VII INTERNAL FACTORS 63 1 



(Owen et al., 1939) and pantothenic acid in the tail of Amphibia (Raunish, 1950). 

 High concentrations of the latter have an inhibitory action. Vitamin Bj2 promotes 

 liver regeneration in rats (Schweigert et al., 1954), and its component, benzylimid- 

 azoline, the healing of fractures (Principe and Bellucci, 1953). Choline chloride, in 

 0.3% concentration, accelerates the regeneration of the newt's limbs (Lecamp, 1 942) . 



[b) Hormones in the control of regeneration 



In general the hormones of vertebrates affect regeneration in a manner consist- 

 ent with their activity on normal growth and morphogenesis. Apparently paradoxi- 

 cal results are common because of the complexity of interactions between the 

 various hormones. In addition, regeneration introduces its own peculiarities, due 

 to the R-phase and to the subsequent reversal of metabolism. Moreover, the brev- 

 ity and speed of the process may render it fatally sensitive to small changes in 

 hormone-concentration, at critical periods. 



(?) Steroid hormones. Probably the most equivocal results are those on the action 

 of the hormones of the adrenal cortex though it seems clear from Table 1 3 that 

 this is due mainly to the familiar contrast between the actions of the cortisone, or 

 ''S "-group of steroids, the gluco-corticoids, which are generally nitrogen-squander- 

 ing and pro-catabolic, and the androgenic or "N" group, nitrogen-sparing and 

 growth-promoting (Cope et al., 1943; Derbes and Weiss, 1951). The mineralo- 

 corticoids resemble the latter group. The former might be expected to promote 

 regeneration in the R-phase and the latter in the P-phase, and in fact cortisone- 

 administration does induce all essential components (Cuthbertson, 1954) of the 

 GAS. Moreover these components are essential for regeneration (Schotte and 

 Chamberlain, 1955). Deoxycorticosterone (DOCS), one of the mineralocorticoids, 

 promotes the proliferation of connective tissue-cells (Selye, 1955), increases the 

 protein-content of the liver during its regeneration (Berman et al., 1947; Fried- 

 good et al., 1950) and also of the serum (Roberts, 1951), which frequently reflects 

 changes in the liver. 



The promotion of regeneration directly, by extracts of the adrenal cortex, or 

 indirectly by the adrenocorticotropic (ACTH) factor of the pituitary, seems to 

 be limited to these early stages (Hall and Schotte, 1951 ; Schotte and Hall, 1952; 

 Schotte and Lindberg, 1954; Schotte and Chamberlain, 1955; Giberti and Bian- 

 chini, 1954). Wolffian lens-regeneration in the newt involves little R-phase activ- 

 ity and appears not to be affected by hypophectomy at any stage of regeneration 

 (Schotte and Murphy, 1953, Stone and Steinitz, 1953). The presumption is that 

 corticoids have little effect on the process in the P-phase, or possibly that any 

 favourable effect of the N-group is counteracted by inhibitory action of the S- 

 group, at that stage. Administered cortisone in fact does inhibit in the P-phase 

 (Table 13), acting mainly on cell-division (Perez-Tamayo, 1953; Mene, 1953; 

 Einhorn, et al., 1954; Taleisnik, 1954; Thomas, 1954; Manner, 1955), ^^^^ 

 possibly also on cellmigration (Thomas, 1954). It also inhibits the growth of nerve- 

 axons (Lytton and Murray, 1954), — altogether it shows a remarkable resemblance 

 to the action of colchicine. The action of the adrenal S-corticoids, like the de- 

 differentiation caused by colchicine, by denervation and by irradiation, normally 

 requires the additional stimulus of trauma (Selye, 1955). 



Lileralure p. 64g 



