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t-BHQ Protects Against Oxidative Damage and Maintains the Antioxidant Response in Malnourished Rats

OBJECTIVE: Tert-butylhydroquinone (t-BHQ) protective effect against oxidative damage in thymus from malnourished pops-rats was evaluated. METHODS: Malnutrition in pops-rats was induced during the lactation period and first-, second-, and third-degree malnourished rats were studied (MN1, MN2, and MN3...

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Detalles Bibliográficos
Autores principales: Gavia-García, Graciela, Rosas-Trejo, María de los Ángeles, García-Mendoza, Eduardo, Toledo-Pérez, Rafael, Königsberg, Mina, Nájera-Medina, Oralia, Luna-López, Armando, González-Torres, María Cristina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6156215/
https://www.ncbi.nlm.nih.gov/pubmed/30263018
http://dx.doi.org/10.1177/1559325818796304
Descripción
Sumario:OBJECTIVE: Tert-butylhydroquinone (t-BHQ) protective effect against oxidative damage in thymus from malnourished pops-rats was evaluated. METHODS: Malnutrition in pops-rats was induced during the lactation period and first-, second-, and third-degree malnourished rats were studied (MN1, MN2, and MN3). To determine t-BHQ protective effect, lipid peroxidation (LPx) was assessed, as well as the carbonyl content. The reduced glutathione and glutathione disulfide content were determined and antioxidant enzyme activities were measured. RESULTS: Oxidative protein damage, LPx, and Nuclear Factor-κB (NF-κB) content, increased in the MN2 and MN3 compared to well-nourished rats, associated with lower protein content and antioxidant activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase. Tert-butylhydroquinone treatment induced a protective effect against lipids and proteins oxidative damage, as well as decrease in NF-κB in MN rats and restored the antioxidant mechanisms, mostly GPx and SOD. No differences were found between male and female animals. CONCLUSIONS: Results show that higher body weight deficit leads to increased oxidative damage and probably inflammation, attributable to alterations in antioxidant mechanisms. These effects were reversed by the t-BHQ-treatment, which restores the antioxidant response. Our findings suggest that t-BHQ could be an interesting pharmacological intervention, but it needs to be studied further.