Glutathione Is Undoubtedly A Key Factor in Determining The Symptomatic Manifestations Of The COVID-19 Virus in Patients.

The important role of glutathione in determining an individual's receptivity to COVID-19 infection and its pathogenesis. Utility of glutathione as a solution that may cure and/or prevent the SARS-CoV-2 virus. The claim that a significant deficiency of glutathione is the most likely cause of severe manifestations and death in COVID-19 patients is based on a comprehensive analysis and a range of observations. It reveals the mysteries of the risk factors associated with severe cases of SARS-CoV-2 and higher mortality rates presented by epidemiological data. This article also discusses possible options for treating and suppressing COVID-19.

Studies have shown higher rates of severe illness and death from the virus among older adults with underlying medical conditions, suggesting that the biological processes and age associated with the disease make these individuals more susceptible to infectious agents of the virus. Associated oxidative stress and impaired redox homeostasis play an important role in biological processes that lead to increased vulnerability.

This is a multifaceted pathological condition that reflects the inability of the relevant biological components to repair the resulting damage or detoxify reactive intermediates due to an imbalance that leads to the rapid production of ROS (reactive oxygen species). Studies have shown that ROS is closely related to aging because they trigger an immediate response to the damage caused by age.

Supporting studies have also shown that inflammation associated with excess production of ROS due to oxidative stress and decreased antioxidant defenses promotes the pathogenesis of various chronic diseases. Some of these diseases include respiratory and cardiovascular diseases, diabetes, and more, all of which contribute to the risk of severe symptoms and/or even death from COVID-19.

Another key determinant of disease and various related viral disease progression is when intonation of virus-induced antioxidant properties is present in the host. A broad understanding of the antioxidant rejection mechanisms that protect patients from oxidative stress is essential. Only then can we fully understand the devices that cause resistance or non-specific sensitivity to infectious mediators.

The popular hypothesis is currently being studied in the scientific community that VD (vitamin D) deficiency is associated with severe manifestations (and in some cases deaths) in COVID-19 patients. More research suggests that glutathione levels are positively correlated with active vitamin D. Lower levels of L-cysteine and glutathione have been reported to be positively correlated with lower levels of vitamin D (VD) and vitamin D-binding protein (VDBP) in T2D patients.

A recent study showed that increased oxidative stress associated with glutathione deficiency alters vitamin D regulatory genes. Because of this, suppressed genes reduce vitamin D biosynthesis, ultimately leading to vitamin D-induced deficiency.

However, GSH supplementation by L-cysteine administration positively altered the methyltransferase of epigenetic enzymes and amplified the activity of VD metabolic genes. Overall, the study demonstrated that glutathione is essential for controlling endogenous vitamin D biosynthesis. It also demonstrates how glutathione treatment can be beneficial in reducing VD deficiency. Broken down further, this study suggests that glutathione deficiency rather than VD deficiency is a more plausible factor contributing to biochemical abnormalities, including lower rates of VD biosynthesis and therefore more strongly associated with severe symptoms and even death in COVID-19 patients.

Many studies have shown that an individual's positive response to viral attack is associated with higher levels of glutathione. Glutathione primarily uses its antioxidant mechanism to protect the host's immune cells. It is also essential for the optimal functioning of the numerous cells that make up the immune system. Notably, at different stages of the viral life cycle, glutathione hinders cell replication, thereby preventing the subsequent massive release of harmful inflammatory cells and increasing viral load into the lungs.

The great antiviral properties of glutathione were further established in the experiments of De Flora et al. During the study period, clinically significant influenza was found to be significantly suppressed by six months of treatment with prophylactic N-acetylcysteine (NAC, glutathione precursor). It has also been noted that precursors suppress their associated episodes, especially in older people.

In addition, cases of pathophysiological conditions such as lung cell damage and cases of persistent inflammation experienced by patients with severe ARDS were carefully selected as targets for NAC treatment and observation.

During treatment, patients with ARDS with deficiencies associated with lower levels of glutathione in the alveolar fluid were observed to experience enhanced lung cell damage due to inflammation and oxidative stress / ROS. The administration of glutathione and NAC mitigates the damage, which, among other things, will help increase coagulation dysfunction in COVID-19 patients.

Glutathione is undoubtedly a key factor in determining the symptomatic manifestations of the COVID-19 virus in patients. However, its antiviral effect remains nonspecific.

Tag: Glutathione

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