Experimental and theoretical investigation on photodegradation mechanisms of naproxen and its photoproducts.

The photochemical degradation of the pharmaceuticals and personal care products (PPCPs) has attracted increasing attention. In this study, a deep inspection of the photolysis mechanisms of naproxen and its photoproducts has been performed by employing experimental and theoretical methods. Contributions of different reactive oxygen species (ROS, such as OH, 1O2, and O2-) in the photolysis reaction also have been clarified. Based on the detected intermediates and DFT calculations, several photodegradation pathways of naproxen and its photoproducts have been proved. Furthermore, the deprotonated form of naproxen has been confirmed to be more reactive than the protonated one, and the lowest triplet state of naproxen is the reactive state. The decarboxylation mechanism of naproxen has been fully discussed. Meanwhile, the free energy barriers of OH-induced photolysis reactions (ΔG‡eff(1a) = 7.6 kcal mol-1, ΔG‡eff(4a) = 7.0 kcal mol-1) are much lower than the free energy barriers induced by O2- and 1O2. It proves that OH is the most favourable one among the three ROS. The similar inhabition rates and free energy barriers of reactions induced by O2- and 1O2, respectively, have demonstrated that O2- and 1O2 equally contribute to the degradation. Additionally, the computational results are coincident with the observed experimental findings. Hence, this work has verified a part of naproxen photodegradation mechanism under UV irradiation and brought about a rational way to investigate contributions of different ROS in the complex photochemical system of PPCPs.

Photodegradation of naproxen in water under simulated solar radiation: mechanism, kinetics, and toxicity variation.

The main objective of this study was to investigate the degradation mechanism, the reaction kinetics, and the evolution of toxicity of naproxen in waters under simulated solar radiation. These criteria were investigated by conducting quenching experiments with reactive oxygen species (ROS), oxygen concentration experiments, and toxicity evaluations with Vibrio fischeri bacteria. The results indicated that the degradation of naproxen proceeds via pseudo first-order kinetics in all cases and that photodegradation included degradation by direct photolysis and by self-sensitization via ROS; the contribution rates of self-sensitized photodegradation were 1.4%, 65.8%, and 31.7% via ·OH, (1)O2 and O2(•-), respectively. Furthermore, the oxygen concentration experiments indicated that dissolved oxygen inhibited the direct photodegradation of naproxen, and the higher the oxygen content, the more pronounced the inhibitory effect. The toxicity evaluation illustrated that some of the intermediate products formed were more toxic than naproxen.

[Photodegradation of naproxen in aqueous systems by UV irradiation: mechanism and toxicity of photolysis products].

This paper studies the degradation mechanism, the reaction kinetics and the toxicity of photolysis products of naproxen in waters under UV irradiation (120 W mercury lamp) by quenching experiments of reactive oxygen species (ROS), oxygen concentration experiment and toxicity evaluation using Vibrio fischeri bacteria. The results demonstrated that NPX could be degraded effectively by UV irradiation and the photolysis pathways was the sum of the degradation by direct photolysis and self-sensitization via ROS, and the contribution rates of self-sensitized photodegradation were 0.1%, 80.2%, 35.7% via *OH, (1)O2, O2*-, respectively. The effect of oxygen concentration illustrated that dissolved oxygen had an inhibitory effect on the direct photodegradation of NPX, and the higher the oxygen content, the more obvious the inhibitory effect. The toxicity evaluation illustrated the formation of some intermediate products that were more toxic than NPX during the photodegradation of NPX. The process of NPX degradation in all cases could be fitted by the pseudo first-order kinetics model.

[Biomarkers of endothelial dysfunction and risk of early organ damage: a comparison between patients with primary aldosteronism and essential hypertension].

OBJECTIVE: To compare plasma concentrations of biomarkers of endothelial dysfunction between patients with primary aldosteronism (PA) and essential hypertension (EH), and to determine whether elevated levels of these biomarkers could predict development of early organ damage. METHODS: Thirty-six PA patients and 39 EH patients matched for age, sex, blood pressure and duration of hypertension were included in this study. Plasma levels of biomarkers reflecting endothelial dysfunction (von Willebrand factor, vWF; soluble intercellular adhesion molecule 1, sICAM-1; and oxidized low density lipoprotein, ox-LDL) were detected and compared between PA and EH patients. Left ventricular mass index (LVMI) determined by echocardiography, 24-hour urinary protein quantitative determination and urinary albumin excretion rate (UAER) were analyzed to evaluate early organ damage. Left ventricular hypertrophy was defined as LVMI > 125 g/m(2) in men and > 120 g/m(2) in women, and UAER between 20 µg/min and 200 µg/min was defined as microalbuminuria. RESULTS: vWF [(122.3 ± 53.8)% vs. (113.1 ± 68.3)%], sICAM-1 [(401.0 ± 74.1) µg/L vs. (300.9 ± 87.0) µg/L], ox-LDL [(13.6 ± 10.0) U/L vs. (8.1 ± 5.9) U/L], LVMI [(124.7 ± 33.6) g/m(2) vs. (109.1 ± 25.7) g/m(2)], 24-hour urinary protein quantitation [24 h UPQ, (0.17 ± 0.10) g vs. (0.09 ± 0.04) g] and UAER [(25.9 ± 7.7) µg/min vs. (9.7 ± 5.9) µg/min] were significantly higher in PA group than in EH group (all P < 0.05). Elevated plasma vWF, sICAM-1 levels and plasma aldosterone concentration independently predicted microalbuminuria. Whereas, elevated plasma vWF and ox-LDL levels, plasma aldosterone concentration and systolic blood pressure independently predicted left ventricular hypertrophy. CONCLUSION: Patients with PA have severer endothelial dysfunction reflected by multiple biomarkers and earlier organ damage than patients with EH, and plasma aldosterone concentration and multiple endothelial dysfunction biomarkers could independently predict early organ damage.