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This study evaluated strain reactions in young athletes (mean age: 17.6 years). Of 35 male rowers, 21 were selected by rowing ergometer tests to take part in a 26-day training camp before the World Championships in 1989. Blood samples were obtained in the morning of the day after rowing ergometer tests and on the 16th and 26th day. Cortisol (C), testosterone (T), sexual-hormone-binding globulin (SHBG), urea and creatine kinase (CK) were determined in serum and free testosterone (FT) was calculated. In the nonselected rowers C was 10% higher, FT 20% lower, and CK 42% higher compared to the selected rowers. During training, C was related to the intensity of training. It remained constant in phase 1 (12 days, increased volume of training) and increased in phase 2 (10 days, decreased volume and higher intensity). FT decreased in phase 1 and increased in phase 2. Urea showed a close relationship to training volume. CK levels decreased during the training volume. CK levels decreased during the training period as an adaptation to the training. Despite a high training load, there were no indications of overstrain reactions in these young athletes.

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The combined effects of amino acid antagonists with proven or potential inhibitory activities on aminoacyl-tRNA synthetases were investigated on the murine leukemic cell line P388 D1. As the best result a summation of the antiproliferative effects was observed. Combinations with established cytostatic agents like platinum complexes or other antitumor compounds also yielded partly additive effects. In experiments performed with asparaginase L-aspartic acid-beta-hydroxamate gave synergistic growth inhibition of P388 D1 cells in vitro, which was reflected by additive effects against murine leukemia P388 in vivo.

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Experiments on the P 388 D1 cell line (48 h exposure) demonstrate that [1,2-bis-(fluorophenyl)ethylenediamine]platinum(II) complexes are comparably active on the cell number and 3H-thymidine incorporation, irrespective of the position of the fluorine atom (ortho, meta, or para) and the nature of the "leaving group" (Cl- or H2O). However, the compounds of the R,R/S,S series are more active than those of the R,S series and comparable to cisplatin. In the "tumor colony forming assay" the R,R/S,S configurated compounds are about ten times as active as cisplatin. The R,R/S,S configurated diaqua[1,2-bis(4-fluorophenyl)ethylenediamine]platinum(II) salts reach their half maximum effect more readily (t1/2 approximately equal to 1.6 h) than their R,S configurated analogues (t1/2 approximately equal to 20 h). A time limited contact of the cells with R,R/S,S configurated diaqua[1,2-bis(4-fluorophenyl)ethylenediamine]platinum(II) salts (-1h) leads to a similar inhibition like a permanent drug exposure indicating a fast uptake of the complex by the tumor cell. In experiments on the Ehrlich ascites tumor of the mouse and on the L 1210 leukemia cell line R,R/S,S-[1,2-bis(4-fluorophenyl)ethylenediamine]dichloroplatinum(II) turns out to be equipotent with cisplatin.

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Amino acid antagonists with proven or potential inhibitory activities on aminoacyl-tRNA synthetases were tested for their antiproliferative effect against the murine leukemic cell line P388D1. Micromolar concentrations of the compounds S-tritylcysteine (18), fenitropan and beta-chloroalanine gave strong growth inhibition. In the mouse only 18 was effective against leukemia P388 (T/C = 211%). The inhibitory effect on aminoacyl-tRNA synthetases and the antiproliferative action on P388D1 or P388 could not be correlated.

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Amino acid antagonists with proven or potentially inhibitory activities on aminoacyl-tRNA synthetases were tested for their antiproliferative effect against E. coli B. The compounds 4- and 6-fluoro-tryptophan, 5-methyltryptophan, selenocystine and beta-(2-thienyl)alanine gave strong growth inhibition in minimal medium, which disappeared after addition of structurally related natural amino acids or in an enriched broth. The inhibitory effect on amino-acyl-tRNA synthetases and the minimal inhibitory concentration for growth inhibition in minimal medium could not be correlated.

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Melphalan and analogous aniline mustard derivatives were tested on antitumor activity in vitro. All compounds showed similar antiproliferative effects against melanoma B16, sarcoma 180 and leukemia P388D1. Thus, the singular clinical efficiency of melphalan may not simply be explained by a selective uptake employing amino acid carrier systems of tumor cells.

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The antimycobacterial effects of benzylamines are not related to an inhibition of aminoacyl-tRNA synthetases.

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Tests for antimycobacterial properties (Mycobacterium tuberculosis H37 Ra, Middlebrook-7H9-broth) of the phenothiazines 1-11 are described. The growth inhibition of these compounds can be blocked by the addition of histamine.

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