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PubMed2002

Influence of hydroxypropyl-beta-cyclodextrin on photo-induced free radical production by the sunscreen agent, butyl-methoxydibenzoylmethane.

The aim of the study was to investigate the effect of hydroxypropyl-beta-cyclodextrin (HP-beta-CD) on the photo-induced production of free radicals by the sunscreen agent, butyl-methoxydibenzoylmethane (BMDBM). Spin-trapping/electron paramagnetic resonance spectroscopy was used to evaluate the formation of radicals and the extent of BMDBM photodegradation was measured by high-performance liquid chromatography. The stable 2,2,6,6-tetramethylpiperidine-1-oxyl, nitroxide radical (TEMPO) was used as spin-trap. Any free radicals generated during irradiation of the sunscreen agent will couple with the TEMPO radicals giving diamagnetic species and thus a decrease of the signal intensity in the electron paramagnetic resonance spectrum. Following 2-h illumination with simulated sunlight, the solution containing free BMDBM exhibited a 93.9% decrease of the intensity of the TEMPO signal. Under the same irradiation conditions, only a 12.2% reduction of the TEMPO concentration was measured in the sample containing BMDBM complexed with HP-beta-CD. Moreover, the decrease of the spin-trap level observed for the HP-beta-CD/BMDBM complex was not significantly different from that produced when solutions containing TEMPO only or TEMPO in the presence of HP-beta-CD alone were subjected to irradiation. In addition, the photodegradation of the sunscreen agent was reduced by complexation with HP-beta-CD (the extent of degradation was 27.6% for the complex compared with 63.1% for free BMDBM). The results obtained indicate that the free radicals generated by BMDBM when exposed to simulated sunlight are effectively scavenged by inclusion complexation of the sunscreen agent with HP-beta-CD.

2-Hydroxypropyl-beta-cyclodextrin↗
PubMed1976

Cerebrovascular response to infused noradrenalin and its modification by a catecholamine metabolism blocker.

Despite many studies, the cerebrovascular action of infused noradrenalin is still unclear. The study reported here tested the hypothesis that infused noradrenalin is prevented from reaching the adrenoreceptors by being avidly taken up and metabolized in the vascular smooth muscle. Cerebral blood flow was measured by the xenon133 clearance technique in nine baboons before and during blockade of the enzyme catechol-O-methyl transferase, which is known to be important in inactivation of circulating noradrenalin. The cerebral blood flow responses to noradrenalin infused at 8, 16, and 32 mug per minute were also determined. Responses indicated vasodilatation before but vasoconstriction after blockade, with a significant noradrenalin. It is suggested that the cerebral circulation is normally protected against sympathetic vasoconstriction by the avid uptake and metabolism of noradrenalin in extraneuronal and possibly neuronal sites.

Animals↗
PubMed1984

Bupropion in Parkinson's disease.

Bupropion is an antidepressant, thought to be an indirect dopaminergic agonist. No significant sympathomimetic, anti-cholinergic, or MAO inhibitor effects have been reported. We evaluated this drug in 20 patients with idiopathic Parkinson's disease. Parkinsonism lessened by at least 30% (Northwestern University Disability Scale or Modified New York University Parkinson's Disease Scale) in half the patients. Depression, present in 12 of 20, was alleviated in only 5. Bupropion is mildly efficacious in Parkinson's disease, although side effects were frequent and were dose-limiting in five patients.

Adult↗
PubMed2005

Induction of apoptosis in human promyelocytic leukemia cell line HL-60 by C-benzylated dihydrochalcones, uvaretin, isouvaretin and diuvaretin.

Uvaretin, isouvaretin and diuvaretin, cytotoxic C-benzylated dihydrochalcones isolated from Uvaria acuminata, displayed growth inhibitory effects against human promyelocytic leukemia HL-60 cells. We examined the mechanism of the cytotoxicity. From the morphological study by staining with Hoechst 33258, the cells treated with C-benzylated dihydrochalcones exhibited significant chromosomal condensation and nuclear degradation. The cell cycle analysis showed the accumulation of cells in the G1 phase and the appearance of a sub-G1 peak. These results suggest apoptotic cell death. Further, from the detection of DNA fragmentation and the activation of caspase-3, the biological hallmarks of apoptosis, these C-benzylated dihydrochalcones appeared to induce apoptosis against HL-60 cells. The cytotoxicity of uvaretin and diuvaretin was stronger than that of isouvaretin, which suggest that the 5'-substitution of the 2-hydroxybenzyl group increased the cytotoxicity.

Apoptosis↗
PubMed1990

Acidic drug transport in vivo through the blood-brain barrier. A role of the transport carrier for monocarboxylic acids.

The relationship of the transports between acidic drugs and monocarboxylic acids through the blood-brain barrier (BBB) was examined using the carotid artery injection technique in rats. The BBB uptakes of [3H]acetic acid and [14C]salicylic acid were significantly reduced by the presence of the respective unlabeled compounds, valproic acid, lactic acid, benzoic acid, nicotinic acid or beta-lactam antibiotics (benzylpenicillin, propicillin and cefazolin), but was not reduced by choline, phenylalanine and a basic drug, eperisone. A remarkable pH dependency was observed for the BBB uptake of [14C]salicylic acid at the pH region of 4.0 to 7.4. Interestingly, 10 mM of salicylic acid diminished significantly the pH dependent BBB uptake of [14C]salicylic acid. Similar results were obtained in the BBB uptake of [14C]nicotinic acid. No significant difference was observed in the transport of monocarboxylic acids through the BBB between normotensive Wistar KY rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). From these observations, acidic drugs could be transported by a carrier-mediated system for monocarboxylic acids at the BBB and the transport system was not changed by the disease state.

Acetates↗
PubMed1990

In vivo and in vitro evidence for a common carrier mediated transport of choline and basic drugs through the blood-brain barrier.

The blood-brain barrier (BBB) transport system for choline and basic drugs was characterized by the in vivo carotid artery injection technique (Oldendorf, Brain Res., 24, 372-376, 1970) and in vitro uptake into isolated bovine brain capillaries (Pardridge et al., J. Neurochem., 44, 1178-1184, 1985). Basic drugs such as eperisone, thiamine and scopolamine significantly inhibited choline uptake by the BBB with the half inhibitory concentration, IC50 value of 1.45, 2.06, and 0.47 mM, respectively. On the contrary, the uptake of choline was not inhibited by amino acids (L-phenylalanine and L-arginine) and acidic drugs (nicotinic acid, salicylic acid and valproic acid). Choline was taken up by the isolated brain capillaries in concentration and temperature dependent manners. The uptake of choline by the isolated bovine brain capillaries was significantly inhibited by eperisone, scopolamine and thiamine in consistent with the in vivo results. Furthermore, eperisone inhibited competitively the uptake of choline with the inhibition constant, Ki value of 455 microM. According to these results it was suggested that in the BBB choline and basic drugs would share a common carrier-mediated transport system.

Animals↗