A dye-andrographolide assembly as a turn-on sensor for detection of phthalate in both cells and fish.

Phthalates can penetrate the environment and enrich various aquatic organisms through the food chain, which is involved in promoting the growth of breast cancer. It is of current interest to develop new sensors for phthalates. We herein reported a hydrogen-bond competing fluorescent sensor, BANP, for the detection of dibutyl phthalate (DBP). The BANP compound was synthesized by assembling andrographolide (Andro), nitro- and cyano-substituted BODIPY dye (BCN), and polyethylene glycol derivatives (DSPE-mPEG5000). BANP was found to be a turn-on fluorescent probe for DBP in water with a detection limit of 0.13 µg/g; the DBP-water system acts as a hydrogen bond switch to turn on the fluorescence. And BANP fluorescently detected DBP in contaminated fish meat. Moreover, BANP sensed the DBP-induced growth of human breast cancer MCF-7 cells, and the release of Andro in the DBP-cultivated cancer cells inhibited the proliferation of the MCF-7 cells. Taken together, BANP is a DBP-responsive probe for sensitive DBP detection in water, cells, and fish meats. The BANP sensor may be used in both in vitro fluorescence and cellular imaging analyses. Our results show that guest-induced reassembly brings forth significant fluorescence change, which is a promising way of designing new fluorescent probes for the analysis of phthalates in the environment and food.

A Mn(II) complex of boradiazaindacene (BODIPY) loaded graphene oxide as both LED light and H2O2 enhanced anticancer agent.

Cancer cells are more susceptible to H2O2 induced cell death than normal cells. H2O2-activatable and O2-evolving nanoparticles could be used as photodynamic therapy agents in hypoxic environments. In this report, a photo-active Mn(II) complex of boradiazaindacene derivatives (Mn1) was used as a dioxygen generator under irradiation with LED light in water. Moreover, the in vitro biological evaluation for Mn1 and its loaded graphene oxide (herein called Mn1@GO) on HepG-2 cells in normal and hypoxic conditions has been performed. In particular, Mn1@GO can react with H2O2 resulting active anticancer species, which show high inhibition on both HepG-2 cells and CoCl2-treated HepG-2 cells (hypoxic cancer cells). The mechanism of LED light enhanced anticancer activity for Mn1@GO on HepG-2 cells was discussed. Our results show that Mn(II) complexes of boradiazaindacene (BODIPY) derivatives loaded GO can be both LED light and H2O2-activated anticancer agents in hypoxic environments.

Effects of the N-salicylaladehyde Aminoglucose Schiff Base Complexes no O(2)(-). and DNA.

The effects of SG schiff base complexes with Cu(II), Zn(II), Co(III) on O(2)(-). and DNA were studied. The results showed that both CuSG and ZnSG could an inhibit the synthesis of O(2)(-). markedly. The inhibiting effect of CuSG was larger than that of ZnSG. Complexes CuSG and CoSG could also combine with the salmon sperm DNA. The intrinsic association constant (K(0)) for CuSG and CoSG were estimated to be 2.86x10(4) M(-1 and 1.29x105) M-1 respectively. The numbers of binding sites per 100 nucleotide (n) were 2.5 and 7.5 respectively.

Nomega-Nitro-L-Arginine Benzyl Ester Enhances Pulmonary Vasopressor Responses to Hypoxia and to Angiotensin II.

The effects of Nomega-nitro-L-arginine benzyl ester (L-NABE), an inhibitor of nitric oxide (NO) synthase, were investigated on pulmonary arterial responses during baseline or low tone conditions and during elevated tone conditions induced by ventilatory hypoxia or by AII in the isolated blood-perfused rat lung. We also tested the influence L-NABE on the vasodilator responses to acetylcholine (ACh) and nitroglycerin (GTN) during elevated pulmonary arterial tone conditions. Under baseline conditions, L-NABE in doses of 10--1000 &mgr;g, induced small increases in pulmonary arterial perfusion pressure that were significant for the higher doses studied. Ventilation with an hypoxic gas mixture or administration of AII significantly increased pulmonary arterial perfusion pressure and the responses were reproducible with respect to time. Following administration of L-NABE, the pulmonary arterial responses to hypoxic ventilation (HPV) were significantly enhanced, and L-NABE significantly enhanced the pulmonary arterial pressor responses to angiotensin II. During elevated pulmonary arterial tone conditions induced with hypoxic ventilation, L-NABE inhibited the vasodilator responses to acetylcholine (ACh); however, the vasodilator responses to nitroglycerin (GTN) were not altered. The small effect of L-NABE on baseline pulmonary arterial pressure in the isolated blood-perfused rat lung suggests that NO plays only a small role in maintaining pulmonary vascular tone at low resting levels. However, the augmentation of the pressor responses by L-NABE during HPV and to AII suggests that NO plays an important role in modulating these pulmonary pressor responses during elevated tone conditions. Additionally, the inhibition of pulmonary vasodilator response to ACh supports the hypothesis that NO release plays a major role in mediating vasodilator responses to endothelial-dependent agents such as ACh, but not to endothelial-independent agents such as GTN. In conclusion, these data suggest that NO release is more important under stimulated conditions than under basal conditions.

Hemodynamic Responses to Papaverine: Do Nitric Oxide, Cyclic GMP, or Calcium Mediate the Vasodilation?

Papaverine is a commonly used vasodilator of the internal mammary artery in cardiac surgery. The effects of papaverine with and without N(omega)-L-arginine methyl ester (L -NAME) (a nitric oxide production inhibitor) and/or zaprinast (a cyclic GMP inhibitor) or verapamil (calcium channel antagonist) on systemic vascular resistance in vivo have not been well documented. This study examines the hemodynamic responses to papaverine and attempts to identify the role of nitric oxide, cyclic guanosine monophosphate (GMP), and calcium in the vasodilation. The effects of varying doses of papaverine were evaluated with and without L-NAME and/or zaprinast or verapamil on the hindlimb vascular resistance in the male rat. With institutional approval, 40 male Sprague--Dawley rats (400--450 g) were anesthetized with intraperitoneal pentobarbital (50 mg kg(minus sign1)). The carotid artery, jugular vein, and abdominal aorta were cannulated by cutdown; mean arterial pressure (MAP) and hindlimb perfusion pressure (HPP) were recorded. Rats were heparinized (1000 U kg(minus sign1)). Papaverine (1, 3, 10, 30, and 100 &mgr;g) was injected into the hindlimb, whereas MAP was maintained constant, and the HPP was recorded. Both L-NAME (25 mg kg(minus sign1)) and/or verapamil and then papaverine (1, 3, and 10 &mgr;g) were injected into the hindlimb, and changes in HPP were recorded. A Student's t-test was used for statistical analysis, with a p < 0.05 considered significant. Papaverine, in increasing doses, decreased HPP incrementally. L-NAME partially blocked the effects of papaverine (p < 0.05), as did verapamil (p < 0.05). The combination of L-NAME and verapamil further decreased papaverine's vasodilation to almost eliminate it (p < 0.05). We demonstrated the effect of papaverine on the hindlimb vasculature is similar to its effects noted in the internal mammary artery. Nitric oxide is known to be an agent causing vasodilation. It was demonstrated that papaverine vasodilation in the hindlimb vascular bed is modified by L-NAME, which suggests that nitric oxide production inhibition is partially responsible for this effect. It was demonstrated that there is an effect of calcium channel blockade on the vasodilation caused by papaverine. Both L-NAME and verapamil together appear to modify further the vasodilation caused by papaverine, suggesting both calcium channel and nitric oxide mechanisms for vasodilation. Zaprinast, a specific cyclic GMP phosphodiesterase inhibitor, did not effect the vasodilation caused by papaverine, acetylcholine, nitroglycerin, or verapamil.

The Effect of Cromakalim on the Hindlimb Vascular Bed of the Male Rat: Do Glybenclamide and/or Nitric Oxide Modulate the Vasodilation?

Cromakalim, a benzopyran derivative, is a member of a novel class of antihypertensive agents that increase membrane K(+) conductance through ATP-sensitive K(+) channels. The effects of glybenclamide and N(omega)-L-arginine methyl ester (L-NAME), a specific inhibitor of nitric oxide synthesis from L-arginine were investigated on the vasodilator response to cromakalim in the hindlimb vascular bed in the male rat, as well as the combination glybenclamide and L-NAME. Thirty male Sprague--Dawley rats (350--450 g) were studied. Cromakalim in three doses (10, 30, 100 &mgr;g) injected into the hindlimb through a catheter induced a significant dose-dependent decrease in both mean arterial pressure (MAP) and hindlimb perfusion pressure (HPP). These responses were significantly modified by either glybenclamide or L-NAME. The role of a combination of glybenclamide and L-NAME on the vasodilator responses to cromakalim, acetylcholine, and nitroglycerin were also investigated. Three doses of either acetylcholine, nitroglycerin, or cromakalim caused dose-dependent reduction in HPP of the rats. The responses to acetylcholine were significantly blocked by L-NAME, but the responses to nitroglycerin were not. The vasodilation induced by cromakalim was not only partly blocked by glybenclamide but also by L-NAME. This blockade was significantly augmented when both glybenclamide and L-NAME were infused. These results suggest that nitric oxide may play an important role in regulating hindlimb vascular tone under physiologic conditions. The data also suggest that nitric oxide may be an additional mediator for cromakalim vasodilation as well as K(APT)(+) channel activation in the hindlimb vascular bed of the male rat.