A useful and sensitive marker in the prediction of COVID-19 and disease severity: Thiol

Kalem, Ayşe Kaya; Kayaaslan, Bircan; Neşeli̇oğlu, Salim; Eser, Fatma; Hasanoğlu, İmran; Aypak, Adalet; Akıncı, Esragül; Akça, Halise; Erel, Özcan; Güner, Rahmet

doi:10.1016/j.freeradbiomed.2021.02.009

Cited by 28 publications

(42 citation statements)

References 27 publications

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“…No significant change was found in the disulphide levels between the pre- and post-treatment values. A similar finding reported no significant change in the disulphide levels in severe COVID-19 patients compared to healthy controls ( Kalem et al, 2021 ). Collectively, these findings imply that endogenous thiol contents are depleted and dynamic thiol/disulphide homeostasis is modified by COVID-19.…”

Section: Discussionmentioning

confidence: 61%

“…This data supports the results presented by Erel et al (2020) , who reported that thiol status is depleted in COVID-19 patients. Kalem et al (2021) also demonstrated that COVID-19 patients had lower native thiol and total thiol levels compared to healthy controls. Thiols are an independent risk factor for COVID-19 severity ( Erel et al, 2020 ).…”

Section: Discussionmentioning

confidence: 83%

“…Measuring of a dynamic thiol/disulphide homeostasis allows determining entire dynamic thiol groups providing a benefit from determining only glutathione level or redox couples (such as reduced/oxidized glutathione, cysteine/cystine, and cysteinilglycine/cystinilglycine) individually. There is limited published data concerning the contribution of thiol/disulphide homeostasis in COVID-19 ( Erel et al, 2020 ; Giustarini et al, 2021 ; Kalem et al, 2021 ). To the best of our knowledge, no published studies have investigated the effects of antiviral drug therapy on the thiol/disulphide status and nitric oxide (NO) levels in COVID-19 patients.…”

Section: Introductionmentioning

confidence: 99%

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Effects of antiviral drug therapy on dynamic thiol/disulphide homeostasis and nitric oxide levels in COVID-19 patients

Mete

Koçak

Saracaloglu

et al. 2021

European Journal of Pharmacology

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The novel coronavirus disease 2019 (COVID-19) has led to a serious global pandemic. Although an oxidative stress imbalance occurs in COVID-19 patients, the contributions of thiol/disulphide homeostasis and nitric oxide (NO) generation to the pathogenesis of COVID-19 have been poorly identified. Therefore, the aim of this study was to evaluate the effects of antiviral drug therapy on the serum dynamics of thiol/disulphide homeostasis and NO levels in COVID-19 patients. A total of 50 adult patients with COVID-19 and 43 sex-matched healthy control subjects were enrolled in this prospective study. Venous blood samples were collected immediately on admission to the hospital within 24 h after the diagnosis (pre-treatment) and at the 15th day of drug therapy (post-treatment). Serum native thiol and total thiol levels were measured, and the amounts of dynamic disulphide bonds and related ratios were calculated. The average pre-treatment total and native thiol levels were significantly lower than the post-treatment values (P < 0.001 for all). We observed no significant changes in disulphide levels or disulphide/total thiol, disulphide/native thiol, or native thiol/total thiol ratios between pre- and post-treatments. There was also a significant increase in serum NO levels in the pre-treatment values when compared to control (P < 0.001) and post-treatment measurements (P < 0.01). Our results strongly suggest that thiol/disulphide homeostasis and nitrosative stress can contribute to the pathogenesis of COVID-19. This study was the first to show that antiviral drug therapy can prevent the depletion in serum thiol levels and decrease serum NO levels in COVID-19 patients.

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Section: Discussionmentioning

confidence: 61%

Section: Discussionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of antiviral drug therapy on dynamic thiol/disulphide homeostasis and nitric oxide levels in COVID-19 patients

Mete

Koçak

Saracaloglu

et al. 2021

European Journal of Pharmacology

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“… 22 , 23 Only little information was available about the relationship between oxidative stress and COVID-19 disease. 24 , 25 SARS-CoV-2 enters the host cell mainly via the cell surface enzyme angiotensin-converting enzyme 2 (ACE2), which plays a pivotal role in the conversion of angiotensin II (ANG II) to ANG-(1–7). The interaction of Ang-(1–7) with its receptor Mas plays an important role in the balance between reactive oxygen species (ROS) production and antioxidant capacity.…”

Section: Discussionmentioning

confidence: 99%

SOD1 is a Possible Predictor of COVID-19 Progression as Revealed by Plasma Proteomics

Lei

Ren

et al. 2021

ACS Omega

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The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a worldwide health emergency. Patients infected with SARS-CoV-2 present with diverse symptoms related to the severity of the disease. Determining the proteomic changes associated with these diverse symptoms and in different stages of infection is beneficial for clinical diagnosis and management. Here, we performed a tandem mass tag-labeling proteomic study on the plasma of healthy controls and COVID-19 patients, including those with asymptomatic infection (NS), mild syndrome, and severe syndrome in the early phase and the later phase. Although the number of patients included in each group is low, our comparative proteomic analysis revealed that complement and coagulation cascades, cholesterol metabolism, and glycolysis-related proteins were affected after infection with SARS-CoV-2. Compared to healthy controls, ELISA analysis confirmed that SOD1, PRDX2, and LDHA levels were increased in the patients with severe symptoms. Both gene set enrichment analysis and receiver operator characteristic analysis indicated that SOD1 could be a pivotal indicator for the severity of COVID-19. Our results indicated that plasma proteome changes differed based on the symptoms and disease stages and SOD1 could be a predictor protein for indicating COVID-19 progression. These results may also provide a new understanding for COVID-19 diagnosis and treatment.

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“…Although the contribution of oxidative stress to disease pathogenesis had been explored in several viral infection [ 28 , 29 ], its relevance to COVID-19 respiratory infection deserves more attention [ 25 , 26 ]. This is due to the fact that immune derangement during SARS-CoV-2 infection could switch on a lethal cycle of oxidative stress, inflammation and lung tissue injury.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of oxidative stress gene markers during SARS-COV-2 viral infection

Sharif-Askari

Mdkhana

et al. 2021

Free Radical Biology and Medicine

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Severe viral infections, including SARS-COV-2, could trigger disruption of the balance between pro-oxidant and antioxidant mediators; the magnitude of which could reflect the severity of infection and lung injury. Using publicly available COVID-19 transcriptomic datasets, we conducted an in-silico analyses to evaluate the expression levels of 125 oxidative stress genes, including 37 pro-oxidant genes, 32 oxidative-responsive genes, and 56 antioxidant genes. Seven oxidative stress genes were found to be upregulated in whole blood and lung autopsies (MPO, S100A8, S100A9, SRXN1, GCLM, SESN2, and TXN); these genes were higher in severe versus non-severe COVID-19 leucocytes. Oxidative genes were upregulated in inflammatory cells comprising macrophages and CD8 + T cells isolated from bronchioalveolar fluid (BALF), and neutrophils isolated from peripheral blood. MPO, S100A8, and S100A9 were t/opmost upregulated oxidative markers within COVID-19's lung autopsies, whole blood, leucocytes, BALF derived macrophages and circulating neutrophils. The calprotectin's, S100A8 and S100A9 were upregulated in SARS-COV-2 infected human lung epithelium. To validate our in-silico analysis, we conducted qRT-PCR to measure MPO and calprotectin's levels in blood and saliva samples. Relative to uninfected donor controls, MPO, S100A8 and S100A9 were significantly higher in blood and saliva of severe versus asymptomatic COVID-19 patients. Compared to other different viral respiratory infections, coronavirus infection showed a prominent upregulation in oxidative stress genes with MPO and calprotectin at the top of the list. In conclusion, SARS-COV-2 induce the expression of oxidative stress genes via both immune as well as lung structural cells. The observed correlation between oxidative stress genes dysregulation and COVID-19 disease severity deserve more attention. Mechanistical studies are required to confirm the correlation between oxidative stress gene dysregulation, COVID-19 severity, and the net oxidative stress balance.

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A useful and sensitive marker in the prediction of COVID-19 and disease severity: Thiol

Cited by 28 publications

References 27 publications

Effects of antiviral drug therapy on dynamic thiol/disulphide homeostasis and nitric oxide levels in COVID-19 patients

Effects of antiviral drug therapy on dynamic thiol/disulphide homeostasis and nitric oxide levels in COVID-19 patients

SOD1 is a Possible Predictor of COVID-19 Progression as Revealed by Plasma Proteomics

Upregulation of oxidative stress gene markers during SARS-COV-2 viral infection

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