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
Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana-Iztapalapa, CDMX, Mexico.
Posgrado en Biología Experimental, Universidad Autónoma Metropolitana-Iztapalapa, CDMX, Mexico.
Dose Response. 2018 Sep 25;16(3):1559325818796304. doi: 10.1177/1559325818796304. eCollection 2018 Jul-Sep.
Tert-butylhydroquinone (t-BHQ) protective effect against oxidative damage in thymus from malnourished pops-rats was evaluated.
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.
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.
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.
评估叔丁基对苯二酚(t-BHQ)对营养不良的断奶大鼠胸腺氧化损伤的保护作用。
在哺乳期诱导断奶大鼠营养不良,研究一级、二级和三级营养不良的大鼠(MN1、MN2和MN3)。为了确定t-BHQ的保护作用,评估了脂质过氧化(LPx)以及羰基含量。测定了还原型谷胱甘肽和谷胱甘肽二硫化物的含量,并测量了抗氧化酶活性。
与营养良好的大鼠相比,MN2和MN3组的氧化蛋白损伤、LPx和核因子κB(NF-κB)含量增加,同时超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)和过氧化氢酶的蛋白含量及抗氧化活性降低。叔丁基对苯二酚处理对MN大鼠的脂质和蛋白质氧化损伤具有保护作用,并降低了NF-κB水平,恢复了抗氧化机制,主要是GPx和SOD。在雄性和雌性动物之间未发现差异。
结果表明,较高的体重不足会导致氧化损伤增加,可能还会引发炎症,这归因于抗氧化机制的改变。t-BHQ处理可逆转这些影响,恢复抗氧化反应。我们的研究结果表明,t-BHQ可能是一种有趣的药物干预手段,但需要进一步研究。