60 The Chemistry of the Injured Cell 



diet is followed by inadequate synthesis of these coenzymes, a fall 

 in their tissue level and failure of the enzymic reactions for which 

 they are required. The clinical syndrome of pellagra is due partly 

 to this cause, partly to other poorly understood factors. 



Riboflavin 



This member of the vitamin B complex may be lacking in the 

 diet in malnutrition and in pellagra. Riboflavin is a component of 

 two respiratory coenzymes, flavine mononucleotide and flavine 

 adenine dinucleotide. The former is required for the shunt path- 

 way of glycolysis in the oxidation of glucose-6-phosphate to 6-phos- 

 phogluconic acid (Fig. 5) . Flavine adenine dinucleotide is part of 

 the flavoprotein molecule which acts as a carrier in electron trans- 

 port in respiration. Experimental dietary deficiency of riboflavin is 

 followed by a progressive decline in the tissue levels of these flavo- 

 proteins. 



Pantothene 



Lack of pantothene may produce disease in rats, if not in man. 

 The substance is part of coenzyme A, one of the most vital compon- 

 ents of respiration and biosynthesis (Fig. 6) . 



Copper 



Deficiency of copper produces disease in cattle and sheep. Many 

 enzymes require a metal cofactor (prosthetic group) for proper 

 function and copper is probably needed in this fashion by the 

 respiratory enzyme cytochrome oxidase. Decreased activity of this 

 enzyme is characteristic of copper deficiency and may well be re- 

 sponsible for many of the clinical symptoms, and eventually for 

 death of the animal (Gallagher et. al., 1956) . 



INJURY TO NON-RESPIRATORY ENZYMES 



Non specific injury, e.g. the cutting off of blood supply to cells 

 leads first to disorganisation of respiration and energy production 

 and only secondarily to disruption of non-respiratory metabolism, 

 e.g. biosynthesis and detoxication. However, special types of injury 

 exist which damage specifically certain non-respiratory enzyme 



