Sodium chloride accelerated rancidity in blended cod muscle at 0 C. This salt-induced rancidity was retarded by commercial antioxidants and chelating compounds. The active agent appeared to be the Na+rather than the whole salt or the Cl−.Other metal salts had similar pro-oxidant action on the cod muscle when used in relatively high concentrations (0.1 N and above). The relative activity, using metal chlorides, was as follows: Fe > Co > Cd > Li > Ni > Mg > Zn > Na > K. Ca and Ba had no effect.Many of these "pro-oxidant" salts also had a strong antioxidant effect on the development of copper-induced rancidity in the muscle.The relationship between TBA values and the type and intensity of odours is not the same for sodium chloride-induced and copper-induced rancidities. Some of the reasons for this have been discussed.It has been suggested that one mechanism by which sodium chloride influences the rate of lipid oxidation in the fish muscle is by the changes it produces in the accompanying proteins.

Addition of free amino acids to blended cod muscle affected the subsequent development of rancidity. In the presence of trace amounts of Cu++, the aromatic, heterocyclic, and sulphur-containing amino acids exerted varying degrees of antioxidant acitivity. In the absence of added metallic ions the aliphatic amino acids and cysteine showed strong pro-oxidant activity. Tests were carried out to determine the effect of pH and the concentration of amino acid on these reactions.Amino acid-induced rancidity was inhibited by the commercial antioxidants NDGA, PG, and BHT and by the chelating agent, EDTA; but not by tocopherol; ascorbic acid enhanced the oxidation. A limited number of tests indicated that the fish muscle did not undergo a seasonal variation in sensitivity to the amino acid-induced rancidity, and thus differed from the Cu++-induced rancidity.Those amino acids which inhibited metal-induced rancidities did not retard rancidity induced by the addition of sodium chloride.

In a study of copper-catalyzed rancidity of cod fillets it has been found that: (1) muscle from the tail section goes rancid faster than muscle from the head or centre sections; (2) there is no apparent difference in the development of rancidity in the inner and outer halves of fillets that have been sliced lengthwise; and (3) sensitivity to rancidity changes with the season and is greater in the winter and early spring than in the summer and fall.

A method that can be carried out within 24–72 hr is suggested for determining the tendency of fish muscle to become rancid. It consists of adding measured, trace amounts of copper ion to muscle that has been blended with water (1:3) followed by storage at 0 °C. Rancidity is observed subjectively by noting the odours that develop and objectively by means of the thiobarbituric acid reaction.

Actively growing bacteria suppress the development of copper-catalyzed rancidity in lean fish muscle. Apart from the antioxidant effect of the bacteria themselves, it could not be shown that fish muscle undergoing microbial deterioration became any less susceptible to oxidative rancidity as spoilage progressed.