We studied the effects of UV radiation on the degree of phosphatidylcholine (PC) liposome membrane oxidation in the presence of such toxic organometallic compounds (TOC) as diphenyltin dichloride (DPhT), triphenyltin chloride (TPhT), dibutyltin dichloride (DBT), tributyltin chloride (TBT), triphenyllead chloride (TPhL) and tributyllead chloride (TBL). PC liposome oxidation was also investigated in the presence of quercetin (Que) and equimolar mixtures of Que and TOC in order to determine the protective properties of this natural antioxidant with respect to liposome membrane oxidation induced by UV light. Concentration of the compounds studied was 10 µM. The degree of liposome oxidation was measured using the TBARS (Thiobarbitutric Reactive Substances) test. The sequence thus obtained of relative induction of PC oxidation due to TOC was as follows: TBT > TPhT = DBT > DPhT = TPhL > TBL. The results of studies with Que indicate its high efficacy in the antioxidative action of equimolar mixtures of Que and TOC. From our study it follows that quercetin forms complexes both with phenyl- and butyl- tin and lead compounds. A high antiradical (towards DPPH radical) activity of the associates with respect to the activity of quercetin alone was also found. This result can partly explain the antioxidative properties of Que in the studied solution, connected with their antiradical action and chelating posibility towards the organometallic compounds studied. A factor that differentiates the antioxidant activity of the complexes Que-TOC is probably their differentiated location in the liposome membrane bilayer. A factor that differentiates the antioxidant activity of the complexes Que-TOC is probably their differentiated location in the liposome membrane bilayer.
3
Dostęp do pełnego tekstu na zewnętrznej witrynie WWW
It is widely appreciated that inflammation and oxidant stress contribute to atherogenesis. Curcumin, a polyphenolic natural compound has been reported to possess anti-inflammatory and anti-oxidant actions. We hypothesized that curcumin could inhibit the development of atherosclerosis in the apoE/LDLR - double knockout mice fed with Western diet (21% fat, 0.15% cholesterol w/w, without cholic acid). Curcumin (purity 98%), premixed with diet, was given for 4 months at a dose of 0.3 mg/per day/per mouse. In this model curcumin inhibited atherogenesis, measured both by "en face" method (25,15±2,9% vs. 19,2±0,6%, p<0,05) and "cross-section" method (565867±39764 µm2 vs. 299201±20373 µm2, p<0,05). Importantly, curcumin influenced neither the concentrations of cholesterol and triglycerides in blood nor animal body weight. To our knowledge, this is the first report that shows the anti-atherogenic effect of low dose of curcumin in fine model of atherosclerosis: gene-targeted apoE/LDLR - double knockout mice.
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.