Chronic heart failure (HF) is an important clinical, social, and economic problem. A key role in HF progression is played by oxidative stress. Free oxygen radicals, formed under the conditions of hypoxia and reperfusion, participate in myocardial stunning and other forms of post-reperfusion damage. HF patients also suffer from disorders connected with saliva secretion. However, still little is known about the mechanisms that impair the secretory function of salivary glands in these patients. In the presented study, we were the first to compare the antioxidant barrier, protein glycoxidation, and nitrosative/nitrative stress in non-stimulated (non-stimulated whole saliva (NWS)) and stimulated (SWS) saliva of HF patients. The study included 50 HF patients with normal saliva (NS) secretion (n = 27) and hyposalivation (HS) (n = 23), as well as an age- and gender-matched control group (n = 50). We demonstrated that, in NWS of HF patients with HS, the concentration of low-molecular-weight non-enzymatic antioxidants decreased (↓total polyphenols, ↓ascorbic acid, ↓reduced glutathione, ↓albumin) compared to HF patients with normal saliva (NS) secretion, as well as the control group (except albumin). We also observed increased content of protein glycoxidation products (↑dityrosine, ↑kynurenine, ↑glycophore) in NWS and SWS of HF patients with HS compared to healthy controls. Interestingly, the content of dityrosine, N-formylkynurenine, and glycophore in NWS was also significantly higher in HF patients with HS compared to those with NS secretion. The concentration of NO was considerably lower, while the levels of peroxynitrite and nitrotyrosine were significantly higher in NWS and SWS of HF subjects with HS compared to the controls. Salivary gland dysfunction occurs in patients with chronic HF with the submandibular salivary glands being the least efficient. Oxidative/nitrosative stress may be one of the mechanisms responsible for the impairment of salivary gland secretory function in HF patients.

中文翻译：

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亚硝化应激以及蛋白质的氧化和糖化会加剧慢性心力衰竭患者的唾液腺功能障碍

慢性心力衰竭（HF）是一个重要的临床、社会和经济问题。氧化应激在心力衰竭进展中发挥着关键作用。在缺氧和再灌注条件下形成的自由基参与心肌顿抑和其他形式的再灌注后损伤。心力衰竭患者还患有与唾液分泌有关的疾病。然而，对于损害这些患者唾液腺分泌功能的机制仍然知之甚少。在本研究中，我们首次比较了心力衰竭患者非刺激唾液（非刺激全唾液（NWS））和刺激唾液（SWS）的抗氧化屏障、蛋白质糖氧化和亚硝化/硝化应激。该研究包括 50 名唾液 (NS) 分泌正常 ( n = 27) 和唾液分泌不足 (HS) ( n = 23) 的心衰患者，以及年龄和性别匹配的对照组 ( n = 50)。我们证明，与唾液正常的心力衰竭患者（NS ）分泌量，以及对照组（白蛋白除外）。我们还观察到，与健康对照相比，患有 HS 的心力衰竭患者的 NWS 和 SWS 中蛋白质糖氧化产物（↑二酪氨酸、↑犬尿氨酸、↑糖基团）含量增加。有趣的是，与分泌 NS 的心力衰竭患者相比，伴有 HS 的心力衰竭患者 NWS 中二酪氨酸、N-甲酰犬尿氨酸和糖基团的含量也显着升高。与对照组相比，患有 HS 的 HF 受试者的 NWS 和 SWS 中 NO 浓度显着降低，而过氧亚硝酸盐和硝基酪氨酸水平显着升高。慢性心力衰竭患者会出现唾液腺功能障碍，其中下颌下唾液腺的效率最低。氧化/亚硝化应激可能是心衰患者唾液腺分泌功能受损的机制之一。