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РЖ ВИНИТИ 76 (BI29) 97.08-04Н1.352

Melnick, R. L.
1,3-Butadiene induces cancer in experimental animals at all concentrations from 6.25 to 8000 parts per million [Text] / R. L. Melnick, J. E. Huff // Butadiene and Styrene: Assess. Health Hazards. - Lyon, 1993. - P309-322 . - ISBN 92-832-2127-3
Перевод заглавия: 1,3-бутадиен индуцирует рак у экспериментальных животных при всех концентрациях от 6,25 до 8000 ppm
Аннотация: 1,3-Butadiene, a chemical produced in large volumes, induces cancer in many organs in rats (at 1000 and 8000 ppm) and mice (at 6.25 to 1250 ppm); however, the sites of tumour induction (seven in rats and nine in mice) and the magnitudes of response differ between the two species. Particularly noteworthy in the studies of mice exposed by inhalation were the early, extensive induction of malignant lymphomas, the induction of uncommon haemangiosarcomas of the heart and the development of malignant lung tumours at 6.25 ppm, the lowest concentration ever used in a long-term carcinogenicity study of this gas. In order to account for the impact of early mortality on the expression of late development of tumours, survival-adjusted tumour rates were computed for mice exposed to butadiene at 6.25-625 ppm. The results provide a more accurate characterization of concentration-dependent responses for butadiene-induced cancers. Stop-exposure studies revealed that the atmospheric concentration of butadiene was a greater contributing factor to the development of lymphomas than was duration of exposure. The studies in mice show a good correspondence with the reported associations between occupational exposure to butadiene and excess mortality from lymphatic and haematopoietic cancers; mice are thus a better experimental surrogate for humans. Although further work is needed to improve the understanding of the mechanisms of tumour induction by butadiene, pursuit of that research must not delay reduction of human exposure to this carcinogenic chemical. США, Environmental Carcinogenesis Program, Nat. Inst. of Env. Health Sci., Res. Triangle Park, North Carolina. Библ. 82

ГРНТИ	76.29.49

ВИНИТИ 761.29.49.21.07.11
Рубрики: КАНЦЕРОГЕНЕЗ ХИМИЧЕСКИЙ
КАНЦЕРОГЕНЫ ПРОМЫШЛЕННЫЕ
1,3-БУТАДИЕН
КОНЦЕНТРАЦИОННЫЕ ЗАВИСИМОСТИ
ОПУХОЛИ ЗЛОКАЧЕСТВЕННЫЕ
ЛАБОРАТОРНЫЕ ЖИВОТНЫЕ

Доп.точки доступа:
Huff, J.E.

РЖ ВИНИТИ 34 (BI34) 97.09-04Т4.145

Melnick, R. L.
1,3-Butadiene induces cancer in experimental animals at all concentrations from 6.25 to 8000 parts per million [Text] / R. L. Melnick, J. E. Huff // Butadiene and Styrene: Assess. Health Hazards. - Lyon, 1993. - P309-322 . - ISBN 92-832-2127-3
Перевод заглавия: 1,3-бутадиен индуцирует рак у экспериментальных животных при всех концентрациях от 6,25 до 8000 ppm
Аннотация: 1,3-Butadiene, a chemical produced in large volumes, induces cancer in many organs in rats (at 1000 and 8000 ppm) and mice (at 6.25 to 1250 ppm); however, the sites of tumour induction (seven in rats and nine in mice) and the magnitudes of response differ between the two species. Particularly noteworthy in the studies of mice exposed by inhalation were the early, extensive induction of malignant lymphomas, the induction of uncommon haemangiosarcomas of the heart and the development of malignant lung tumours at 6.25 ppm, the lowest concentration ever used in a long-term carcinogenicity study of this gas. In order to account for the impact of early mortality on the expression of late development of tumours, survival-adjusted tumour rates were computed for mice exposed to butadiene at 6.25-625 ppm. The results provide a more accurate characterization of concentration-dependent responses for butadiene-induced cancers. Stop-exposure studies revealed that the atmospheric concentration of butadiene was a greater contributing factor to the development of lymphomas than was duration of exposure. The studies in mice show a good correspondence with the reported associations between occupational exposure to butadiene and excess mortality from lymphatic and haematopoietic cancers; mice are thus a better experimental surrogate for humans. Although further work is needed to improve the understanding of the mechanisms of tumour induction by butadiene, pursuit of that research must not delay reduction of human exposure to this carcinogenic chemical. США, Environmental Carcinogenesis Program, Nat. Inst. of Env. Health Sci., Res. Triangle Park, North Carolina. Библ. 82

ГРНТИ	34.47.03

ВИНИТИ 341.47.03.19.19
Рубрики: КАНЦЕРОГЕНЕЗ ХИМИЧЕСКИЙ
КАНЦЕРОГЕНЫ ПРОМЫШЛЕННЫЕ
1,3-БУТАДИЕН
КОНЦЕНТРАЦИОННЫЕ ЗАВИСИМОСТИ
ОПУХОЛИ ЗЛОКАЧЕСТВЕННЫЕ
ЛАБОРАТОРНЫЕ ЖИВОТНЫЕ

Доп.точки доступа:
Huff, J.E.

РЖ ВИНИТИ 34 (BI52) 89.11-04Т6.104

Chong, Saeho.
Kinetic mechanisms for the concentration dependency of in vitro degradation of nitroglycerin and glyceryl dinitrates in human blood: Metabolite inhibition or cosubstrate depletion? [Text] / Saeho Chong, Ho-Leung Fung // J. Pharm. Sci. - 1989. - Vol. 78, N 4. - P295-302 . - ISSN 0022-3549
Перевод заглавия: Кинетические механизмы концентрационной зависимости деградации нитроглицерина и глицерилдинитратов в крови человека in vitro: ингибирование метаболизма или косубстратное истощение?
Аннотация: В препаратах цельной крови человека, в реконституированных эритроцитах (РЭ), лизированных эритроцитах (ЛЭ) и в плазме исследовали влияние добавки тиолов (N-ацетилцистеина, I; L-цистеина, II; D-цистеина, III; глутатиона, IV) на скорость деградации (СД) [{1}{4}C]-нитроглицерина (V). I-III увеличивали СД в цельной крови, тогда как IV не влиял на СД. I-IV и дитиотреитол в 3- 14 раз увеличивали СД в плазме. Рассматривая I-IV как косубстраты процесса истощения, обсуждают полученные данные в связи с зависимостью СД V от исходной конц-ии V. США, Dep. of Pharmaceutics, School of Pharmacy, State Univ. of New York at Buffalo, Buffalo, NY 14260. Библ. 34.

ГРНТИ	34.45.25

ВИНИТИ 341.45.25.29.11.19.09
Рубрики: НИТРОГЛИЦЕРИН
ГЛИЦЕРИЛДИНИТРАТ
МЕТАБОЛИЗМ
КОСУБСТРАТНОЕ ИСТОЩЕНИЕ
КОНЦЕНТРАЦИОННЫЕ ЗАВИСИМОСТИ
КИНЕТИЧЕСКИЕ МЕХАНИЗМЫ
ЭРИТРОЦИТЫ
ЧЕЛОВЕК

Доп.точки доступа:
Fung, Ho-Leung

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