E)izymes 



63 



the acetyl CoA that would normally condense with oxaloacetate 

 is free to condense with other acetyl CoA to form acetoacetic acid 

 which in turn forms acetone and /3-hydroxybutyric acid, in other 

 words, the ketone bodies excreted in the urine in severe diabetes 



(Fig. 8) . 



Oxaloacetate 



Tricarboxylic 

 Acid Cycle 



Acetyl CoA + Acetyl CoA 

 [CH3COC0A + CH3COC0A] 



Cholestrol 

 Synthesis 



Acetoacetate 



[CHoC0-CH 2 C00H 



2CoA 



2CoA] 



Acetone 



[CH3COCH3] 



/3 hydroxy buty rate 

 [CH3CHOH -CH 2 C00H] 



Fig. 8. The Formation of Ketone Bodies and Excess Cholesterol in Diabetes. 



Another possible result of the disturbance is that acetyl CoA is 

 diverted to another reaction in which it is involved, namely, choles- 

 terol synthesis, thus leading to hypercholesterolaemia and perhaps 

 to its deposition in blood vessels (atheroma) . Both these abnormali- 

 ties are common complications of diabetes. 



EXOGENOUS POISONS 



Well documented examples in this group are scarce. The anti- 

 cholinesterases, e.g. DFP, parathion, mipafox, apiol produce severe 

 neurological symptoms accompanied by demyelination and death. 

 Their only major common property appears to be inhibition of 

 certain carbonic esterases notably cholinesterase, and esterase 

 linked proteases, e.g. chymotrypsin, but the connection between 

 their effect on these enzymes and their toxic properties is uncertain. 



The opposite effect, that of a specialised enzyme producing in- 



