Evaluation of the Antioxidant Properties of Propofol and its Nitrosoderivative. Comparison with Homologue Substituted Phenols

Abstract

Propofol (2,6-diisopropylphenol), some substituted phenols (2,6-dimethylphenol and 2,6-ditertbutylphenol) and their 4-nitrosoderivatives have been compared for their scavenging ability towards 1,1-diphenyl-2-picrylhydrazyl and for their inhibitory action on lipid peroxidation. These products were also compared to the classical antioxidants butylated hydroxytoluene and butylated hydroxyanisole. When measuring the reactivity of the various phenolic derivatives with 1,1-diphenyl-2-picrylhydrazyl the following order of effectiveness was observed: butylated hydroxyanisole > propofol > 2,6-dimethylphenol > 2,6-di-tertbutylphenol > butylated hydroxytoluene. In cumene hydroperoxide-dependent microsomal lipid peroxidation, propofol acts as the most effective antioxidant, while butylated hydroxyanisole, 2,6-di-tertbutylphenol and butylated hydroxytoluene exhibit a rather similar effect, although lower than propofol. In the iron/ascorbate-dependent lipid peroxidation propofol, at concentrations higher than 10 microM, exhibits antioxidant properties comparable to those of butylated hydroxytoluene and butylated hydroxyanisole, 2,6-Dimethylphenol is scarcely effective in both lipoperoxidative systems. The antioxidant properties of the various molecules depend on their hydrophobic characteristics and on the steric and electronic effects of their substituents. However, the introduction of the nitroso group in the 4-position almost completely removes the antioxidant properties of the examined compounds. The nitrosation of the aromatic ring of antioxidant molecules and the consequent loss of antioxidant capacity can be considered a condition potentially occurring in vivo since nitric oxide and its derivatives are continuously formed in biological systems.

A Search for Hepatoprotective Activity of Fruit Extract of Mangifera indica L. Against Oxidative Stress Cytotoxicity

“…b: Significant difference in comparison with CHP treated hepatocytes (P<0.05) organelle (mitochondria/lysosomes) membrane damage are regarded as an important mechanism underlying the toxicity of several oxidative xenobiotics [29]. CHP induced microsomal lipid peroxidation is a common model for evaluating the effectiveness of antioxidants [30]. In this study, Mango Extracts were able to inhibit the lipid peroxidation and all the sub-cellular subsequent events induced by CHP.…”

Laccase oxidation and removal of toxicants released during combustion processes

“…This means that the generated nitric oxide immediately reacted with laccase oxidized toxicants leading to its removal. Previously, Rigobello et al, 2004 andPessêgo et al, 2011 also noted that nitric oxide readily reacted with phenolic compounds. This is quite interesting since nitric oxide like carbon monoxide have been shown not be amenable to adsorption and cannot be selectively reduced by filtration (Liu et al, 2011).…”

Mechanistic Study on the Production of Hydrogen Peroxide in the Anthraquinone Process

“…The BDE of AHQ is 16.7 kcal/mol lower than that of 2,6-dimethylphenol, which is widely used as a radical scavenger species. [30][31][32] Figure 2 shows the singly occupied molecular orbital (SOMO) of AQH · . The unpaired electron is delocalized on the whole aromatic ring; a calculated spin density on the carbonyl oxygen atom is only 0.2.…”