1,721,045 research outputs found
New insights into N-tert-Butyl-α-phenylnitrone (PBN) as a Spin Trap. Part 2. The Reactivity of PBN and 5,5-dimethyl-4,5-dihydropyrrole-N-oxide (DMPO) toward N-heteroaromatic bases
No full textNitroxide radicals protect against DNA damage in rat epithelial cells induced by nitric oxide, nitroxyl anion and peroxynitrite.
No full textIn order to gain more knowledge on the antioxidant role of nitroxide radicals, in this study we investigate their possible protective action against DNA damage induced by nitric oxide (NO) and reactive nitrogen oxide species deriving from it, namely nitroxyl anion (NO(-)) and peroxynitrite (ONOO(-)). Rat trachea epithelial cells were exposed under aerobic conditions to (1) NO generated by 150 microM S-nitrosoglutathione monoethyl ester (GSNO-MEE), (2) NO(-) generated by 200 microM Angeli's salt (Na(2)N(2)O(3)) (3) ONOO(-) generated by 1mM SIN-1 (3-morpholino-sydnonimine) and (4) 100 microM synthesized ONOO(-), in the absence and presence of 5 microM of two indolinonic nitroxides synthesized by us and the piperidine nitroxide TEMPO (2,2,6,6-tetramethylpiperidine-1-oxyl). DNA damage was assessed using the comet assay-a rapid and sensitive, single-cell gel electrophoresis technique used to detect primary DNA damage in individual cells. The parameter tail moment, used as an index of DNA damage, showed that in all cases the nitroxides remarkably inhibited DNA strand breaks induced by the different nitrogen oxide species. All three nitroxides protect to the same extent, except in the case of synthesized peroxynitrite where the aromatic nitroxides 1 and 2 are more efficient than TEMPO. These findings are consistent with the antioxidant character of nitroxide compounds and give additional information on the potential implications for their use as therapeutic agents
Lack of in vitro protection by a common sunscreen ingredient on UVA-induced cytotoxicity in keratinocytes
Full text linkAs an extension of our previous investigations on sunscreen ingredients, the present work was aimed at assessing the possible
protective effects of a common UVA-absorbing agent, Parsol 1789 (4-tert-butyl-4-methoxydibenzoylmethane) in contact with
human keratinocytes under UVA illumination. Cell viability was evaluated by determining lactate dehydrogenase (LDH) release,
uptake of propidium iodide and fluorescein diacetate, total protein content and percentage of cell detachment. Apoptosis was
detected by recognition of translocated phosphatidylserine using annexin V-FITC uptake. Oxidative stress was evaluated through
the carboxy-H2DCFDA assay while the total oxyradical scavenging capacity (TOSC) assay was used for determining the total
antioxidant capacity level in these cells. Lipid peroxidation was also assessed by checking hydroperoxide (HP) levels. The
results obtained show that UVA exposure induces significant cell mortality, decrease in protein concentration, release of LDH,
increase in apoptosis, oxidative stress and lipid peroxidation with a concomitant reduction in the response of the antioxidant
cellular defense system. The presence of 10M Parsol 1789 did not minimize these UVA-induced effects, on the contrary,
for some parameters measured such as lipid hydroperoxides, there was a significant enhancement. Furthermore, the presence
of glutathione (GSH) alone decreased the level of ROS and lipid hydroperoxides, but in combination with Parsol 1789, this
protective effect was reduced. The overall results indicate that the compound does not protect these cells from UVA exposure
under our experimental conditions confirming previous findings on the lack of photoprotective efficiency of this sunscreen in
contact with biologically relevant molecules. However, the biological role and significance of these results to the consequences
of sunscreen use in humans are not known, hence extrapolation from laboratory experiments must be done with caution.
© 2004 Elsevier Ireland Ltd. All rights reserved
Aromatic Secondary Amines as Antioxidants for Polyolefins. Part 2: Phenothiazines
No full textAbstract: The thermoxidation of polypropylene (PP) at 200 degrees C in the presence of phenothiazine (1) and 3,7-di-tert-butylphenothiazine (2) was studied by measuring the oxygen consumption. The rate of oxygen consumption during the induction period passes through a minimum when the antioxidant concentration increases. Both compounds studied have the same critical concentrations but at high concentrations 2 is more efficient than 1. The results obtained may be explained by the differences in the evaporation rate of 1 and 2 during oxidation. ESR signals of radicals originating from 1 and 2 after polymer oxidation at 160 degrees C were observed
Diastereoselectivity in 1,3-dipolar cycloaddition reactions between indolic nitrones and electron-deficient alkenes
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