scholarly journals Re-Print- Artificial Respiration in Severe COVID-19 Cases: A Beneficial or Deleterious Treatment

2021 ◽  
Vol 4 (1) ◽  
pp. 01-09
Author(s):  
Kurt E. Müller
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Manganese Superoxide Dismutase ◽  
Inflammatory Diseases ◽  
Artificial Respiration ◽  
Electron Flow ◽  
Intensive Care Treatment ◽  
Manganese Superoxide ◽  
Number Of Patients ◽  
Treatment Measures

The world over artificial respiration is employed as one of the intensive care treatment measures in severe cases of COVID-19 because of the significant respiratory distress patients develop. Nevertheless, the outcome is poor. Lethality varies from country to country and clinic to clinic between 50% and 90%. So the question arises as to whether the use of oxygen can be a risk factor in the treatment of acute inflammatory diseases in general and of COVID-19 in particular. Oxidative stress is the first and oldest step of cellular defense and starts before the activation of the immune system. This leads to an increase of intracellular oxygen in the mitochondria, followed by an elevated electron flow and the formation of superoxide as well as other reactive oxygen species and reactive nitrogen species. Superoxide reacts with nitric oxide, which is always present in inflammation, forming peroxynitrite, the strongest inducer of oxidative stress. This step induces the activation of nuclear factor kB, followed by the production of proinflammatory cytokines. The elevated levels of inducible nitric oxide synthase keep this cycle running. High amounts of superoxide have to be compensated and catabolized by manganese-superoxide dismutase 2 into hydrogen peroxide and in a second step by catalase into water. When using artificial respiration, these steps are accelerated considerably in the inflamed tissue of the lung, leading to a significant increase of the electron flow as well as an elevation of superoxide, oxidative stress, and water. As SARS-CoV-2 generally induces the production of proteins (and not only those necessary for viral reproduction), the water will remain in the tissue, causing edema and thus a wet lung syndrome associated with a growing oxygen diffusion distance to red blood cells. Ultimately, patients do not suffocate in spite of, but because of, the presence of high levels of oxygen. The limited number of patients who survive this deleterious treatment describe it as having had a sensation of drowning. The reasons will be discussed.

scholarly journals Decreases in manganese superoxide dismutase expression and activity contribute to oxidative stress in persistent pulmonary hypertension of the newborn

2012 ◽  
Vol 303 (10) ◽  
pp. L870-L879 ◽  
Author(s):  
Adeleye J. Afolayan ◽  
Annie Eis ◽  
Ru-Jeng Teng ◽  
Ivane Bakhutashvili ◽  
Sushma Kaul ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Superoxide Dismutase ◽  
Manganese Superoxide Dismutase ◽  
Pulmonary Arteries ◽  
Tyrosine Nitration ◽  
Enos Expression ◽  
Manganese Superoxide ◽  
Expression And Activity

A rapid increase in the synthesis and release of nitric oxide (NO) facilitates the pulmonary vasodilation that occurs during birth-related transition. Alteration of this transition in persistent pulmonary hypertension of the newborn (PPHN) is associated with impaired function of endothelial nitric oxide synthase (eNOS) and an increase in oxidative stress. We investigated the hypothesis that a decrease in expression and activity of mitochondrial localized manganese superoxide dismutase (MnSOD) in pulmonary artery endothelial cells (PAEC) increases oxidative stress and impairs eNOS function in PPHN. We isolated PAEC and pulmonary arteries from fetal lambs with PPHN induced by prenatal ductus arteriosus ligation or sham ligation (control). We investigated MnSOD expression and activity, tyrosine nitration of MnSOD, and mitochondrial O2− levels in PAEC from control and PPHN lambs. We introduced exogenous MnSOD via an adenoviral vector (ad-MnSOD) transduction into PAEC and pulmonary arteries of PPHN lambs. The effect of ad-MnSOD was investigated on: mitochondrial O2− levels, MnSOD and eNOS expression and activity, intracellular hydrogen peroxide (H2O2) levels, and catalase expression in PAEC. MnSOD mRNA and protein levels and activity were decreased and MnSOD tyrosine nitration was increased in PPHN-PAEC. ad-MnSOD transduction of PPHN-PAEC increased its activity two- to threefold, decreased mitochondrial O2− levels, and increased H2O2 levels and catalase expression. ad-MnSOD transduction improved eNOS expression and function and the relaxation response of PPHN pulmonary arteries. Our observations suggest that decreased MnSOD expression and activity contribute to the endothelial dysfunction observed in PPHN.

scholarly journals Genetic Polymorphisms of MnSOD Modify the Impacts of Environmental Melamine on Oxidative Stress and Early Kidney Injury in Calcium Urolithiasis Patients

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 152
Author(s):  
Chia-Chu Liu ◽  
Chia-Fang Wu ◽  
Yung-Chin Lee ◽  
Tsung-Yi Huang ◽  
Shih-Ting Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Manganese Superoxide Dismutase ◽  
Kidney Injury ◽  
Normal Function ◽  
Nucleotide Polymorphisms ◽  
Tubular Injury ◽  
Single Nucleotide ◽  
Manganese Superoxide ◽  
Calcium Urolithiasis ◽  
Renal Tubular

Environmental melamine exposure increases the risks of oxidative stress and early kidney injury. Manganese superoxide dismutase (MnSOD), glutathione peroxidase, and catalase can protect the kidneys against oxidative stress and maintain normal function. We evaluated whether their single-nucleotide polymorphisms (SNPs) could modify melamine’s effects. A total of 302 patients diagnosed with calcium urolithiasis were enrolled. All patients provided one-spot overnight urine samples to measure their melamine levels, urinary biomarkers of oxidative stress and renal tubular injury. Median values were used to dichotomize levels into high and low. Subjects carrying the T allele of rs4880 and high melamine levels had 3.60 times greater risk of high malondialdehyde levels than those carrying the C allele of rs4880 and low melamine levels after adjustment. Subjects carrying the G allele of rs5746136 and high melamine levels had 1.73 times greater risk of high N-Acetyl-β-d-glucosaminidase levels than those carrying the A allele of rs5746136 and low melamine levels. In conclusion, the SNPs of MnSOD, rs4880 and rs5746136, influence the risk of oxidative stress and renal tubular injury, respectively, in calcium urolithiasis patients. In the context of high urinary melamine levels, their effects on oxidative stress and renal tubular injury were further increased.

scholarly journals Effects of SLIRP on Sperm Motility and Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Dan Shan ◽  
Samuel Kofi Arhin ◽  
Junzhao Zhao ◽  
Haitao Xi ◽  
Fan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Manganese Superoxide Dismutase ◽  
Mrna Level ◽  
Atp Content ◽  
Human Male ◽  
Manganese Superoxide ◽  
Polymerase Chain ◽  
And Oxidative Stress ◽  
Relative Mrna Expression

Background. Deficient spermatozoon motility is one of the main causes of male infertility. However, there are still no accurate and effective treatments in a clinical setting for male asthenospermia. Exploring the genes and mechanism of asthenospermia has become one of the hot topics in reproductive medicine. Our aim is to study the effect of SLRIP on human spermatozoon motility and oxidative stress. Methods. Sperm samples were collected including a normospermia group (60 cases) and an asthenospermia group (50 cases). SLIRP protein expression in spermatozoa was examined by western blotting, and relative mRNA expression of SLIRP in spermatozoa was quantified by reverse transcription polymerase chain reaction. Levels of reactive oxygen species (ROS), adenosine triphosphate (ATP) content, and the activity of manganese superoxide dismutase (MnSOD) in spermatozoa were also measured. Results. The mRNA level and protein expression of SLIRP in the asthenospermia group were significantly reduced compared with those in the normospermia group. The ROS active oxygen level in the asthenospermia group significantly increased; however, the ATP content decreased significantly as well as the activity of MnSOD. Conclusion. SLIRP regulates human male fertility, and SLIRP and sperm progressive motility are positively correlated. The expression of SLIRP is declined, oxidative damage is increased, and energy metabolism is decreased in spermatozoa of asthenospermia patients compared to normospermia participants.

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