Severity of oxidative stress as a hallmark in COVID-19 patients.

INTRODUCTION: Understanding the mechanisms and identifying effective treatments for the COVID-19 outbreak are imperative. Therefore, this study aimed to assess the antioxidant status and oxidative stress parameters as potential pivotal mechanisms in asymptomatic, non-severe, and severe COVID-19 patients. METHODS: This study is a case-control study that was performed on patients referred to the Persian Gulf Martyrs Hospital of Bushehr University of Medical Sciences, Bushehr, Iran, from May 2021 to September 2021. A total of 600 COVID-19 patients (non-severe and severe group) and 150 healthy volunteers of the same age and sex were selected during the same period. On the first day of hospitalization, 10 ml of venous blood was taken from subjects. Then, hematological, biochemical, serological, antioxidant and oxidative stress parameters were determined. RESULTS: Our results indicated that ESR, CRP, AST, ALT, and LDH significantly augmented in the severe group as compared to the non-severe and normal groups (P ≤ 0.05). It was observed that the levels of FRAP, G6PD activity, and SOD activity significantly reduced in the non-severe patients in comparison with the severe and normal groups (P ≤ 0.05). We found that MDA content and NO metabolite markedly increased in severe patients as compared to the non-severe group. CONCLUSIONS: Taken together, it seems that the balance between antioxidants and oxidants was disturbed in COVID-19 patients in favor of oxidant markers. In addition, this situation caused more aggravation in severe patients as compared to the non-severe group.

Crosstalk between autophagy and insulin resistance: evidence from different tissues.

Insulin is a critical hormone that promotes energy storage in various tissues, as well as anabolic functions. Insulin resistance significantly reduces these responses, resulting in pathological conditions, such as obesity and type 2 diabetes mellitus (T2DM). The management of insulin resistance requires better knowledge of its pathophysiological mechanisms to prevent secondary complications, such as cardiovascular diseases (CVDs). Recent evidence regarding the etiological mechanisms behind insulin resistance emphasizes the role of energy imbalance and neurohormonal dysregulation, both of which are closely regulated by autophagy. Autophagy is a conserved process that maintains homeostasis in cells. Accordingly, autophagy abnormalities have been linked to a variety of metabolic disorders, including insulin resistance, T2DM, obesity, and CVDs. Thus, there may be a link between autophagy and insulin resistance. Therefore, the interaction between autophagy and insulin function will be examined in this review, particularly in insulin-responsive tissues, such as adipose tissue, liver, and skeletal muscle.

In vitro and Molecular Docking Analysis of Quercetin as an Anti-inflammatory and Antioxidant.

INTRODUCTION: Quercetin (3,3',4',5,7-pentahydroxyflavone) is a dietary flavonoid with good antioxidant and anti-inflammatory properties. AIMS: The present study aims to determine these effects in peripheral blood mononuclear cells (PBMCs) evoked by lipopolysaccharides (LPS). METHODS: The mRNA expression and protein secretion of inflammatory mediators were evaluated by enzyme- linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (PCR), respectively. Western blotting was utilized for assessing p65-NF-κB phosphorylation. Ransod kits evaluated the glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity in the cell lysates. Ultimately, the molecular docking approach was performed to investigate the biological activity of Quercetin against NF-κB pathway proteins and antioxidant enzymes. RESULTS: The findings revealed that quercetin significantly attenuated the expression and secretion of inflammatory mediators and p65-NF-κB phosphorylation in LPS-induced PBMCs. Additionally, quercetin dose-dependently improved the activities of SOD and GPx enzymes and decreased LPS-mediated oxidative stress in PBMCs. Moreover, quercetin has a considerable binding affinity to IκKb, the core element of the NF-κB pathway and the antioxidant enzyme SOD. CONCLUSION: The data show that quercetin plays a vital role in ameliorating inflammation and oxidative stress caused by LPS in PBMCs.

A comparative study on the effect of blood collection tubes on stress oxidative markers.

Oxidative stress has a major role in disease pathogenesis. However, limited studies have investigated the effect of various sample collection tubes on oxidative biomarkers. The present study aimed to evaluate the effect of different collection tubes on the variation of malondialdehyde (MDA), nitric oxide (NO), total thiol (t-SH), and ferric reducing ability of plasma (FRAP) levels. A total of 35 individuals participated in this study and each collected sample was separated into three different tubes: glass tubes (GTs), plain plastic tubes (PTs), and gel separator tubes (GSTs). The results of PTs and GSTs were compared to those of GTs as the reference tube. The comparison between the means of biomarkers in various tubes indicated that there was no significant difference in MDA results between tubes. In contrast, t-SH and NO content were significantly decreased in GSTs and PTs compared to GTs. However, the Bland-Altman analysis showed an acceptable concordance for the mentioned analytes and the statistically significant differences were not clinically significant for NO, MDA, and t-SH antioxidant parameters. Moreover, the FRAP level was considerably lower in GSTs compared to GTs. Nevertheless, the Bland-Altman analysis showed a high bias percentage for the FRAP assay when using PTs and GSTs. According to the present results, it can be concluded that switching to plastic blood collection tubes or serum separation tubes could influence the FRAP results. However, there was no interference for the interpretation of other antioxidant assays in different types of collection tubes. Hence, it is suggested to use GTs for total antioxidant capacity evaluations, especially the FRAP assay.

Iron Chelator or Iron Supplement Consumption in COVID-19? The Role of Iron with Severity Infection.

Iron is a trace element that is used to replicate the virus and has a role in the vital functions of the body and the host's innate immune system. The mechanism of iron in COVID-19 severity is still not well understood. The aim of this study was to evaluate the association of the iron with COVID-19 severity. A case-control study was performed on 147 patients with a positive PCR test result and 39 normal individuals admitted to the Persian Gulf Martyrs Hospital in Bushehr, Iran. The iron profiles and related tests were measured along with hematological analytes. Hemoglobin (Hb), Fe, and saturated transferrin decreased in all the groups compared to the controls, but ferritin increased in the patient groups. After adjusting for age and sex, we found that increased ferritin levels augmented the odds ratio (OR) of the disease in the moderate (OR = 2.95, P = 0.007), severe (OR = 6.1, P < 0.001), and critical groups (OR = 8.34, P < 0.001). The decreased levels of Fe reduced the OR of the disease in the mild (OR = 0.96, P < 0.001), moderate (OR = 0.96, P < 0.001), severe (OR = 0.95, P < 0.001), and critical (OR = 0.98, P = 0.001) groups. Fe (AUC = 85.95, cutoff < 75.5 µg/dL, P < 0.001) and ferritin (AUC = 84.45, cutoff > 157.5 ng/dL, P < 0.001) have higher AUC for disease prognosis, but only ferritin (AUC = 74.89, cutoff > 261.5 ng/dL, P < 0.001) has higher AUC for disease severity assays. It could be concluded that the use of iron chelators to reduce iron intake can be considered a therapeutic goal. In addition, measuring Fe and ferritin is beneficial for the diagnosis of the disease and determining its severity.

The effects of malvidin on oxidative stress parameters and inflammatory cytokines in LPS-induced human THP-1 cells.

Malvidin is an anthocyanin which is involved in inhibiting inflammatory-related mediators in inflammatory diseases; however, its mechanism of action in THP-1 cells is not yet known. THP-1 is a human monocytic cell line that is derived from patients with acute monocytic leukemia. The present study aimed to investigate the effect of malvidin on inflammatory responses and oxidative stress in lipopolysaccharide (LPS)-induced THP-1 cells. THP-1 cells were stimulated with LPS (50 ng/ml) to induce inflammation in the presence or absence of malvidin. The anti/proinflammatory cytokines were evaluated by real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Total protein levels/phosphorylation of c-Jun N-terminal kinase (JNK), P65-NF-κB, and IKKα/IKKß were evaluated by western blot analysis. Malondialdehyde (MDA) and nitric oxide (NO) metabolite levels, ferric reducing antioxidant power (FRAP), total thiol (T-SH) content, and superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity were measured to evaluate the antioxidant activity of malvidin in THP-1 cells. Treatment of LPS-stimulated THP-1 cells with malvidin (100 and 200 µM) led to the significant inhibition of interleukin-6 (IL-6), tumor necrosis factor-α, and IL-1ß messenger RNA (mRNA) expression and protein levels as well as a significant increase in the IL-10 mRNA expression and protein secretion. Moreover, 200 µM malvidin treatment reduced the phosphorylation of JNK, IKKα/IKKß, and P65-NF-κB. These findings showed that malvidin not only decreased the MDA and NO metabolite levels but also increased the FRAP and T-SH content as well as SOD and GPx activities. The findings of the present study demonstrated the potential role of malvidin in blocking inflammation and oxidative stress induced by LPS in THP-1 cell line, suggesting that malvidin is likely to be a therapeutic agent for inflammatory diseases.