EFFECTS IN THE WHOLE ANIMAL 513 



hyperexcitability in the spinal cord. Masing (1882) showed that the con- 

 vulsions induced by ?)-benzohydroquinone in frogs are actually augmented 

 by destruction of the higher centers, although they are abolished by sev- 

 ering the peripheral nerves, and Labes (1929 c) obtained convulsions by 

 injecting both the hydroquinone and the quinone into the lumbar artery 

 of decapitated cats. Stimulation of supracord levels is indicated by restless- 

 ness, respiratory changes, emesis, various autonomic disturbances, and 

 clonic convulsions. Higher central excitation is also seen in the fact that 

 menadione can cause animals to come out of anesthesia (Smith et al., 

 1943). These stimulating actions have been thought to be the result of 

 the oxidative reactions catalyzed by the quinones, but there is no evidence. 

 There might be some insight into possible mechanisms if there were more 

 agreement on the relative actions of the different quinones and polyphenols; 

 but Marquardt et al. (1947), for example, who reported interesting differ- 

 ences in the responses of mice to p-benzohydroquinone, catechol, resorcinol, 

 pyrogallol and phloroglucinol, are quite at variance with some other 

 workers. The substances were injected subcutaneoulsy in this study and, 

 since many of them are locally irritating, some of the reactions may have 

 related to the intense pain. 



An interesting central effect was reported by Bijlsma and Versteegh 

 (1922) in mice and guinea pigs following administration of p-benzoquinone. 

 This is a rolling motion of the body always following a rotation of the 

 head, duplicating the response to a unilateral labyrinthine extirpation, but 

 it was found that the labyrinth is not essential for this response and that 

 the effect is central. Increasing dosage causes a loss of the position reflex 

 and compensatory ocular adjustments; a cerebellar site of action is not 

 impossible. It may be recalled that 2-phenyl-p-benzoquinone at relatively 

 low doses causes a peculiar writhing in mice, this being antagonized by 

 acetylsalicylate and other analgetics (Hendershot and Forsaith, 1959). 



The antipyretic activity of p-benzohydroquinone was discovered by 

 Brieger (1880) and its ability to reduce fever in typhoid was reported. 

 Doses of 400-500 mg produce some cardiac weakness but no other toxic 

 effects were noted. Steffen (1882) investigated this further and used a dose 

 of 300-500 mg in small children and 1 g in larger children, claiming a sig- 

 nificant antipyretic effect without toxicity. However, Oettel (1936) went 

 over Steffen's data and found evidence of several toxic reactions and felt 

 that the claims were unjustified. Since these doses correspond to around 

 25 mg/kg, it is not surprising, as Oettel points out, that this treatment was 

 soon discontinued. It is interesting to speculate whether these actions 

 are similar to those of the salicylates, but they could also be due to a direct 

 depression of metabolism. 



In view of the different functions of the benzo- and naphthoquinones in 

 electron transport, it would be important to be able to compare the central 



