Abstract:Thiols (sulfhydryl groups) are effective antioxidants that can preserve the correct structure of proteins, and can protect cells and tissues from damage induced by oxidative stress. Abnormal levels of thiols have been measured in the blood of patients with moderate-to-severe chronic kidney disease (CKD) compared to healthy subjects, as well as in end-stage renal disease (ESRD) patients on haemodialysis or peritoneal dialysis. The levels of protein thiols (a measure of the endogenous antioxidant capacity invers… Show more
“…These latter include the transcriptional and metabolic processes associated with adaptive homeostasis mechanisms discussed earlier in Section 2 , and these defects are exacerbated in case of premature aging and oxidative stress induced by chronic and degenerative ailments. For example, in chronic kidney disease, defects in the cellular levels of reduced pyridine nucleotides and GSH metabolism are associated with poor capacity to prevent oxidative damages of blood cells and to restore the extracellular redox [ 41 , 45 , 46 , 47 , 48 ]; even more evident is the case of chronic respiratory syndromes that induce defects in the levels of lung GSH and in the redox buffering of protein Cys (reviewed in [ 7 , 34 , 35 , 36 , 49 ] and references therein). Worthy of note is the fact that such prototypical examples of chronic ailments, and others associated with oxidative stress, are included in the comorbidity that increases the risk of severe COVID-19 [ 6 , 50 ].…”
Section: Age-dependent Changes Of Lung Thiols and The Role Of Gsh In ...mentioning
SARS-CoV-2 infection can cause a severe respiratory distress syndrome with inflammatory and thrombotic complications, the severity of which increases with patients’ age and presence of comorbidity. The reasons for an age-dependent increase in the risk of severe COVID-19 could be many. These include defects in the homeostatic processes that control the cellular redox and its pivotal role in sustaining the immuno-inflammatory response to the host and the protection against oxidative stress and tissue degeneration. Pathogens may take advantage of such age-dependent abnormalities. Alterations of the thiol redox balance in the lung tissue and lining fluids may influence the risk of infection, and the host capability to respond to pathogens and to avoid severe complications. SARS-CoV-2, likewise other viruses, such as HIV, influenza, and HSV, benefits in its replication cycle of pro-oxidant conditions that the same viral infection seems to induce in the host cell with mechanisms that remain poorly understood. We recently demonstrated that the pro-oxidant effects of SARS-CoV-2 infection are associated with changes in the cellular metabolism and transmembrane fluxes of Cys and GSH. These appear to be the consequence of an increased use of Cys in viral protein synthesis and to ER stress pathway activation that interfere with transcription factors, as Nrf2 and NFkB, important to coordinate the metabolism of GSH with other aspects of the stress response and with the pro-inflammatory effects of this virus in the host cell. This narrative review article describes these cellular and molecular aspects of SARS-CoV-2 infection, and the role that antivirals and cytoprotective agents such as N-acetyl cysteine may have to limit the cytopathic effects of this virus and to recover tissue homeostasis after infection.
“…These latter include the transcriptional and metabolic processes associated with adaptive homeostasis mechanisms discussed earlier in Section 2 , and these defects are exacerbated in case of premature aging and oxidative stress induced by chronic and degenerative ailments. For example, in chronic kidney disease, defects in the cellular levels of reduced pyridine nucleotides and GSH metabolism are associated with poor capacity to prevent oxidative damages of blood cells and to restore the extracellular redox [ 41 , 45 , 46 , 47 , 48 ]; even more evident is the case of chronic respiratory syndromes that induce defects in the levels of lung GSH and in the redox buffering of protein Cys (reviewed in [ 7 , 34 , 35 , 36 , 49 ] and references therein). Worthy of note is the fact that such prototypical examples of chronic ailments, and others associated with oxidative stress, are included in the comorbidity that increases the risk of severe COVID-19 [ 6 , 50 ].…”
Section: Age-dependent Changes Of Lung Thiols and The Role Of Gsh In ...mentioning
SARS-CoV-2 infection can cause a severe respiratory distress syndrome with inflammatory and thrombotic complications, the severity of which increases with patients’ age and presence of comorbidity. The reasons for an age-dependent increase in the risk of severe COVID-19 could be many. These include defects in the homeostatic processes that control the cellular redox and its pivotal role in sustaining the immuno-inflammatory response to the host and the protection against oxidative stress and tissue degeneration. Pathogens may take advantage of such age-dependent abnormalities. Alterations of the thiol redox balance in the lung tissue and lining fluids may influence the risk of infection, and the host capability to respond to pathogens and to avoid severe complications. SARS-CoV-2, likewise other viruses, such as HIV, influenza, and HSV, benefits in its replication cycle of pro-oxidant conditions that the same viral infection seems to induce in the host cell with mechanisms that remain poorly understood. We recently demonstrated that the pro-oxidant effects of SARS-CoV-2 infection are associated with changes in the cellular metabolism and transmembrane fluxes of Cys and GSH. These appear to be the consequence of an increased use of Cys in viral protein synthesis and to ER stress pathway activation that interfere with transcription factors, as Nrf2 and NFkB, important to coordinate the metabolism of GSH with other aspects of the stress response and with the pro-inflammatory effects of this virus in the host cell. This narrative review article describes these cellular and molecular aspects of SARS-CoV-2 infection, and the role that antivirals and cytoprotective agents such as N-acetyl cysteine may have to limit the cytopathic effects of this virus and to recover tissue homeostasis after infection.
“…The nonenzymatic antioxidants include vitamins A, C, and E, bilirubin, and glutathione, while the enzymatic ones comprise glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (CAT); taking into account that the enzyme defense system is the first rapid line of defense against ROS [ 20 , 21 ]. Total Thiol sulfhydryl (TSH) is an effective antioxidants that can preserve the correct structure of proteins, and can protect cells and tissues from damage induced by oxidative stress [ 22 ]. Free radicals can damage all macromolecules such as carbohydrates, proteins, lipids, and nucleic acids [ 19 ].…”
Background. Asthma is known as a disease that causes breathing problems in children and adults and is also associated with chronic inflammation and oxidative stress of the airways. Nasturtium officinale (NO) possesses a wide range of pharmacological properties, particularly anti-inflammation and antioxidant potentials. Thus, this study for the first time was aimed to investigate anti-inflammatory and antioxidative activities of NO extract (NOE) in an ovalbumin-induced rat model of asthma. Materials and Methods. Forty-four male Wistar rats were sensitized with ovalbumin (OVA) to induce asthma symptoms. The animals were allocated into five groups: control (C), asthmatic (A), A + NOE (500 mg/kg), NOE (500 mg/kg), and A + dexamethasone (DX, 2.5 mg/kg). After 7 days, blood and tissue samples were taken from the rats. Then, the level of inflammatory markers, oxidative stress parameters, and antioxidant enzymes activity were measured. Results. The obtained results showed that OVA-sensitive rats significantly increased the levels of pro-inflammatory cytokines IL-1B, TGF-β, and SMA-α compared to the control group (
p
<
0.05
), while treatment with NOE remarkably reduced the SMA-α gene expression compared to the asthma group (
p
<
0.05
). Furthermore, it decreased the expression of IL-1B and TNF-α genes, although it was not statistically significant. The level of glutathione peroxidase (GPX) significantly reduced in A group compared to the C group (
p
<
0.05
), whereas NOE administration significantly increased this marker (
p
<
0.05
). Moreover, NOE attenuated inflammation and alveolar injury in the lungs of OVA-sensitive rat compared to the nontreated A group. Conclusions. Overall, our findings demonstrated that NOE somewhat is able to reduce airway inflammation by reducing inflammatory and increasing GPX activity. Indeed, further experiments investigating the impact of different extract doses are needed to confirm the antioxidant and anti-inflammatory effects of NOE.
“…Oxidative stress accompanies CKD, and the presence of ROS in the plasma of hemodialyzed patients has been demonstrated experimentally [15]. In patients with CKD, a significant decrease in the level of the thiol groups in proteins has also been shown [16,17]. The studies by Pieniazek and Gwozdzinski also showed conformational changes in hemolysate proteins in patients with CKD [16].…”
The deteriorating function of the kidneys in chronic kidney disease (CKD) is associated, among other things, with the retention of many unnecessary metabolic products in the body. Indoxyl sulfate (IS) belongs to the group of uremic toxins with a high protein binding affinity. Moreover, this compound can generate oxidative stress. We hypothesized that a high concentration of IS might induce oxidative changes in erythrocytes and plasma components, and could therefore contribute to CKD progression. In this study, we evaluated the influence of IS on the oxidative stress parameters in plasma and hemolysate. Moreover, as a result of the action of IS, we observed a decrease in the total antioxidant capacity and a change in the activity of catalase and superoxide dismutase in hemolysate and plasma. The obtained results indicate that IS induces oxidative damage to hemolysate and plasma components. Greater changes in the parameters of oxidative stress were observed in hemolysate than in plasma treated with indoxyl sulfate. The obtained results suggest that the increased concentration of IS in patients with chronic kidney disease may lead to a decrease in the lifespan of erythrocytes in their bloodstream.
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