HOWARD M. LENHOFF 217 



was removed. The time that it took for the mouths to close prob- 

 ably represent the time required both for the dissociation of the 

 glutathione and for the cessation of the cellular events involved 

 in the receptor-effector system. The observations that mouth closure 

 was more rapid the longer Hydra were exposed to glutathione may 

 imply that bound metabolic intermediates or cofactors, postulated 

 to be released by and to take part in this system (12), become 

 depleted as the feeding reHex nears completion. 



When considering the quantitative aspects of the union of gluta- 

 thione with the receptor, we found that the data were more mean- 

 ingful if they were treated according to concepts borrowed from 

 enzymology. Therefore, we investigated the effect of glutathione 

 concentration on the "activity" of the receptor-effector system, the 

 "activity" in this case being expressed as the duration of the feeding 

 reflex (Fig. 3). For each concentration of glutathione, duplicate 

 groups of five animals were used. In experiments employing Hydra 

 starved for two days (solid curve), a maximum response was ob- 

 served at concentrations of 5 X 10 ""^ M and greater. No further 

 increase in the duration of the feeding reflex occurred at higher 

 glutathione concentrations. At lower glutathione concentrations, 

 the duration of the feeding reflex increased in nearly direct propor- 

 tion to the amount of glutathione added. However, at these smaller 

 values there was greater variation in the response of the individual 

 Hydra, some not responding at all, as indicated by the symbols 

 used in Figure 3. The similarity of this plot (Fig. 3) to the Lang- 

 muir adsorption isotherm, and to a curve illustrating the saturation 

 of an enzyme by its substrate is apparent. Accordingly, the results 

 (Fig. 3) are interpreted as indicating that at glutathione concen- 

 trations greater than 5 X 10"** M all of the glutathione-receptors are 

 saturated. In these experiments we have not been able to demon- 

 strate that the glutathione is metabolized in a manner analogous 

 to the metabolism of a substrate by its enzyme. But rather it appears 

 as if the glutathione continues to activate all of the receptor- 

 effector systems until the response ceases. At subsaturation levels 

 of glutathione, the animal does not respond to its fullest capacity 

 (see also Table 1, expt. e). 



Another useful concept, analogous to the Michaelis constant, or 

 K^r, used in enzymology, is the concentration of glutathione eliciting 



