | |
| dc.contributor.author | Fernández Acosta, Roberto | |
| dc.contributor.author | Matos Peralta, Yasser | |
| dc.contributor.author | D’Vries, Richard F. | |
| dc.contributor.author | Marín Prida, Javier | |
| dc.contributor.author | Pardo Andreu, Gilberto L. | |
| dc.date.accessioned | 2025-07-14T15:25:02Z | |
| dc.date.available | 2025-07-14T15:25:02Z | |
| dc.date.issued | 2021 | |
| dc.description.abstract | The disruption of iron homeostasis is an important factor in the loss of mitochondrial function in neural cells, leading to neurodegeneration. Here, we assessed the protective action of gossypitrin (Gos), a naturally occurring flavonoid, on iron-induced neuronal cell damage using mouse hippocampal HT-22 cells and mitochondria isolated from rat brains. Gos was able to rescue HT22 cells from the damage induced by 100 µM Fe(II)-citrate (EC50 8.6 µM). This protection was linked to the prevention of both iron-induced mitochondrial membrane potential dissipation and ATP depletion. In isolated mitochondria, Gos (50 µM) elicited an almost complete protection against iron-induced mitochondrial swelling, the loss of mitochondrial transmembrane potential and ATP depletion. Gos also prevented Fe(II)-citrate-induced mitochondrial lipid peroxidation with an IC50 value (12.45 µM) that was about nine time lower than that for the tert-butylhydroperoxide-induced oxidation. Furthermore, the flavonoid was effective in inhibiting the degradation of both 15 and 1.5 mM 2-deoxyribose. It also decreased Fe(II) concentration with time, while increasing O2 consumption rate, and impairing the reduction of Fe(III) by ascorbate. Gos-Fe(II) complexes were detected by UV-VIS and IR spectroscopies, with an apparent Gos-iron stoichiometry of 2:1. Results suggest that Gos does not generally act as a classical antioxidant, but it directly affects iron, by maintaining it in its ferric form after stimulating Fe(II) oxidation. Metal ions would therefore be unable to participate in a Fenton-type reaction and the lipid peroxidation propagation phase. Hence, Gos could be used to treat neuronal diseases associated with iron-induced oxidative stress and mitochondrial damage. | |
| dc.identifier.citation | Bécquer-Viart, M. Á., Armentero-López, A., Alvarez-Almiñaque, D., Fernández-Acosta, R., Matos-Peralta, Y., D’Vries, R. F., Marín-Prida, J., & Pardo-Andreu, G. L. (2021). Gossypitrin, a naturally occurring flavonoid, attenuates iron-induced neuronal and mitochondrial damage. Molecules, 26(11). https://doi.org/10.3390/MOLECULES26113364 | |
| dc.identifier.issn | 14203049 | |
| dc.identifier.uri | https://repositorio.usc.edu.co/handle/20.500.12421/7430 | |
| dc.language.iso | en | |
| dc.subject | Gossypitrin | |
| dc.subject | HT-22 cells | |
| dc.subject | Iron | |
| dc.subject | Mitochondria | |
| dc.subject | Neurodegeneration | |
| dc.subject | Neuroprotection | |
| dc.title | Gossypitrin, a naturally occurring flavonoid, attenuates iron-induced neuronal and mitochondrial damage | |
| dc.type | Article |