15.9.78 Specialia 116 1 20 I0 ~= 0 6 -10 -20 20 15 10 5 80 60 40 20 600 500 400 E 300 250 20O 150 100 5O I I i i _DNA I t ~ I i RNA .~.~176 o.~''~176 ~o~ 1 i i L i Protein ~ . i r I i ProteogPycan .release ~ .~ ..,,o. ~176 -''~ I i i 0 2 4 6 Fig.2 Days in culture that hormone or vitamin. Since the effects of the hormonal form of vitamin D3, 1,25-dihydroxycholecalciferol 2~ are also known to depend upon continous RNA and protein synthesis, it is most likely that cellular effects of certain vitamins, like those of some hormones, are mediated by regulation of protein synthesis, presumably at the transcrip- tional level. However, further work is needed to ascertain whether the vitamin A effect only represents a quantitative or rather a qualitative change in protein synthesis. Fig. 2. Time course of retinoic acid-induced changes in length, DNA, RNA and protein content and in the release of proteoglycan in limb bones of late fetal rats. Humeri (4 per dish) were incubated in supplemented culture medium F- 10 (final volume 5 ml) at 36 ~ Before incubation, and then every 2 days, the contour of the magnified bones (x 14.1, using a reversed microscope and a pro- jecting prisma) was drawn and the length determined. At the time indicated, the humeri, after washing in Ringer's salt solution, were extracted in 1 ml of 10% (w/v) trichloroacetic acid and the extract discarded. Nucleic acids were extracted with 10% (w/w) perchloric acid at 70 ~ for 30 rain and the DNA and RNA determined 23,24. The remaining tissue was dissolved in 1N NaOH and the protein measured 25. Aliquots of the culture medium were collected and the amount of proteoglycan released into the medium was measured by the Alcian blue assay 22, using chondroitinsulfate as standard. Since the humeri were distributed randomly, it was assumed that the values at day 0 were similar for all groups. Except for the proteoglycan release, the results are the mean of 4 determinations, + SD. Treatments were: controls; A, 0.6 I~M retinoic acid; O, 20 IxM retinoic acid, * p < 0.01. 1 Acknowledgments. We thank Prof. R. Weber and Dr G. Ryf- fel for helpful discussions and critical reading of this manus- cript. The skillful technical assistance of Miss B. Schr6ter and Mrs B. Galli is gratefully acknowledged. We wish to thank Mrs G. Sutter for providing culture medium and excellent labora- tory facilities. 2 T. Moore, in: The vitamines, vol. 1, p. 245. Ed. W.H. Sebrell and R. S. Harris. Academic Press, New York 1972. 3 W. Bollag, Eur. J. Cancer 8, 689 (1972). 4 W. Bollag, Eur. J. Cancer 10, 731 (1974). 5 W. Bollag, Eur. J. Cancer 11, 721 (1975). 6 M.B. Sporn, N.M. Dunlop, D.L Newton and J.M. Smith, Fedn Proc. 35, 1332 (1976). 7 H.B. Fell and E. Mellanby, J. Physiol. 116, 320 (1952). 8 D.S. Goodman, J.E. Smith, R.M. Hembry and J.T. Dingle, J. Lipid Res. 15, 406 (1974). 9 H.B. Fell and J.T. Dingle, Biochem. J. 87, 403 (1963). 10 D.R. Bard and I. Lasnitzki, Br. J. Cancer 35, 115 (1977). 11 B.P. Sani and D.L. Hill, Biochem. biophys. Res. Commun. 61, 1276 (1974). 12 D.E. Ong and F. Chytil, J. biol. Chem. 250, 6113 (1975). 13 F. Chytil and D.E. Ong, Nature 260, 49 (1976). 14 B.P. Sani and D.L. Hill, Cancer Res. 36, 409 (1976). 15 B.P. Sani and T.H. Corbett, Cancer Res. 37, 209 (1977). 16 B.P. Sani, Biochem. biophys. Res. Commun. 75, 7 (1977). 17 L. Prutkin, Cancer Res. 31, 1080 (1971). 18 J.T. Dingle, Br. reed. Bull. 24, 141 (1968). 19 B.W. O'Malley, R.J. Schwartz and W.T. Schrader, J. Steroid Biochem. 7, 1151 (1976). 20 H.F. DeLuca, Fedn Proc. 33, 2211 (1974). 21 A.W. Norman and H. Henry, Rec. Progr. Hormone Res. 30, 431 (1974). 22 P. Whiteman, Biochem. J. 131, 343 (1973). 23 K. Burton, Biochem. J. 62, 315 (1956). 24 G. Cerriotti, J. biol. Chem. 214, 59 (1955). 25 O.H. Lowry, N.J. Rosebrough, A.L Farr and R.J. Randall, J. biol. Chem. 193, 265 (1951). Effect of infection of mice with Friend leukemia complex viruses on background antibody-forming cell produc- tion in vitro ~ M. Bendinelli, D. Matteucci, A. Toniolo and H. Friedman Institute of Microbiology, University of Pisa, 1-56100 Pisa (Italy) and Department of Microbiology and Immunology, Albert Einstein Medical Center, Philadelphia (Pa. 19141, USA), 16 February 1978 Summary. Friend leukemia complex (FLC) and Rowson-Parr virus (RPV) infections of donor mice depress the production of background antibody-forming cells by splenocytes cultured in the absence of specific antigenic stimulation. During investigations on the immunodepressive properties forming cells to various antigens 2,3. Obviously, this is a of Friend leukemia complex (FLC), it was shown that adult paradoxical effect, since in the same mice artifically stimu- mice infected with viruses belonging to this complex exhi- lated antibody responses are suppressed 4. Here it is shown bit increased numbers of splenic background antibody- that after infection of donor mice with FLC viruses the