Dynamic thiol–disulfide homeostasis in acute ischemic stroke patients
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Dynamic thiol–disulfide homeostasis plays a critical role in the cellular protection provided by antioxidation. The aim of this study was to investigate whether there is a change in thiol–disulfide homeostasis in acute ischemic stroke patients. Patients diagnosed with acute ischemic stroke that had undergone magnetic resonance diffusion-weighted imaging within the first 24 h were prospectively included in this study. The thiol, disulfide, and total thiol levels were measured during the first 24 and 72 h, and the National Institutes of Health Stroke Scale (NIHSS), modified Rankin Scale (mRS), and Barthel Index (BI) of the patients were recorded. Overall, the relationships between the thiol–disulfide levels of the patients and the infarct volumes, NIHSS, mRS, and BI scores were investigated. In this study, 54 patients and 53 healthy controls were included. The mean of the native thiol levels in the stroke group was 356.572 ± 61.659 μmol/L (min/max 228.00/546.40), while it was 415.453 ± 39.436 μmol/L (min/max 323.50/488.70) in the control group (p < 0.001). A negative, significant correlation was observed between the infarct volumes and native thiol levels (ρ = −0.378; p = 0.005), and the disulfide levels were similar between the groups (Z = 0.774; p = 0.439). Significant difference was found between the thiol levels of the mild and moderate-severe NIHSS groups (p = 0.026). The changes in the thiol levels under oxidative stress may be associated with the severity of the stroke. Substitution of thiol deficiency and correction of thiol–disulfide imbalance may be beneficial in ischemic stroke.
keywordsThiol levels Ischemic stroke Infarct volume Disulfide
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This research received no grant from any funding agency in the public, commercial, or non-profit sectors.
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The authors declare that there are no conflicts of interest.
- 10.Calabrese V, Lodi R, Tonon C, D’Agata V, Sapienza M, Scapagnini G, Mangiameli A, Pennisi G, Stella AM, Butterfield DA (2005) Oxidative stress, mitochondrial dysfunction and cellular stress response in Friedreich’s ataxia. J Neurol Sci 233(1–2):145–162. doi: 10.1016/j.jns.2005.03.012 CrossRefPubMedGoogle Scholar
- 22.Matsuo Y, Kihara T, Ikeda M, Ninomiya M, Onodera H, Kogure K (1995) Role of neutrophils in radical production during ischemia and reperfusion of the rat brain: effect of neutrophil depletion on extracellular ascorbyl radical formation. J Cereb Blood Flow Metab 15(6):941–947CrossRefPubMedGoogle Scholar
- 26.Murakami K, Kondo T, Kawase M, Li Y, Sato S, Chen SF, Chan PH (1998) Mitochondrial susceptibility to oxidative stress exacerbates cerebral infarction that follows permanent focal cerebral ischemia in mutant mice with manganese superoxide dismutase deficiency. J Neurosci 18(1):205–213PubMedGoogle Scholar
- 27.Fujimura M, Morita-Fujimura Y, Kawase M, Copin JC, Calagui B, Epstein CJ, Chan PH (1999) Manganese superoxide dismutase mediates the early release of mitochondrial cytochrome C and subsequent DNA fragmentation after permanent focal cerebral ischemia in mice. J Neurosci 19(9):3414–3422PubMedGoogle Scholar
- 32.Sen CK, Packer L (2000) Thiol homeostasis and supplements in physical exercise. Am J Clin Nutr 72(2):653–669Google Scholar