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

机译:t-BHQ可保护营养不良的大鼠免受氧化损伤并维持其抗氧化反应

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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.
机译:评估了叔丁基对苯二酚(t-BHQ)对营养不良的持久性有机污染物大鼠胸腺中氧化损伤的保护作用。在哺乳期期间,在持久性有机污染物大鼠中引起营养不良,并研究了一级,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。测定还原的谷胱甘肽和谷胱甘肽二硫化物含量并测量抗氧化酶活性。与营养丰富的大鼠相比,MN2和MN3中的氧化蛋白损伤,LPx和核因子-κB(NF-κB)含量增加,与较低的蛋白含量和超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GPx)的抗氧化活性相关)和过氧化氢酶。叔丁基氢醌处理诱导了对脂质和蛋白质氧化损伤的保护作用,以及MN大鼠中NF-κB的降低,并恢复了抗氧化剂机制,主要是GPx和SOD。雄性和雌性动物之间没有发现差异。结果表明,较高的体重不足会导致氧化损伤增加,并可能引起炎症,这归因于抗氧化剂机制的改变。通过t-BHQ处理可逆转这些作用,从而恢复抗氧化反应。我们的发现表明,t-BHQ可能是一种有趣的药理干预措施,但需要进一步研究。

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