Is Antioxidant Therapy a Useful Complementary Measure for Covid-19 Treatment? An Algorithm for Its Application

Abstract

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) causes the corona virus disease-19 which is accompanied by severe pneumonia, pulmonary alveolar collapses and which stops oxygen exchange. Viral transmissibility and pathogenesis depend on recognition by a receptor in the host, protease cleavage of the host membrane and fusion. SARS-CoV-2 binds to the angiotensin converting enzyme 2 receptor. Here, we discuss the general characteristics of the virus, its mechanism of action and the way in which the mechanism correlates with the comorbidities that increase the death rate. We also discuss the currently proposed therapeutic measures and propose the use of antioxidant drugs to help patients infected with the SARS-CoV-2. Oxidizing agents come from phagocytic leukocytes such as neutrophils, monocytes, macrophages and eosinophils that invade tissue. Free radicals promote cytotoxicity thus injuring cells. They also trigger the mechanism of inflammation by mediating the activation of NFkB and inducing the transcription of cytokine production genes. Release of cytokines enhances the inflammatory response. Oxidative stress is elevated during critical illnesses and contributes to organ failure. In corona virus disease-19 there is an intense inflammatory response known as a cytokine storm that could be mediated by oxidative stress. Although antioxidant therapy has not been tested in corona virus disease-19, the consequences of antioxidant therapy in sepsis, acute respiratory distress syndrome and acute lung injury are known. It improves oxygenation rates, glutathione levels and strengthens the immune response. It reduces mechanical ventilation time, the length of stay in the intensive care unit, multiple organ dysfunctions and the length of stay in the hospital and mortality rates in acute lung injury/acute respiratory distress syndrome and could thus help patients with corona virus disease-19.

Keywords: ACE2 receptor; COVID-19; SARS-CoV-2; antioxidant therapy; sepsis.

Figure 1

Ultrastructural lung features from a postmortem patient of COVID-19. The patient was a 68-year-old female from our Institute, with type II diabetes, ischemic heart disease, hypertension and morbid obesity as associated comorbidities. The pictures of the electron microscopy panels (A,B) were made at 25,000× and 50,000× respectively with a Jeol JEM-1011 electronic microscope. Panel (A) shows the separation of the two muscular cells of the middle zone of a bronchiole with viral particles. Panel (B) shows the middle zone of a bronchiole with viral particles, the viral particles found measured between 56.2 and 102 nm and this agrees with the reported size of the virus. Abbreviations: C = cellule, CM = cellular membrane, VP = viral particle.

Figure 2

Postmortem lung biopsy of a 28 year old male patient with acute myocardial infarction and aortic stenosis as control subject. The bronchiole without viral particles. The pictures of the electron microscopy panels (A,B) were made at 25,000× and 50,000× respectively with a Jeol JEM-1011 electronic microscope. Abbreviations: C = cellule, CM = cellular membrane.

Figure 3

Interaction of SARS-COV-2 with the ACE2 receptor, target organs and its effect on them. Abbreviations: ACE2 = Angiotensin converting enzyme 2, RAAS = Inhibitors of the renin-angiotensin-aldosterone system, ATR1 = receptor type 1 losartan. ALT = alanine aminotransferase, AST = aspartate aminotransferase.

Figure 4

Ultrastructural features of a heart sample from a patient with COVID-19 postmortem. The patient was a 68-year-old female of our Institute that had as associated comorbidities type II diabetes, ischemic heart disease, hypertension, morbid obesity. The picture to 40,000× of the electron microscopy was made with a Jeol JEM-1011 electronic microscope. The Picture describes inter fibrillate mitochondria with viral particles in the heart with loss of cytoplasmic content and loss of internal membrane and loss and shortening of chalk with alterations of the external membrane, rupture of heart fibers. Abbreviations: M = Mitochondria, S = Sarcomere, VP = viral particle.

Figure 5

Ultrastructural features of a heart sample from biopsy postmortem of patient 54 years old female with atrial fibrillation as control subject without viral particles. The mitochondria show regular ridges and shorts sarcomere. The picture to 40,000× of the electron microscopy was made with a Jeol JEM-1011 electronic microscope. Abbreviations: M = Mitochondria, S = Sarcomere.

Figure 6

Ultrastructural liver features from postmortem of COVID-19 patient. The patient was a 68-year-old. The pictures of the electron microscopy panels A and B were made at 25,000× and 50,000× respectively with a Jeol JEM-1011 electronic microscope. The panel (A) shows vaccination drops from viral damage. The panel (B) shows mitochondrial damage, mitochondria with loss of cytoplasmic content, internal membrane and loss of chalk with alterations of the external membrane. The measurement of something viral particles they were found between 98 and 150 nm and agrees with the reported size of the virus. Abbreviations: GAC = Golgi apparatus cisterns, N = nucleus, M = Mitochondria, VD = vaccination drops, VP = viral particle.

Figure 7

Postmortem lung biopsy of a 28 year old male patient with acute myocardial infarction and aortic stenosis as control subject. The liver without viral particles. The pictures of the electron microscopy panels (A,B) were made at 25,000× and 50,000× respectively with a Jeol JEM-1011 electronic microscope. Abbreviations: GAC = Golgi apparatus cisterns, N = nucleus, M = Mitochondria.