80 The Chemistry of the Injured Cell 



the chief one of which, a toxin, is a very active lecithinase that 

 splits the phospholipid lecithin in the cell wall and mitochondrial 

 membranes to yield phosphoryl choline and the diglyceride. In this 

 way the cells and mitochondria are disrupted at least in vitro 

 (Payling Wright, 1955) . 



Botulinum toxin, perhaps the most toxic of all known poisons, 

 produces no specific structural disturbance in the cell, but it in- 

 jures the terminal, largely unmyelinated portion of cholinergic 

 nerves whether they are pre- or post-ganglionic components of the 

 autonomic nervous system or somatic nerves supplying skeletal 

 muscle. So far no biochemical lesion has been spotted in affected 

 cells. The clinical features are satisfactorily explained on the basis 

 of some lesion produced by the toxin at the myoneural junction 

 which renders that structure incapable of releasing acetylcholine in 

 quantities sufficient to evoke a contraction of the muscle fibre 

 (Payling Wright, 1955) . 



Tetanus toxin, it is generally agreed, operates at some site 

 within the central nervous system to give widespread skeletal 

 muscle spasticity and convulsions. No characteristic cellular changes 

 have been discovered and its mode of action is uncertain. On the 

 whole it appears to behave "less as a general neural poison than 

 as a specific impediment to acetylcholine formation and release— 

 a property which it shares with botulinum toxin" (Payling Wright, 

 1955) . Tetanus toxin, however, selects central cholinergic mechan- 

 isms as its main site of action, botulinum toxin chooses peripheral 

 mechanisms. Tetanus toxin also impairs reflex inhibition in the 

 spinal cord. The biochemical lesions responsible for these disturb- 

 ances are not known. 



Typhimurium toxin gives cloudy swelling and focal necrosis in 

 the liver of rats. Mitochondria from affected liver cells show un- 

 coupling of oxidative phosphorylation in vitro, a biochemical le- 

 sion possibly responsible for the appearance of cloudy swelling, if 

 not for necrosis (Fonnescu and Severi, 1956) . 



REFERENCES 



Abood, L. G. (1955) : Proc. Soc. ex per. Biol. Med., 88:688. 

 Aldridge, W. N. and Cremer, J. E. (1955) : Biochem. ] ., 61:406. 



