Susceptible milk

However, its presence is not the only determinant of whether or not oxidative deterioration occurs. Olson and Brown (1942) showed that washed cream (free of ascorbic acid) from susceptible milk did not develop an oxidized flavor when contaminated with copper and stored for three days. Subsequently, the addition of ascorbic acid to washed cream, even in the absence of added copper, was observed to promote the development of an oxidized flavor (Pont 1952). Krukovsky and Guthrie (1945) and Krukovsky (1961) reported that 0.1 ppm added copper did not promote oxidative flavors in milk or butter depleted of their Vitamin C content by quick and complete oxidation of ascorbic acid to dehydroascorbic acid. Krukovsky (1955) and Krukovsky and Guthrie (1945) further showed that the oxidative reaction in ascorbic acid-free milk could be initiated by the addition of ascorbic acid to such milk. Accordingly, these workers and others have concluded that ascorbic acid is an essential link in a chain of reactions resulting in the development of an oxidized flavor in fluid milk. 

Susceptible milk does not oxidize spontaneously but does develop oxidized flavor following contamination with iron or copper. Use of noncorrodible dairy equipment has reduced the incidence of copper contamination. 

Non-susceptible milk does not oxidize even in the presence of iron or copper. 

Mixing of normal milk with susceptible milk in a ratio of 4 1 prevents spontaneous rancidity and therefore the problem is not serious except in small or abnormal herds. The incidence of spontaneous rancidity increases with advancing lactation and with dry feeding. 

Susceptible milks which are susceptible to oxidation on addition of Cu or Fe but not without. 

Non-susceptible milks that do not become oxidized even in the presence of added Cu or Fe. 

It has been proposed that spontaneous milks have a high content (10 times normal) of xanthine oxidase (XO). Although addition of exogenous XO to non-susceptible milk induces oxidative rancidity, no correlation has been found between the level of indigenous XO and susceptibility to oxidative rancidity. The Cu-ascorbate system appears to be the principal pro-oxidant in susceptible milk. A balance between the principal antioxidant in milk, a-tocopherol (Chapter 6), and XO may determine the oxidative stability of milk. The level of superoxide dismutase (SOD) in milk might also be a factor but there is no correlation between the level of SOD and the propensity to oxidative rancidity. 

Other examples are glycine — formaldehyde, alanine — acetaldehyde, valine — isobutyraldehyde, phenylalanine — phenylacetaldehyde, and methionine — methional (106). Products such as dried skim milk, dried eggs, and dehydrated vegetables and fmits are particularly susceptible to deteriorative flavor changes ascribed to this reaction (Table 10). 

Cs, I, and Sr) in her milk which is usuaUy consumed fairly near the cow within a few days after production. Other foodstuffs may be stored for months, allowing the short-lived radionuclides to decay away. Moreover, milk is a major food for children who are more susceptible to radiation... 

Human adult needs for this vitamin (vitamins) are not established quantitatively. Most human studies have involved preventing or curing rickets in infants or children, and the recommended daily allowance of the Food and Nutrition Board is 400 units. Even among "normal" children, however, there is evidence of variation in vitamin D needs. According to Spies and Butt,38 "The activated milk does not exhibit sufficient potency in vitamin D for the prevention of rickets in cases in which a susceptibility exists" (italics added). They note that "susceptible" children may require 5,000 to 10,000 units daily. 

It is unclear why certain foreign proteins can also stimulate the B-cells to secrete IgE antibodies, to result in allergy or hypersensitivity. The terms are used interchangeably, although the latter is usually restricted to milder forms of the response. The term anaphylaxis is used to describe the severe response (Box 17.4). Both reactions arise in genetically susceptible individuals and they are precipitated by exposure to environmental antigens such as pollen, some organic compounds, tobacco smoke, animal hairs or even components of some common foods such as milk and cereals. 

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