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Selenium-induced antioxidant protection recruits modulation of thioredoxin reductase during excitotoxic/pro-oxidant events in the rat striatum.
Neurochem Int. 2012 Jul; 61(2):195-206.NI

Abstract

Selenium (Se) is a crucial element exerting antioxidant and neuroprotective effects in different toxic models. It has been suggested that Se acts through selenoproteins, of which thioredoxin reductase (TrxR) is relevant for reduction of harmful hydroperoxides and maintenance of thioredoxin (Trx) redox activity. Of note, the Trx/TrxR system remains poorly studied in toxic models of degenerative disorders. Despite previous reports of our group have demonstrated a protective role of Se in the excitotoxic/pro-oxidant model induced by quinolinic acid (QUIN) in the rat striatum (Santamaría et al., 2003, 2005), the precise mechanism(s) by which Se is inducing protection remains unclear. In this work, we characterized the time course of protective events elicited by Se as pretreatment (Na(2)SO(3), 0.625 mg/kg/day, i.p., administered for 5 consecutive days) in the toxic pattern produced by a single infusion of QUIN (240 nmol/μl) in the rat striatum, to further explore whether TrxR is involved in the Se-induced protection and how is regulated. Se attenuated the QUIN-induced early reactive oxygen species formation, lipid peroxidation, oxidative damage to DNA, loss of mitochondrial reductive capacity and morphological alterations in the striatum. Our results also revealed a novel pattern in which QUIN transiently stimulated an early TrxR cellular localization/distribution (at 30 min and 2 h post-lesion, evidenced by immunohistochemistry), to further stimulate a delayed protein activation (at 24 h) in a manner likely representing a compensatory response to the oxidative damage in course. In turn, Se induced an early stimulation of TrxR activity and expression in a time course that "matches" with the reduction of the QUIN-induced oxidative damage, suggesting that the Trx/TrxR system contributes to the resistance of nerve tissue to QUIN toxicity.

Authors+Show Affiliations

Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía, Mexico 14269, Mexico.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22579569

Citation

Maldonado, Perla D., et al. "Selenium-induced Antioxidant Protection Recruits Modulation of Thioredoxin Reductase During Excitotoxic/pro-oxidant Events in the Rat Striatum." Neurochemistry International, vol. 61, no. 2, 2012, pp. 195-206.
Maldonado PD, Pérez-De La Cruz V, Torres-Ramos M, et al. Selenium-induced antioxidant protection recruits modulation of thioredoxin reductase during excitotoxic/pro-oxidant events in the rat striatum. Neurochem Int. 2012;61(2):195-206.
Maldonado, P. D., Pérez-De La Cruz, V., Torres-Ramos, M., Silva-Islas, C., Lecona-Vargas, R., Lugo-Huitrón, R., Blanco-Ayala, T., Ugalde-Muñiz, P., Vázquez-Cervantes, G. I., Fortoul, T. I., Ali, S. F., & Santamaría, A. (2012). Selenium-induced antioxidant protection recruits modulation of thioredoxin reductase during excitotoxic/pro-oxidant events in the rat striatum. Neurochemistry International, 61(2), 195-206. https://doi.org/10.1016/j.neuint.2012.05.004
Maldonado PD, et al. Selenium-induced Antioxidant Protection Recruits Modulation of Thioredoxin Reductase During Excitotoxic/pro-oxidant Events in the Rat Striatum. Neurochem Int. 2012;61(2):195-206. PubMed PMID: 22579569.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Selenium-induced antioxidant protection recruits modulation of thioredoxin reductase during excitotoxic/pro-oxidant events in the rat striatum. AU - Maldonado,Perla D, AU - Pérez-De La Cruz,Verónica, AU - Torres-Ramos,Mónica, AU - Silva-Islas,Carlos, AU - Lecona-Vargas,Ramón, AU - Lugo-Huitrón,Rafael, AU - Blanco-Ayala,Tonali, AU - Ugalde-Muñiz,Perla, AU - Vázquez-Cervantes,Gustavo Ignacio, AU - Fortoul,Teresa I, AU - Ali,Syed F, AU - Santamaría,Abel, Y1 - 2012/05/09/ PY - 2011/12/31/received PY - 2012/03/28/revised PY - 2012/05/01/accepted PY - 2012/5/15/entrez PY - 2012/5/15/pubmed PY - 2012/12/12/medline SP - 195 EP - 206 JF - Neurochemistry international JO - Neurochem Int VL - 61 IS - 2 N2 - Selenium (Se) is a crucial element exerting antioxidant and neuroprotective effects in different toxic models. It has been suggested that Se acts through selenoproteins, of which thioredoxin reductase (TrxR) is relevant for reduction of harmful hydroperoxides and maintenance of thioredoxin (Trx) redox activity. Of note, the Trx/TrxR system remains poorly studied in toxic models of degenerative disorders. Despite previous reports of our group have demonstrated a protective role of Se in the excitotoxic/pro-oxidant model induced by quinolinic acid (QUIN) in the rat striatum (Santamaría et al., 2003, 2005), the precise mechanism(s) by which Se is inducing protection remains unclear. In this work, we characterized the time course of protective events elicited by Se as pretreatment (Na(2)SO(3), 0.625 mg/kg/day, i.p., administered for 5 consecutive days) in the toxic pattern produced by a single infusion of QUIN (240 nmol/μl) in the rat striatum, to further explore whether TrxR is involved in the Se-induced protection and how is regulated. Se attenuated the QUIN-induced early reactive oxygen species formation, lipid peroxidation, oxidative damage to DNA, loss of mitochondrial reductive capacity and morphological alterations in the striatum. Our results also revealed a novel pattern in which QUIN transiently stimulated an early TrxR cellular localization/distribution (at 30 min and 2 h post-lesion, evidenced by immunohistochemistry), to further stimulate a delayed protein activation (at 24 h) in a manner likely representing a compensatory response to the oxidative damage in course. In turn, Se induced an early stimulation of TrxR activity and expression in a time course that "matches" with the reduction of the QUIN-induced oxidative damage, suggesting that the Trx/TrxR system contributes to the resistance of nerve tissue to QUIN toxicity. SN - 1872-9754 UR - https://www.unboundmedicine.com/medline/citation/22579569/Selenium_induced_antioxidant_protection_recruits_modulation_of_thioredoxin_reductase_during_excitotoxic/pro_oxidant_events_in_the_rat_striatum_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-0186(12)00164-7 DB - PRIME DP - Unbound Medicine ER -