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1.
Journal of Pharmaceutical Negative Results ; 13:555-561, 2022.
Article in English | Web of Science | ID: covidwho-2111710

ABSTRACT

Background: Despite several scientific efforts against COVID 19, conundrum of biomolecular deterioration in Post COVID syndrome patients are still in dark at an unprecedented scale globally and affected the patient's health multidimensionally. It is conceivable that patients recovered from COVID-19 after second wave are at enhanced risk of secondary complications.Aim: The present study was carried out to estimate the serum vitamin D and total antioxidant activity (TAC) along with markers of oxi-inflammatory stress in post COVID patients diagnosed RT-PCR negative after second wave of COVID-19 and to determine their role in predicting secondary complications.Methodology: 50 subjects (30-55 years) of Delhi-NCR region were recruited and categorized into two groups (n=25 in each group;on the basis of their history of COVID infection). By using standard methods, study group parameters were estimated in Post COVID patients and statistically compared it with that of 25 non affected healthy controls by using student's t-test.Result: Serum CRP, TNF-alpha, MDA and uric acid levels were significantly high (p<0.05) in Post COVID patients as compared to healthy controls. Conversely, serum vitamin D and TAC levels along with SOD activities were found to be significantly low (P<0.001) in Post COVID patients as compared healthy controls. However, ceruloplasmin level was altered insignificantly (p<0.1) with respect to Group I subjects. Vitamin D levels were positively correlated with TAC and SOD activity (P<0.001) and negatively correlated with MDA, CRP, TNF-alpha and uric acid levels in post COVID patients.Conclusion: Therefore, the present study emphasizes the dire need of special attention to Post COVID population by providing vitamin D supplementation, antioxidant and mineral rich diet along with adoption of regular aerobic exercise not only to rejuvenate the biomolecular homeostasis but also to reduce oxi-inflammatory stress mediated future complications.

2.
Viruses ; 14(4)2022 03 30.
Article in English | MEDLINE | ID: covidwho-1834925

ABSTRACT

Oxidative stress (OS) induced by SARS-CoV-2 infection may play an important role in COVID-19 complications. However, information on oxidative damage in pregnant women with COVID-19 is limited. OBJECTIVE: We aimed to compare lipid and protein oxidative damage and total antioxidant capacity (TAC) between pregnant women with severe and non-severe COVID-19. METHODS: We studied a consecutive prospective cohort of patients admitted to the obstetrics emergency department. All women positive for SARS-CoV-2 infection by reverse transcription-polymerase chain reaction (RT-qPCR) were included. Clinical data were collected and blood samples were obtained at hospital admission. Plasma OS markers, malondialdehyde (MDA), carbonylated proteins (CP), and TAC; angiogenic markers, fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF); and renin-angiotensin system (RAS) markers, angiotensin-converting enzyme 2 (ACE-2) and angiotensin-II (ANG-II) were measured. Correlation between OS, angiogenic, and RAS was evaluated. RESULTS: In total, 57 pregnant women with COVID-19 were included, 17 (28.9%) of which had severe COVID-19; there were 3 (5.30%) maternal deaths. Pregnant women with severe COVID-19 had higher levels of carbonylated proteins (5782 pmol vs. 6651 pmol; p = 0.024) and total antioxidant capacity (40.1 pmol vs. 56.1 pmol; p = 0.001) than women with non-severe COVID-19. TAC was negatively correlated with ANG-II (p < 0.0001) and MDA levels (p < 0.0001) and positively with the sFlt-1/PlGF ratio (p = 0.027). CONCLUSIONS: In pregnant women, severe COVID-19 is associated with an increase in protein oxidative damage and total antioxidant capacity as a possible counterregulatory mechanism.


Subject(s)
COVID-19 , Antioxidants , Female , Humans , Placenta Growth Factor , Pregnancy , Pregnant Women , Prospective Studies , SARS-CoV-2 , Vascular Endothelial Growth Factor Receptor-1/metabolism
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