228 J. E. Lovelock 



temperatures below 0° are taken from the data of Miner 

 and Dalton (1953) and of Blum and Kauzman (1954). 



The diagram illustrates how very much more rapidly the 

 rate of metabolism slows than does the diffusion when the 

 temperature is lowered. At — 20°, assuming the relative rates 

 are equivalent at + 40°, diffusion proceeds 20 times more 

 rapidly than metabolism. 



Both the rate of death of the cells and their spontaneous 

 haemolysis show a cubic type of relationship with temperature. 

 The rates of death and haemolysis decrease at first with falling 

 temperature until in the region between + 5° and — 20° there 

 is a halt in the death rate and an increase in the rate of 

 haemolysis. At still lower temperatures both rates resume their 

 decrease with decreasing temperature. At the lower tempera- 

 tures both rates fall approximately as fast as the calculated 

 rates of diffusion. In the region between — 20° and 8° 

 metabolism proceeds at an appreciable rate and its beneficial 

 effects may be responsible for the observed temporary de- 

 crease in the rates of death and haemolysis as the tempera- 

 ture rises. 



More direct evidence in support of the notion that the 

 structure of the red cell is in dynamic equilibrium comes from 

 experiments on the transfusion of red cells after storage and 

 other treatment in vitro. Burnett (1951) has shown that red 

 cells, exposed to enzymes which modify their surface so that 

 they are no longer able to absorb virus particles, are restored 

 to their normal condition within a few days after their 

 transfusion. Gabrio, Stevens and Finch (1954) have shown 

 that red cells recover from damage suffered during cold 

 storage after they are transfused into a recipient. They have 

 also shown that the damage suffered during cold storage 

 can to some extent be reversed in vitro, which suggests that 

 the capacity for repair is possessed by the cell rather than 

 the recipient. These experimental findings seem sufficient to 

 justify the speculation that the factor determining the survival 

 of the cell, either in vivo or after storage, is its ability to repair 

 losses by diffusion or other changes. In addition, it would 



