Recent studies have shown that oxidative stress is the one of the molecular changes underlying the pathogenesis of Alzheimer's disease. In this study, we have investigated the dynamic thiol-disulphide homeostasis in patients with Alzheimer's disease, using a novel method.
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.
The monocyte-to-high density lipoprotein ratio (MHR) has recently been implemented as an indicator of inflammation and oxidative stress. The present study characterized MHR in patients with diabetic polyneuropathy (DPN), in which oxidative stress and microvascular damage play a role in pathogenesis, relative to patients with non-DPN, diabetic patients without polyneuropathy, and healthy individuals. We further aimed to evaluate the association between MHR and the decreased compound muscle action potential (CMAP) amplitude of patients with diabetic axonal polyneuropathy.We enrolled 90 patients with DPN, 75 patients with nonDPN, 92 diabetic patients without polyneuropathy, and 67 healthy individuals; The monocyte, high-density lipoprotein cholesterol (HDL-C) values were obtained for all participants and MHR was calculated for each individual. Intergroup comparison was performed. The relationship between MHR and the posterior tibial nerve CMAP amplitudes was examined.Statistically significant negative correlation was observed between MHR and the posterior tibial nerve CMAP amplitudes of patients with DPN. The MHR values of the patients with DPN were significantly higher than those of the patients with non-DPN, diabetic patients without polyneuropathy and the control group.This study demonstrated that diabetic patients with higher MHR values may be more likely to develop polyneuropathy.
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