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[化学致癌物诱导小鼠T细胞淋巴瘤发生]

[T-cell lymphomagenesis induced by chemical carcinogens in mice].

作者信息

Seidel H J

出版信息

Eksp Onkol. 1984;6(3):21-4.

PMID:6333977
Abstract

Investigations were performed on models of murine leukemogenesis induced by butylnitrosourea or methylnitrosourea in DBA/2, C57B1/6, NMRI, BDF and CBA mice. The latency period in CBA mice was longer than in mice of the other strains. The first transplantable cells appeared mostly in the thymus, and only in two cases in the bone marrow. Methylnitrosourea suppressed the activity of natural killer cells, but not to the same extent as leukemogenic irradiation. Heterogeneity of leukemic T-cell phenotypes with respect to the expression of the ly-1 and ly-2 antigens was detected. At the same time leukemic cells revealed consistent inability to be agglutinated by peanut agglutinine. When hydrocortisone was injected to mice after the carcinogene treatment or within 24 h before it, the leukemogenesis was delayed.

摘要

对丁基亚硝脲或甲基亚硝脲诱导的DBA/2、C57B1/6、NMRI、BDF和CBA小鼠白血病模型进行了研究。CBA小鼠的潜伏期比其他品系的小鼠长。最早出现的可移植细胞大多出现在胸腺中,仅在两例中出现在骨髓中。甲基亚硝脲抑制自然杀伤细胞的活性,但程度不如致白血病辐射。检测到白血病T细胞表型在ly-1和ly-2抗原表达方面的异质性。同时,白血病细胞表现出始终无法被花生凝集素凝集的特性。在致癌剂处理后或处理前24小时内向小鼠注射氢化可的松,白血病的发生会延迟。

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