Reference

Further studies on the response of intestinal crypt cells of different hierarchical status to eighteen different cytotoxic agents

Further studies on the response of intestinal crypt cells of different hierarchical status to eighteen different cytotoxic agents.Some chemicals with cas registry numbers like 15663-27-1 and 23214-92-8 are also used. Ijiri, K.; Potten, C. S. (Fac. Sci., Univ. Tokyo, Tokyo 113, Japan). Br. J. Cancer, 55(2), 113-23 (English) 1987. CODEN: BJCAAI. ISSN: 0007-0920. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Section cross-reference(s): 8 Adult male mice were treated with 1 or 2 different doses of each of 18 different cytotoxic agents. They were sampled at various times (3-12 h) thereafter, and the spatial distributions of cell death in the small intestinal crypts were studied. Dead or dying cells or cells carrying dead cell fragments were examd. histol., and all of these were recorded (for convenience as apoptotic fragments), relative to the cell position in the crypt. Thus, distributions of apoptotic fragments against cell position were detd. A regression anal. of the data obtained at different times after administration of each cell position were detd. A regression anal. of the data obtained at different times after administration of each agent was undertaken and the position of the median of the spatial distribution of presumptive target cells was deduced for each cytotoxic agent. The accuracy of this median value was detd. to be ±0.5 cell positions. From these median values, the different cytotoxic agents could be divided roughly into 3 groups: 3H-labeled thymidine [50-89-5], isopropylmethanesulfonate [926-06-7], g-rays, bleomycin [11056-06-7] and adriamycin [23214-92-8] all have their median values (susceptible cells) at cell positions 4 to 6; bischlorethylnitrosourea [154-93-8], actinomycin D [50-76-0], cyclophosphamide [50-18-0], and cycloheximide [66-81-9] at cell positions 6-8; mechlorethamine [51-75-2], triethylenethiophosphoramide [52-24-4], vincristine [57-22-7], 5-fluorouracil [51-21-8], hydroxyurea [127-07-1] and methotrexate [59-05-2] at cell positions 8-11. The position of these medians was considered in relation to the killing of clonogenic cells. Preliminary studies on the distributions of dead cells after myleran [55-98-1], cis-platinum [15663-27-1] and heat (hyperthermia) are also reported. There is a general tendency for antibiotics and radiation to attack the lower cell positions in the crypt. Alkylating agents on the other hand have a somewhat broad spectrum of action. Antimetabolites and a microtubule dissocg. agent act on higher cell positions. No difference could be detected between 2 different forms (sources) of actinomycin D. The changes in the yields of apoptotic and mitotic cells with time and the migration velocities of cells in the crypts carrying apoptotic fragments after exposure to cytotoxics are also presented. .

Pulmonary toxicity of cytostatic drugs: cell kinetics

Pulmonary toxicity of cytostatic drugs: cell kinetics. Witschi, Hanspeter; Godfrey, Gayle; Frome, Ed; Lindenschmidt, Robert C. (Biol. Div., Oak Rridge Natl. Lab., Oak Ridge, TN 37831, USA). Fundam. Appl. Toxicol., 8(2), 253-62 (English) 1987. CODEN: FAATDF. ISSN: 0272-0590. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Mice were treated with 3 cytostatic drugs: cyclophosphamide [50-18-0], busulfan [55-98-1], or BCNU [154-93-8]. The alveolar labeling index was measured following drug administration with a pulse of 3H-labeled thymidine and autoradiog. In cyclophosphamide-treated animals, peak alveolar cell proliferation was seen 5 days after injection of the drug. In animals treated with busulfan or BCNU, proliferation was even more delayed (occurring 2-3 wk after administration). 154-93-8 and 50-18-0 which are cas registry numbers of chemicals are mentioned. In contrast, with oleic acid, the highest alveolar cell labeling was found 2 days after i.v. administration. In animals exposed to a cytostatic drug, proliferation of type II alveolar cells was never a prominent feature, whereas in animals treated with oleic acid there was an initial burst of type II cell proliferation. Thus, the patterns of pulmonary repair vary between chem. designed to interfere with DNA replication as compared to agents which produce acute lung damage such as oleic acid. .