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Fish spoilage mechanisms

water activity

Fish spoilage results from three basic mechanisms: Enzymatic autolysis, oxidation, microbial growth.

Autolytic enzymatic spoilage: Shortly after capture, chemical and biological changes take place in dead fish due to enzymatic breakdown of major fish molecules autolytic enzymes reduced textural quality during early stages of deterioration but did not produce the characteristic spoilage off-odors and off-flavors. This indicates that autolytic degradation can limit shelf-life and product quality even with relatively low levels of spoilage organisms. Most of the impact is on textural quality along with the production of hypoxanthine and formaldehyde.

The digestive enzymes cause extensive autolysis which results in meat softening, rupture of the belly wall and drain out of the blood water which contains both protein and oil. Peptides and free amino acids can be produced as a result of autolysis of fish muscle proteins, essential. Which lead towards the spoilage of fish meat as an outcome of microbial growth and production of biogenic amines.

Oxidative spoilage: Lipid oxidation is a major cause of deterioration and spoilage for the pelagic fish species such as mackerel and herring with high oil/fat content stored fat in their flesh. Lipid oxidation involves a three stage free radical mechanism: initiation, propagation and termination. Initiation involves the formation of lipid free radicals through catalysts such as heat, metal ions and irradiation. These free radicals which react with oxygen to form peroxyl radicals. During propagation, the peroxyl radicals reacting with other lipid molecules to form hydroperoxides and a new free radical. Termination occurs when a buildup of these free radicals interact to form nonradical products. Oxidation typically involves the reaction of oxygen with the double bonds of fatty acids. Therefore, fish lipids which consist of polyunsaturated fatty acids are highly susceptible to oxidation. Molecular oxygen needs to be activated in order to allow oxidation to occur. Transition metals are primary activators of molecular oxygen.

In fish, lipid oxidation can occur enzymatically or non-enzymatically. The enzymatic hydrolysis of fats by lipases is termed lipolysis (fat deterioration). During this process, lipases split the glycerides forming free fatty acids which are responsible for: (a) common off-flavour, frequently referred to as rancidity and (b) reducing the oil quality. The lipolytic enzymes could either be endogenous of the food product (such as milk) or derived from psychrotrophic microorganisms. The enzymes involved are the lipases present in the skin, blood and tissue. The main enzymes in fish lipid hydrolysis are triacyl lipase, phospholipase A2 and phospholipase B. Non-enzymatic oxidation is caused by hematin compounds (hemoglobin, myoglobin and cytochrome) catalysis producing hydroperoxides. The fatty acids formed during hydrolysis of fish lipids interact with sarcoplasmic and myofibrillar proteins causing denaturation

Microbial spoilage: Composition of the microflora on newly caught fish depends on the microbial contents of the water in which the fish live. Fish microflora includes bacterial species such as Pseudomonas, Alcaligenes, Vibrio, Serratia and Micrococcus. Microbial growth and metabolism is a major cause of fish spoilage which produce amines, biogenic amines such as putrescine, histamine and cadaverine, organic acids, sulphides, alcohols, aldehydes and ketones with unpleasant and unacceptable off-flavors. Trimethylamine (TMA) levels are used universally to determine microbial deterioration leading to fish spoilage.