Objective: Recent studies have shown that cerebral ischaemia causes not only local, but also systemic oxidative stress. This leads to oxidation of thiol-containing compounds, including low-molecular-weight thiols (cysteine, glutathione, homocysteine and others). Therefore, the aim of this work was to verify the hypothesis that the thiol/disulphide homeostasis of low-molecular-weight thiols is disturbed in the early stages of cerebral ischaemia. Methods: Two experimental rat models of ischaemia were used: a global model of vascular ischaemia (clamping the common carotid arteries + haemorrhage) and focal ischaemia (middle cerebral artery occlusion). The total levels of thiols and their reduced forms were measured before surgery and after 40 minutes of reperfusion (global) or 3 hours (focal) ischaemia. Results: The global ischaemia model caused a marked (2.5–4 times, P < 0.01) decrease in the plasma thiol/disulphide redox state, and focal ischaemia caused an even larger decrease (30–80 times, P < 0.001). Discussion: These results suggest that plasma low-molecular-weight thiols are actively involved in oxidation reactions at early stages of cerebral ischaemia; therefore, their reduced forms or redox state may serve as a sensitive indicator of acute cerebrovascular insufficiency.

Acute brain ischemia is accompanied by a disruption of low-molecular-weight aminothiols (LMWTs) homeostasis, such as homocysteine (Hcy), cysteine (Cys), and glutathione (GSH). We investigated the r...

Objective. Aminothiols (glutathione (GSH), cysteinylglycine (CG)) may play an important role in the pathogenesis of coronavirus disease 2019 (COVID‐19), but the possible association of these indicators with the severity of COVID‐19 has not yet been investigated. Methods. The total content (t) and reduced forms (r) of aminothiols were determined in patients with COVID‐19 (n = 59) on admission. Lung injury was characterized by computed tomography (CT) findings in accordance with the CT0‐4 classification. Results. Low tGSH level was associated with the risk of severe COVID‐19 (tGSH ≤ 1.5 μM, mild vs. moderate/severe: risk ratio (RR) = 3.09, p = 0.007) and degree of lung damage (tGSH ≤ 1.8 μM, CT < 2 vs. CT ≥ 2: RR = 2.14, p = 0.0094). The rGSH level showed a negative association with D‐dimer levels (ρ = −0.599, p = 0.014). Low rCG level was also associated with the risk of lung damage (rCG ≤ 1.3 μM, CT < 2 vs. CT ≥ 2: RR = 2.28, p = 0.001). Levels of rCG (ρ = −0.339, p = 0.012) and especially tCG (ρ = −0.551, p = 0.004) were negatively associated with platelet count. In addition, a significant relationship was found between the advanced oxidation protein product level and tGSH in patients with moderate or severe but not in patients with mild COVID‐19. Conclusion. Thus, tGSH and rCG can be seen as potential markers for the risk of severe COVID‐19. GSH appears to be an important factor to oxidative damage prevention as infection progresses. This suggests the potential clinical efficacy of correcting glutathione metabolism as an adjunct therapy for COVID‐19.