Lipid peroxidation

From WaiWiki
Revision as of 17:41, 10 February 2013 by RRM (talk | contribs) (Susceptibility to oxidation)

Lipid peroxidation is the oxidative degradation of lipids, endogenously, or in cooking. When radicals react with non-radicals, this always creates another radical. When a fatty acid reacts with a radical, a fatty acid-radical is created. This fatty acid-radical may react with oxygen to form a peroxyl-fatty acid radical. This peroxyl-fatty acid radical may react with another free fatty acid, producing two compounds: another fatty acid radical and a lipid peroxide. This cycle is ended by an anti-oxidant, or (if there are lots of radicals) by another radical, because when two radicals react, they produce a non-radical. Anti-oxidants end a radical chain reaction by getting oxidized themselves (not rendering another radical).

Lipid peroxidation yields various compounds of different stability.[1] Such carbonyls are generated by both lipid peroxidation and by autoxidation of sugars. Specific carbonyls, such as alpha-dicarbonyls, may be aldehydic or ketonic (or both) [2], and are very potent Maillard reaction intermediates, yielding advanced glycation end products (AGEs) as well as advanced lipoxidation end products (ALEs). The Maillard reaction and lipid peroxidation are intimately interrelated, and the products of each reaction influence the other, sharing intermediates and products.[3]

Susceptibility to oxidation

Polyunsaturated fatty acids are more susceptible to lipoxidation than other fatty acids because they contain multiple carbon units with double bonds. The carbon unit in between two double-bonded carbon units is called a methylene bridge. This carbon unit has less energy invested in its bonds with the two hydrogen atoms, which makes these hydrogens more reactive. Long chain saturated fatty acids (such as palmitic and stearic acid) are also subject to lipid peroxidation.[4] Oleic acid (monounsaturated fatty acid) is relatively stable.[5] Both oleic acid and palmitoleic acid act as relative lipid peroxidation inhibitors.[6]


All lipids are susceptible to oxidation, though to different degrees. Cooking oils may produce various lipid oxidation products, such as n-alkanes, branched alkanes, alkenes, n-alkanoic acids, n-alkenoic acids, carbonyls, aromatics, polycyclic aromatic hydrocarbons (PAH), and lactones. Carbonyls and fatty acids (n-alkanoic and n-alkenoic acids) make up a significant portion of the organic compounds.[7]

  • Oils and fats experience various degrees of increase in saturation during cooking/frying use, with little consistency of used cooking oil obtained from the same source.[8]
  • Unsaturated oils are more rapidly degraded. Oils with low linoleic acid and high content of palmitic acid are relatively resistant to frying temperatures.[9]
  • After thermal processing, soybean oil contained a 15-fold higher level of free fatty acids (as % of total fat; mainly triglycerides), 8-fold higher peroxide value, 39-fold higher p-anisidine value, 19-fold higher total oxidation value, 8.5-fold more reactive substances, and 2.5 fold more trans fatty acids.[10]
  • The mean trans fat content of sunflower oil used for cooking was 4.2%, compared to vegetable mixture oils 3.1%.[11]
  • Trans fatty acids levels in commercial Spanish foods differe greatly, ranging from 0.1% in refined olive oils to 20.9% in french fries.[12]
  • Olive oil is relatively resistant to frying conditions, due to superior amounts of minor antioxidant compounds, characterized by significantly reduced levels of oxidation and hydrolysis, compared to vegetable oil with higher vitamin E contents.[13] The level of these minor antioxidant compounds (phenolics) in olive oil is reduced with each time the oil is used for frying; retention of phenolics went down from 70-80% (first frying) to 20-30% (eighth frying).[14] In another study extra-virgin olive oil was clearly nongenotoxic, and flax seed oil more genotoxic than sesame seed oil, wheat germ oil and soy oil.[15]
  • Fatty acid compositions of red pepper seed oils did not change with roasting time (6-12 min. at 210°C). Fatty acid profile: 74% linoleic acid, 13% palmitic acid, 10% oleic acid, 2% stearic acid, 0.4% linolenic acid, 0.3% palmitoleic acid and 0.2% myristic acid.[16]
  • After pan-frying fish, omega-6/omega-3 ratio had increased from 0.08 in raw cod to 1.01 (with olive oil) and 6.63 (with sunflower oil) in fried cod. In farmed salmon, the omega-6/omega-3 ratio hardly changed from 0.38 (raw) to 0.39 (olive oil) and 0.58 (sunflower oil) in fried salmon.[17]
  • Linseed oil added to rabbit feed enhanced long-chain polyunsaturated fatty acid biosynthesis, and increased meat oxidation after cooking of the rabbit meat.[18]
  • Supplementation of used coconut oil (20%) to the chick diet resulted in rapid accumulation of (saturated) shorter chain fatty acids (12:0 and 14:0) in liver and hepatic mitochondria, increasing cellular death rates.[19]
  • Beef contains more mono- and di-unsaturated fatty acids than poly-unsaturated fatty acids (PUFAs). Increasing PUFA in meat by increasing PUFA in feedings resulted in a 4-fold increase in lipid oxidation products due to cooking of the meat; most lipidoxidation products coming from (PUFA-initiated) auto-oxidation of the predominant mono- and di-unsaturated fatty acids.[20] In another study, cooking of beef from cattle fed a high-PUFA diet, did not result in changes in the relative distribution of fatty acids upon cooking (140°C for 30min). Cooking did not cause thermal degradation of PUFA, or thermal degradation or oxidative synthesis of conjugated linoleic acid (a trans fatty acid).[21]
  • When peanuts are roasted in a microwave, heating them shortly already significantly increases the formation of fatty acid peroxides.[22]


In general, water-soluble antioxidants (vitamin C, glutathione, lipoic acid, uric acid) act within the cell, and lipid-soluble antioxidants (vitamin E, carotenes, coenzyme Q) protect cell membranes from lipid peroxidation.

  • Vitamin E significantly reduces malonaldehyde (lipid peroxidation product) in cooked chicken.[23]

High dietary omega-3 intakes

Recommendations for minimum PUFA intake to prevent gross EFA deficiency are about 3% of total energy intake. Recommendations for prevention of heart disease are 8-10% of energy. [24] In elderly Japanese subjects, a 3 gram/day increase of dietary ALA could increase serum EPA and DHA in 10 months without any major adverse effects.[25]