Pepsin survival

O Keeffe et al. (1977) reported that some porcine pepsin survives Cheddar cheesemaking and contributes to casein breakdown during cheese curing. However, it has been shown that the breakdown they attributed to pepsin occurs in curd containing neither coagulant nor starter bacteria (Majeed 1984). More recent studies have shown that porcine pepsin does not survive in Cheddar cheese when the milk is set at pH 6.6 (Yiadom-Farkye 1986). This supports earlier reports of Green (1972) and Wang (1969). 

Majeed, G. H. 1984. Survival of porcine pepsin during Cheddar cheesemaking and its effect on casein during cheese ripening. Ph.D. Thesis. Utah State University, Logan. 

Tavares et ah, 2006). The lower concentration of proteolytic enzymes in the gastrointestinal tract of a child may explain fhese cases. In addition, Dubey et al. (1998a,b), reported that tachyzoites may occasionally survive for a shorf period of time (about 2 h) in acid pepsin solutions. 

The solution of pepsin is kept at temperatures varying from 40° to 70° for i and 6 hours. After these exposures i c.c. of enzyme is removed, a certain quantity of albumin milk, is added, and the mixture is left at 50°. Thus in (r) and (2), where the pepdn has been previously heated to 40 or so, the liquefying power survives even after 6 hours of heating. On the other hand, a stay of 6 hours in a bath at 60° lowers the liquefying power to 80. 

As indicated, this paper will concentrate mainly on questions related to stability of enzyme inhibitor proteins and lectins. In particular, differential scanning calorimetric findings on effects of specific interactions on thermal stability will be reviewed. Stabilities of these proteins to other denaturing agents are not considered here. Older work showed that proteinase inhibitors are generally highly stable some resist denaturation at 100 C when dry or in neutral or weakly acidic solutions. Some even survive the action of pepsin, and can thus reach the small intestine intact. 

Bi2(CsH407)] 2K ) which has a complex stmcture. This salt is unstable in the stomach acid and precipitates out to form complex cationic species which form complexes with proteins in the stomach wall protecting ulcers from gastric add and pepsin, and these complexes are also toxic to H. pylori. The basis of the toxidty of bismuth salts to the bacteria may be due to formation of complexes with the tuease (which produces ammonia from urea) that the bacteria produce in large amounts in order to maintain the pH of their environment at around 6 so that they can survive tmder the addic conditions in the stomach/ Bismuth salts are usually used in combination with an H2-receptor antagonist and a tetracydine (see Ch. 22) which is also used to kill the bacteria. 

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