• Journal of the Korean Chemical Society
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• v.43 no.3
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• pp.370-372
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• 1999

• Bulletin of the Korean Chemical Society
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• v.24 no.1
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• pp.129-132
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• 2003

• Bulletin of the Korean Chemical Society
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• v.24 no.7
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• pp.1041-1044
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• 2003

• Proceedings of the PSK Conference
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• 2000.04a
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• pp.129.1-129.1
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• 2000

• BMB Reports
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• v.45 no.2
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• pp.114-119
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• 2012

Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline) is a compound derived from dopamine metabolism and is capable of causing dopaminergic neurodegeneration. Oxidative modification of neurofilament proteins has been implicated in the pathogenesis of neurodegenerative disorders. In this study, oxidative modification of neurofilament-L (NF-L) by salsolinol and the inhibitory effects of histidyl dipeptides on NF-L modification were investigated. When NF-L was incubated with 0.5 mM salsolinol, the aggregation of protein was increased in a time-dependent manner. We also found that the generation of hydroxyl radicals (${\bullet}OH$) was linear with respect to the concentrations of salsolinol as a function of incubation time. NF-L exposure to salsolinol produced losses of glutamate, lysine and proline residues. These results suggest that the aggregation of NF-L by salsolinol may be due to oxidative damage resulting from free radicals. Carnosine, histidyl dipeptide, is involved in many cellular defense processes, including free radical detoxification. Carnosine, and anserine were shown to significantly prevent salsolinol-mediated NF-L aggregation. Both compounds also inhibited the generation of ${\bullet}OH$ induced by salsolinol. The results indicated that carnosine and related compounds may prevent salsolinol-mediated NF-L modification via free radical scavenging.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.3
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• pp.323-330
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• 1998

Tetrahydroisoquinoline (THI) alkaloids can be considered as cyclized derivatives of simple phenylethylamines. Many of them, especially with 6,7-disubstitution, demonstrate a relatively high affinity for catecholamines. Present study examines the pharmacological action of limited series of THI, using rats' isolated atria and aorta. In addition, a $[^3H]$ prazosin displacement binding study with THI compounds was performed, using rat brain homogenates to investigate whether these probes have ?${\alpha}$-adrenoceptor affinity. We also compared the vascular relaxation potency of these probes with dobutamine. YS 49, YS 51, higenamine and dobutamine, concentration-dependently, relaxed endothelium-denuded rat thoracic aorta precontracted with phenylephrine (PE, 0.1 ${\mu}M$) in which $pEC_{50}$ were $5.56{\pm}0.32$ and $5.55{\pm}0.21$, $5.99{\pm}1.16$ and $5.57{\pm}0.34$, respectively. These probes except higenamine also relaxed KCl (65.4 mM)-contracted aorta. In isolated rat atria, all THIs and dobutamine increased heart rate and contractile force. In the presence of propranolol, the concentration response curves of YS 49 and YS 51 shifted to the right and resulted in $pA_2$ values of $8.07{\pm}0.84$ and $7.93{\pm}0.11$, respectively. The slope of each compound was not deviated from unity, indicating that these chemicals are highly competitive at the cardiac ?${\beta}-adrenoceptors$. YS 49, YS 51, and higenamine showed ?${\alpha)-adrenoceptor$ affinity in rat brain, in which the dissociation constant $(K_i)$ was 2.75, 2.81, and 1.02 ${\mu}M$, respectively. It is concluded, therefore, that THI alkaloids have weak affinity to ${\alpha)_1-adrenoceptor$ in rat aorta and brain, respectively, while these probes show relatively high affinity for cardiac ${\beta}-adrenoceptors$. Thus, these chemicals may be useful in the treatment of congestive heart failure.

• YAKHAK HOEJI
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• v.30 no.5
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• pp.245-252
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• 1986

Various structural analogs of higenamine, 1-(4'-hydroxylbenzyl)-6,7-dihydroxy-1, 2, 3, 4-tetrahydroisoquinoline, were synthesized and their inhibitory activities against platelet aggregation induced by either arachidonic acid, ADP or collagen. Among the twenty-five compounds tested, inhibitory activity is favored by the 3, 4-dihydroisoquinoline system with the methyl bridge between the two aromatic rings replaced by either ethyl or ethenyl group. N-Methyl quaternization decreased the inhibitory activities. * 이논문의 내용중 편집상의 오류가 있습니다. 그에대한 정오표는 v.31, n.1의 45p.에 있습니다.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.114-114
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• 2001

Tetrahydropapaveroline (THP), a dopamine-derived 6, 7-dihydroxy-1-(3' ,4'-dihydroxybenzyl)-1,2,3,4-tetrahydroisoquinoline, has been suspected as a possible dopaminergic neurotoxin to elicit Parkinsonism. Autooxidation or enzymatic oxidation of THP and subsequent generation of reactive oxygen species (ROS) may contribute to the degeneration of dopaminergic neurons induced by this isoquinoline alkaloid.(omitted)

• Bulletin of the Korean Chemical Society
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• v.12 no.4
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• pp.373-376
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• 1991

Degradation of (-)-laudanosine, a 1-benzyl-1,2,3,4-tetrahydroisoquinoline alkaloid, with ethyl chloroformate (ECF) afforded an optically active chloro-carbamate as an intermediate. The reason why this intermediate exhibits an optical activity was investigated by comparison with the reactions of some model compounds with ECF. It may be supposed that the chloride group in a hypothetic carbenium ion intermediate stands very closely to the chiral center, so conserving optical activity. However, a neighboring group effect can not be excluded.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.3
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• pp.802-810
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• 2005

The tetrahydroisoquinolines included potent cytotoxic agents that showed antitumor activity,antimicrobial activity, and other biological properties. We studied the effect of CDST, 1-Chloromethyl-6,7-dimethoxy-3,4-dihydro-1H-isoquinoline-2-sulfonic acid amide, a newly synthesized anti-cancer agent. The cytotoxic activity of CDST in HL-60 cells was increased in a dose-dependent manner. CDST, tetrahydroisoquinolines derivative, was cytotoxic to HL-60 cells, with IC50 of $80{\mu}g/ml$. Treatment of CDST to HL-60 cells showed the fragmentation of DNA in a dose- and time dependent manner, suggesting that thesecells underwent apoptosis. Treatment of HL-60 cells with CDST was induced in a dose- and time-dependent activation of caspase-3, caspase-8 and proteolytic cleavage of poly(ADP-ribose) polymerase. In caspase activity assay, caspase-3 and -8 was activated after 12 h and 6 h posttreatment, respectively. CDST also caused the release of cytochrome c from mitochondria into the cytosol. CDST-induced cytochrome c release was mediated by caspase-8-dependent cleavage of Bid and Bax translocation. These results suggest that caspase-8 induced Bid cleavage and Bax translocation, caused mitochondrial cytochrome c release, and induce caspase-3 activationduring CDST-induced apoptosis in HL-60 cells.