492 5. QUINONES 



cussed above probably do not parallel the effects of the simpler qiiinones. 

 For example, Shacter (1956) found only a progressive depression of the 

 respiration of ascites tumor cells by jj-benzoquinone in the presence of 

 glucose, instead of the stimulation seen with phenanthraquinone. It is 

 doubtful if any actions of phenanthraquinone are related to SH groups. 

 The purposes of the investigations in which many types of quinone have 

 been compared for their effects on glycolysis or respiration — e. g., the 

 reports using Schistosoma (Bueding and Peters, 1951), Australorhis (von 

 Brand et at., 1949), or Photobacterium (Spruit and Schuiling, 1945) — 

 did not require a metabolic analysis of the different types of action, so that 

 unfortunately we have no information on the relative importance of the 

 various possible sites of inhibition. 



A few interesting and surprising results obtained in studies on the ef- 

 fects of quinones on respiration will be mentioned briefly. The pyruvate 

 decarboxylase of Monilinia fructicola is quite sensitive to several quinones 

 (Table 5-2) and the inhibition of spore germination generally parallels the 

 enzyme effects, so that it was suggested that the site of the inhibition is 

 the decarboxylase (Foote et al., 1949). However, these quinones scarcely 

 affect respiration and may even stimulate it moderately. Is the respiration 

 of this organism independent of pyruvate, and, if the germination depends 

 on the decarboxylase, how is pyruvate metabolized? Unexpected results 

 on the reversibility of the effects of p-benzoquinone on the respiration and 

 motility of bull spermatozoa were reported by Lardy and Philips (1943 a). 

 The quinone was found to produce an irreversible inhibition, whereas the 

 hydroquinone inhibition is reversible. One might superficially attribute 

 the hydroquinone effects to the quinone formed from it by oxidation, but 

 this does not seem to be the case, since if this were the mechanism the in- 

 hibition would also be irreversible. The quinone may well inhibit by a reac- 

 tion with SH groups, but how does the hydroquinone inhibit? Arsenite 

 inhibits the respiration of bone marrow, leucocytes, and lymphogenous and 

 myelogenous leukemic tumors, and simulteneously there is some increase in 

 aerobic lactate formation (Warren, 1943). This would usually be attributed 

 to a block of pyruvate oxidation. Menadione is able to counteract these 

 effects of arsenite, restoring the respiration and lowering the aerobic gly- 

 colysis, although there is no antagonism of the effects on leucocyte motility 

 or cytological changes. Since methylene blue and thionine are also able 

 to counteract the arsenite effects, it was postulated that menadione action 

 is in some way related to its redox potential, this being substantiated by 

 the fact that phthiocol, with a much lower potential, is without effect. 

 The question here is: How could menadione initiate or activate some oxida- 

 tive sequence which would bypass or overcome the arsenite effect ? Whatever 

 the mechanism, it is always interesting when two inhibitors counteract 

 each other's effects, and a more detailed study of this particular case might 



