BACKGROUND Mental stress (MS) is related to endothelial dysfunction in overweight/obese men. It is believed that the pro-oxidant profile, associated with an imbalance in the vascular remodeling process, may contribute to deleterious effects of MS on endothelial function. However, it is unknown whether administration of ascorbic acid (AA), a potent antioxidant, can prevent oxidative and remodeling dysfunction during MS in these subjects. METHODS Fourteen overweight/obese grade I men (27 ± 7 years; 29.7 ± 2.6 kg·m-2) underwent the Stroop Color Word Test for 5 min to induce MS after AA (3 g) or placebo (PL, 0.9% NaCl) intravenous infusions. Venous blood samples were collected at baseline and the last minute of MS to measure nitrite concentration (chemiluminescence), protein carbonylation, thiobarbituric acid reactive substances (TBARS) and catalase activity (colorimetric assays), superoxide dismutase (SOD; immunoenzymatic assay), activities of active/inactive (pro) forms of metalloproteinases-9 and -2 (MMP; zymography) and its respective tissue inhibitors concentration (TIMP-1 and TIMP-2; immunoenzymatic assays). RESULTS At baseline, MMP-9 activity (p < 0.01), the MMP-9/proMMP-9 ratio (p = 0.02) and TIMP-1 concentration (p = 0.05) were reduced, whereas proMPP-9 activity was increased (p = 0.02) after AA compared to PL infusion. After PL infusion, MS increased protein carbonylation (p < 0.01), catalase (p < 0.01), and the MMP-9/proMMP-9 ratio (p = 0.04) when compared to baseline. AA infusion reduced protein carbonylation (p = 0.02), MMP-9 activity (p < 0.01), and MMP-9/pro-MMP-9 ratio (p < 0.01), while SOD (p = 0.04 vs baseline), proMPP-9 (p < 0.01 vs PL), MMP-2 (p < 0.01 vs PL) and TIMP-2 (p = 0.02 vs baseline) remained elevated during MS. CONCLUSIONS AA appears to minimize the oxidative imbalance and vascular remodeling induced by MS.

中文翻译：

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抗坏血酸抑制超重/肥胖男性精神压力引起的血管重塑。

背景技术精神压力（MS）与超重/肥胖男性中的内皮功能障碍有关。相信与血管重塑过程中的不平衡有关的促氧化剂特征可能有助于MS对内皮功能的有害作用。然而，尚不清楚在这些受试者中，抗坏血酸（AA）（一种有效的抗氧化剂）的使用是否能预防MS期间的氧化和重塑功能障碍。方法对14名超重/肥胖I级男性（27±7岁； 29.7±2.6 kg·m-2）进行了Stroop彩色文字测试5分钟，以AA（3 g）或安慰剂（PL，0.9％NaCl）诱导MS静脉输液。在基线和MS的最后一分钟收集静脉血样本，以测量亚硝酸盐浓度（化学发光），蛋白质羰基化，硫代巴比妥酸反应性物质（TBARS）和过氧化氢酶活性（比色测定），超氧化物歧化酶（SOD;免疫酶测定），金属蛋白酶9和-2的活性/非活性（pro）形式的活性（MMP;酶谱）及其各自的组织抑制剂浓度（TIMP-1和TIMP-2；免疫酶分析）。结果在基线时，MMP-9活性（p <0.01），MMP-9 / proMMP-9比（p = 0.02）和TIMP-1浓度（p = 0.05）降低，而proMPP-9活性增加（p （= 0.02）AA后与PL输注相比。与基线相比，输注PL后，MS可增加蛋白质羰基化（p <0.01），过氧化氢酶（p <0.01）和MMP-9 / proMMP-9比率（p = 0.04）。AA注入可减少蛋白质羰基化（p = 0.02），MMP-9活性（p <0.01）和MMP-9 / pro-MMP-9比率（p <0.01），而SOD（p = 0）。MS期间，proMPP-9（相对于基线为04），proMPP-9（相对于PL为p <0.01），MMP-2（相对于PL为p <0.01）和TIMP-2（相对于基线p = 0.02）仍然升高。结论AA似乎可以最大程度地减少MS引起的氧化失衡和血管重塑。