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1.
РЖ ВИНИТИ 76 (BI28) 96.12-04Н3.81

    Moya-Camarena, S. Y.

    Response of NADH oxidation and growth in K-562 cells to the antitumor sulfonylurea, N-(4-methylphenylsulfonyl)-N'-(4-chlorophenyl)urea (LY181984) [Text] / S. Y. Moya-Camarena, D. J. Morre, D. M. Morre // Protoplasma. - 1995. - Vol. 188, N 3-4. - P151-160 . - ISSN 0033-183X
Перевод заглавия: Ответ окисления NADH и рост клеток К562 на противоопухолевую сульфонилмочевину, N-(4-метилфенилсульфонил)-N'-(4-хлорфенил)мочевину (LY 181948)
Аннотация: Growth of K-562 cells in culture is inhibited by the antitumor sulfonylurea LY 181984 (N-(4-methylphenylsulfonyl)-N'- (4-chlorophenyl)urea) with an ED[50] of about 30 'мю'M. With K-562 cells, NADH oxidation by plasma membranes was transiently stimulated and then inhibited by LY181984. NADH oxidation by whole cells was transiently stimulated and then inhibited by 0.1 to 100 'мю'M LY181984 as well. Both the stimulations and inhibitions of activity were time-dependent. NADH oxidation by lower phase membranes depleted of plasma membranes by aqueous two-phase partition also was inhibited by micromolar and submicromolar concentrations of LY181984. Inhibition did not correlate with mitochondrial presence but rather with membranes that appeared to be fragments of the Golgi apparatus. The oxidation of NADH by whole cells and of plasma membranes that was inhibited by LY181984 was distinguished from mitochondrial NADH oxidation by resistance to inhibition by cyanide and by proceeding under oxygen-depleted conditions or an argon atmosphere. In contrast to the active antitumor agent LY181984, the inactive but chemically-related analog. LY181985 (N-(4-methylphenylsulfonyl)-N'-(4-phenylurea), inhibited neither growth nor NADH oxidation with K-562 cells or cell fractions. Библ. 28
ГРНТИ  
ВИНИТИ 761.29.49.55.07.09.09
Рубрики: ПРОТИВООПУХОЛЕВЫЕ СРЕДСТВА
МЕХАНИЗМ ДЕЙСТВИЯ

СУЛЬФОНИЛМОЧЕВИНА

LY 181984

КУЛЬТУРА КЛЕТОК

ЛЕЙКОЗ K562

ОКИСЛИТЕЛЬНОЕ ФОСФОРИЛИРОВАНИЕ

МИТОХОНДРИИ

IN VITRO


Доп.точки доступа:
Morre, D.J.; Morre, D.M.


2.
РЖ ВИНИТИ 76 (BI29) 97.01-04Н1.214

    Moya-Camarena, S. Y.

    Response of NADH oxidation and growth in K-562 cells to the antitumor sulfonylurea, N-(4-methylphenylsulfonyl)-N'-(4-chlorophenyl)urea (LY181984) [Text] / S. Y. Moya-Camarena, D. J. Morre, D. M. Morre // Protoplasma. - 1995. - Vol. 188, N 3-4. - P151-160 . - ISSN 0033-183X
Перевод заглавия: Ответ окисления NADH и рост клеток К562 на противоопухолевую сульфонилмочевину, N-(4-метилфенилсульфонил)-N'-(4-хлорфенил)мочевину (LY 181948)
Аннотация: Growth of K-562 cells in culture is inhibited by the antitumor sulfonylurea LY 181984 (N-(4-methylphenylsulfonyl)-N'- (4-chlorophenyl)urea) with an ED[50] of about 30 'мю'M. With K-562 cells, NADH oxidation by plasma membranes was transiently stimulated and then inhibited by LY181984. NADH oxidation by whole cells was transiently stimulated and then inhibited by 0.1 to 100 'мю'M LY181984 as well. Both the stimulations and inhibitions of activity were time-dependent. NADH oxidation by lower phase membranes depleted of plasma membranes by aqueous two-phase partition also was inhibited by micromolar and submicromolar concentrations of LY181984. Inhibition did not correlate with mitochondrial presence but rather with membranes that appeared to be fragments of the Golgi apparatus. The oxidation of NADH by whole cells and of plasma membranes that was inhibited by LY181984 was distinguished from mitochondrial NADH oxidation by resistance to inhibition by cyanide and by proceeding under oxygen-depleted conditions or an argon atmosphere. In contrast to the active antitumor agent LY181984, the inactive but chemically-related analog. LY181985 (N-(4-methylphenylsulfonyl)-N'-(4-phenylurea), inhibited neither growth nor NADH oxidation with K-562 cells or cell fractions. Библ. 28
ГРНТИ  
ВИНИТИ 761.29.49.19.11.07
Рубрики: ПРОТИВООПУХОЛЕВЫЕ СРЕДСТВА
МЕХАНИЗМ ДЕЙСТВИЯ

СУЛЬФОНИЛМОЧЕВИНА

LY 181984

КУЛЬТУРА КЛЕТОК

ЛЕЙКОЗ K562

ОКИСЛИТЕЛЬНОЕ ФОСФОРИЛИРОВАНИЕ

МИТОХОНДРИИ

IN VITRO


Доп.точки доступа:
Morre, D.J.; Morre, D.M.


 




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