LA HYPEROXIA DESENCADENA UMA RESPUESTA REDOX BIFÁSICA QUE CONDUCE AL DETERIORO COGNITIVO EM RATONES ADULTOS

Autores/as

  • Ana Luiza Sciandretti de Albuquerque Autor/a
  • Iara Mariana Léllis Ribeiro Autor/a
  • Kenzawin Adliz Pereira Autor/a
  • Thalles de Freitas Castro Autor/a
  • Andressa Aparecida Batista Cota Autor/a
  • Karen del Carmen Barboza Salgado Autor/a
  • Laser Antônio Machado de Oliveira Autor/a
  • Frank Silva Bezerra Autor/a
  • Daiane Fátima Engel Autor/a
  • Katiane de Oliveira Pinto Coelho Nogueira Autor/a

DOI:

https://doi.org/10.56238/arev8n5-130

Palabras clave:

Hiperoxia, Cerebro, Memoria, Comportamiento, Estrés Oxidativo

Resumen

Las especies reactivas de oxígeno (EROs) son subproductos naturales del metabolismo aeróbico y aumentan en condiciones de estrés oxidativo y lesión cerebral. La oxigenoterapia normobárica con 100% de oxígeno se utiliza ampliamente en trastornos neurológicos; sin embargo, la exposición excesiva al O₂ puede comprometer las defensas antioxidantes y contribuir a déficits cognitivos. Este estudio investigó los efectos de la hiperoxia continua sobre la memoria y el equilibrio redox hipocampal en ratones machos adultos C57BL/6. Los animales fueron expuestos a hiperoxia durante 12 o 24 h y evaluados mediante la prueba de reconocimiento de objeto nuevo (NOR). Se analizaron las actividades de superóxido dismutasa (SOD) y catalasa (CAT), además de los niveles de glutatión reducido (GSH) y malondialdehído (MDA). La exposición durante 24 h deterioró la memoria y aumentó los niveles de GSH, mientras que la actividad de SOD y los niveles de MDA se alteraron tras 12 y 24 h. En conjunto, estos hallazgos demuestran que 24 h de exposición al 100% de oxígeno inducen desequilibrio redox hipocampal, potencialmente contribuyendo al daño neuronal y al deterioro de la memoria.

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Referencias

Aebi, H. (1984). Catalase in vitro. In S. P. Colowick & N. O. Kaplan (Eds.), Methods in Enzymology (Vol. 105, pp. 121–126). Academic Press. https://doi.org/10.1016/S0076-6879(84)05016-3 DOI: https://doi.org/10.1016/S0076-6879(84)05016-3

Alva, R., et al. (2023). Oxygen toxicity: Cellular mechanisms in normobaric hyperoxia. Cell Biology and Toxicology, 39(1), 111–143. https://doi.org/10.1007/s10565-022-09689-4 DOI: https://doi.org/10.1007/s10565-022-09773-7

Barbosa, K. B. F., et al. (2010). Oxidative stress: Concept, implications and modulating factors. Revista de Nutrição, 23(4), 629–643. https://doi.org/10.1590/S1415-52732010000400013 DOI: https://doi.org/10.1590/S1415-52732010000400013

Bezerra, F. S., et al. (2019). Exogenous surfactant prevents hyperoxia-induced lung injury in adult mice. Intensive Care Medicine Experimental, 7(1), 53. https://doi.org/10.1186/s40635-019-0261-6 DOI: https://doi.org/10.1186/s40635-019-0233-6

Bradford, M. M. (1976). A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Analytical Biochemistry, 72, 248–254. https://doi.org/10.1016/0003-2697(76)90527-3 DOI: https://doi.org/10.1016/0003-2697(76)90527-3

Brehmer, F., et al. (2012). Interaction of inflammation and hyperoxia in a rat model of neonatal white matter damage. PLoS One, 7(11). https://doi.org/10.1371/journal.pone.0049023 DOI: https://doi.org/10.1371/journal.pone.0049023

Buege, J. A., & Aust, S. D. (1978). Microsomal lipid peroxidation. In S. Fleischer & L. Packer (Eds.), Methods in Enzymology (Vol. 52, pp. 302–310). Academic Press. https://doi.org/10.1016/S0076-6879(78)52032-6 DOI: https://doi.org/10.1016/S0076-6879(78)52032-6

De Paula, G. C., et al. (2021). Hippocampal function is impaired by a short-term high-fat diet in mice: Increased blood–brain barrier permeability and neuroinflammation as triggering events. Frontiers in Neuroscience, 15, 748632. https://doi.org/10.3389/fnins.2021.748632 DOI: https://doi.org/10.3389/fnins.2021.734158

Halliwell, B., & Gutteridge, J. M. C. (2015). Free radicals in biology and medicine (5th ed.). Oxford University Press. DOI: https://doi.org/10.1093/acprof:oso/9780198717478.001.0001

Huang, R. R., et al. (2015). Chronic restraint stress promotes learning and memory impairment due to enhanced neuronal endoplasmic reticulum stress in the frontal cortex and hippocampus in male mice. International Journal of Molecular Medicine, 35(2), 553–559. https://doi.org/10.3892/ijmm.2014.2040 DOI: https://doi.org/10.3892/ijmm.2014.2026

Ighodaro, O. M., & Akinloye, O. A. (2018). First line defence antioxidants—Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX): Their fundamental role in the entire antioxidant defence grid. Alexandria Journal of Medicine, 54(4), 287–293. https://doi.org/10.1016/j.ajme.2017.09.001 DOI: https://doi.org/10.1016/j.ajme.2017.09.001

Invitrogen (ThermoFisher Scientific). (2017). Glutathione colorimetric detection kit product information sheet. https://www.thermofisher.com/us/en/home/global/terms-and-conditions.html

Ishida, Y., et al. (2021). ORi™: A new indicator of oxygenation. Journal of Anesthesia, 35(5), 734–740. https://doi.org/10.1007/s00540-021-02936-7 DOI: https://doi.org/10.1007/s00540-021-02938-4

Körpinar, S., & Uzun, H. (2019). The effects of hyperbaric oxygen at different pressures on oxidative stress and antioxidant status in rats. Medicina, 55(5), 215. https://doi.org/10.3390/medicina55050215 DOI: https://doi.org/10.3390/medicina55050205

Machado, R. S., et al. (2022). Hyperoxia by short-term promotes oxidative damage and mitochondrial dysfunction in rat brain. Respiratory Physiology & Neurobiology, 306, 103929. https://doi.org/10.1016/j.resp.2022.103929

Marklund, S., & Marklund, G. (1974). Involvement of the superoxide anion radical in the autoxidation of pyrogallol and a convenient assay for superoxide dismutase. European Journal of Biochemistry, 47(3), 469–474. https://doi.org/10.1111/j.1432-1033.1974.tb03714.x DOI: https://doi.org/10.1111/j.1432-1033.1974.tb03714.x

Nagato, A. C., et al. (2012). Time course of inflammation, oxidative stress and tissue damage induced by hyperoxia in mouse lungs. International Journal of Experimental Pathology, 93(4), 269–278. https://doi.org/10.1111/j.1365-2613.2012.00822.x DOI: https://doi.org/10.1111/j.1365-2613.2012.00823.x

Ni, Y. N., et al. (2019). The effect of hyperoxia on mortality in critically ill patients: A systematic review and meta-analysis. BMC Pulmonary Medicine, 19(1), 53. https://doi.org/10.1186/s12890-019-0812-9 DOI: https://doi.org/10.1186/s12890-019-0810-1

Pei, J., et al. (2023). Research progress of glutathione peroxidase family (GPX) in redoxidation. Frontiers in Pharmacology, 14, 1165945. https://doi.org/10.3389/fphar.2023.1165945 DOI: https://doi.org/10.3389/fphar.2023.1147414

Perrone, S., Laschi, E., & Buonocore, G. (2020). Oxidative stress biomarkers in the perinatal period: Diagnostic and prognostic value. Seminars in Fetal and Neonatal Medicine, 25(6), 101087. https://doi.org/10.1016/j.siny.2020.101087 DOI: https://doi.org/10.1016/j.siny.2020.101087

Schneider, E., et al. (2021). Larger capacity for unconscious versus conscious episodic memory. Current Biology, 31(16), 3551–3563.e9. https://doi.org/10.1016/j.cub.2021.06.038 DOI: https://doi.org/10.1016/j.cub.2021.06.012

Shin, H. K., et al. (2007). Normobaric hyperoxia improves cerebral blood flow and oxygenation, and inhibits peri-infarct depolarizations in experimental focal ischaemia. Brain, 130(6), 1631–1642. https://doi.org/10.1093/brain/awm092 DOI: https://doi.org/10.1093/brain/awm071

Shrestha, P., & Klann, E. (2016). Lost memories found. Nature, 531(7595), 450–451. https://doi.org/10.1038/531450a DOI: https://doi.org/10.1038/nature17312

Yusa, T., et al. (1987). Hyperoxia increases H2O2 production by brain in vivo. Journal of Applied Physiology, 63(1), 353–358. https://doi.org/10.1152/jappl.1987.63.1.353 DOI: https://doi.org/10.1152/jappl.1987.63.1.353

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Publicado

2026-05-27

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Cómo citar

DE ALBUQUERQUE, Ana Luiza Sciandretti et al. LA HYPEROXIA DESENCADENA UMA RESPUESTA REDOX BIFÁSICA QUE CONDUCE AL DETERIORO COGNITIVO EM RATONES ADULTOS. ARACÊ , [S. l.], v. 8, n. 5, p. e13282, 2026. DOI: 10.56238/arev8n5-130. Disponível em: https://periodicos.newsciencepubl.com/arace/article/view/13282. Acesso em: 29 may. 2026.