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Reactive oxygen species are known to have a harmful activity in living systems. It attracts the attention of researchers due to their capability of damaging crucial biomolecules such as nucleic acids, lipids, proteins, polyunsaturated fatty acids, and carbohydrates and which results many human ailments: atherosclerosis, cancer, diabetes, inflammation, cardiovascular diseases, and neurological disorders. Hence, the investigation of the already known compounds exhibiting antioxidant properties is still an important scientific challenge. So reaction with Co(II)-bound superoxo complex, [(NH3)5Co(O2)Co(NH3)5]5+(MBSC) and Popofol (PPF), Ferulic Acid (FA) is chosen to study the antioxidant activity of PPF and FA. Redox properties of Popofol (PPF) and Ferulic Acid (FA) which are two phenolic antioxidants are studied through the reduction of Co(II)-bound superoxo complex, [(NH3)5Co(O2)Co(NH3)5]5+(MBSC) in aqueous acidic media ([H+] = 0.02–0.70 M) under pseudo-first-order condition. For both the PPF and FA, the observed rate increase with the increase in [PPF] and [FA] and the decrease with media [H+] and ionic strength, I. The kinetic analysis reveals that the deprotonated conjugate bases from PPF and FA reduces MBSC with the diffusion-controlled rate of ~ 108and ~ 1011M−1s−1. Since, the decrease in kovalues with increase in V/V D2O were not significant, we can propose for a simple electron-transfer (ET) mechanism, rather than proton-coupled electron transfer (PCET) or hydrogen-atom transfer (HAT) mechanism for the reduction in bound superoxide by PPF and FA. The antioxidant property of propofol and ferulic acid has been evaluated by various methods but in our study, the novelty lies on the exploration of the real insight of their antioxidant property by studying the chemical mechanism of their redox properties with MBSC.

The coronavirus disease 2019 (COVID-19) has led to serious health and economic damage to all over the world, and it still remains unstoppable. The SARS-CoV-2, by using its S-glycoprotein, binds with an angiotensin-converting enzyme 2 receptor, mostly present in alveolar epithelial type II cells. Eventually pulmonary surfactant depletion occurs. The pulmonary surfactant is necessary for maintaining the natural immunity as well as the surface tension reduction within the lung alveoli during the expiration. Its insufficiency results in the reduction of blood oxygenation, poor pulmonary regeneration, lung fibrosis, and finally the respiratory system collapses. Exogenous surfactants have previously shown great promise in the treatment of infant respiratory distress syndrome, and they may also aid in the healing of damaged alveolar cells and the prevention of respiratory failure. Surfactant based therapy has been advised for the prevention of COVID-19, and the trials have begun around the world. Furthermore, greater research on the timing, dose, and the distribution of surfactant to the COVID-19 patients is required before this technique can be implemented in clinical practice.