Meloxicam is a non-steroidal anti-inflammatory drug, which has a preferential inhibitory effect to cyclooxyganase-2 (COX-2). Although the drug inhibits prostaglandin synthesis, the exact mechanism of meloxicam is still unknown. This is the first study to assess the effect of meloxicam on protein glyco-oxidation as well as antioxidant activity. For this purpose, we used an in vitro model of oxidized bovine serum albumin (BSA). Glucose, fructose, ribose, glyoxal and methylglyoxal were used as glycating agents, while chloramine T was used as an oxidant. We evaluated the antioxidant properties of albumin (2,2-di-phenyl-1-picrylhydrazyl radical scavenging capacity, total antioxidant capacity and ferric reducing antioxidant power), the intensity of protein glycation (Amadori products, advanced glycation end products) and glyco-oxidation (dityrosine, kynurenine, N-formylkynurenine, tryptophan and amyloid-β) as well as the content of protein oxidation products (advanced oxidation protein products, carbonyl groups and thiol groups). We have demonstrated that meloxicam enhances the antioxidant properties of albumin and prevents the protein oxidation and glycation under the influence of various factors such as sugars, aldehydes and oxidants. Importantly, the antioxidant and anti-glycating activity is similar to that of routinely used antioxidants such as captopril, Trolox, reduced glutathione and lipoic acid as well as protein glycation inhibitors (aminoguanidine). Pleiotropic action of meloxicam may increase the effectiveness of anti-inflammatory treatment in diseases with oxidative stress etiology.

Valsartan belongs to angiotensin II type 1 (AT1) receptor blockers (ARB) used in cardiovascular diseases like heart failure and hypertension. Except for its AT1‐antagonism, another mechanism of drug action has been suggested in recent research. One of the supposed actions refers to the positive impact on redox balance and reducing protein glycation. Our study is aimed at assessing the antiglycooxidant properties of valsartan in an in vitro model of oxidized bovine serum albumin (BSA). Glucose, fructose, ribose, glyoxal (GO), methylglyoxal (MGO), and chloramine T were used as glycation or oxidation agents. Protein oxidation products (total thiols, protein carbonyls (PC), and advanced oxidation protein products (AOPP)), glycooxidation products (tryptophan, kynurenine, N‐formylkynurenine, and dityrosine), glycation products (amyloid‐β structure, fructosamine, and advanced glycation end products (AGE)), and albumin antioxidant activity (total antioxidant capacity (TAC), DPPH assay, and ferric reducing antioxidant power (FRAP)) were measured in each sample. In the presence of valsartan, concentrations of protein oxidation and glycation products were significantly lower comparing to control. Moreover, albumin antioxidant activity was significantly higher in those samples. The drug’s action was comparable to renowned antiglycation agents and antioxidants, e.g., aminoguanidine, metformin, Trolox, N‐acetylcysteine, or alpha‐lipoic acid. The conducted experiment proves that valsartan can ameliorate protein glycation and oxidation in vitro in various conditions. Available animal and clinical studies uphold this statement, but further research is needed to confirm it, as reduction of protein oxidation and glycation may prevent cardiovascular disease development.

Background: Prolongation of the QT interval is directly related to the risk of ventricular arrhythmias and sudden cardiac death. Age, comorbidities, and treatment schemes have been shown to influence its prolongation and may also significantly affect the course of SARS-CoV-2 infection. Fluoroquinolones, widely used during the COVID-19 pandemic, are known for their ability to prolong the QT interval. Risk of ventricular arrhythmias has also been reported in patients with infectious diseases, and this risk may have been associated with high levels of interleukin-6 (IL-6). Purpose: The aim of this study is to evaluate the effect of levofloxacin on the corrected QT interval in patients with COVID-19, as well as to identify sociodemographic, clinical, and biochemical parameters associated with QTc interval prolongation among patients with COVID-19. Patients and Methods: The medical records of 93 patients hospitalized for COVID-19 were retrospectively analyzed, focusing on the presence of comorbidities and treatment with levofloxacin. Selected sociodemographic, clinical, and biochemical parameters were then statistically analyzed, with emphasis on their effect on the corrected QTc interval. The QTc interval was calculated according to the Bazett formula. Results: Levofloxacin use was not significantly associated with QTc interval. Statistical analysis identified creatinine, heart failure and atrial fibrillation as significant predictors of QTc interval prolongation. The trends towards QTc interval prolongation observed with hypokalaemia and hypertension suggest that these factors may also contribute to QTc interval variability and should be taken into account when assessing arrhythmia risk. Conclusions: Our retrospective study indicates that QTc prolongation results from the interplay of multiple factors.