626 



JF. Dickens 



Figure 1 includes a number of other possible routes of electron transport 

 from DPNH to oxygen (the oxidation of TPNH will be mentioned separately 

 below); oxidation of succinate via succinic dehydrogenase (fp.,) is also 

 included. Recent work (Crane, Hatefi, Lester and Widmer, 1957; Pumphrey, 

 Redfearn and Morton, 1958a, b; Pumphrey and Redfearn, 1959) indicates 



TPNH 



fR 



TPN DPN E 



DPNH-^fp^(Mg) 



fPi 



DPNH C 

 fMFe) 



cyt bp 



^cyt c, — >-cyt c— ^cyt {a-^-oj-^^O^ 

 TPNH D 



Fig. I. Pyridine Nucleotides and Succinate in relation to the respiratory ciiain. 



A. Mitochondria: phosphorylating: antimycin sensitive. 



B. Microsomal (Strittmatter and Velick, 1956a, b; 1957a, b). 



C. DPNH-cyt c reductase. 



D. TPNH-cyt c reductase. 



E. Pyridine nucleotide transhydrogenase (mitochondrial). 



F. Vitamin K reductase (Martius). 



that a mitochondrial quinone (ubiquinone, Q275 or mitoquinone, hereafter 

 referred to as ubiquinone) restores the activity of succinic oxidase after lipid 

 extraction, a-tocopherol being inactive in this respect. On the other hand, 

 a-tocopherol or vitamin K can restore the DPNH-cytochrome c reductase 

 activity of aged and extracted preparations of muscle particles (Donaldson, 

 Nason and Garrett, 1958; Deul, Slater and Veldstra, 1958). Slater (1958a) in 

 his review of this subject discusses fully whether these quinones in fact 

 participate in the metabolic pathways; this view is favoured by the most 

 recent work on succinate oxidation from R. A. Morton's laboratory as far 

 as the role of ubiquinone in oxidation of succinate is concerned (Pumphrey 

 and Redfearn, 1959). There is also a lack of agreement about the exact site 

 of the inhibitory action of Antimycin, which inhibits not only succinate 

 oxidation but also that of DPNH (Slater, 1958b). The principal features of 



