지질 과산화, 과산화지질, 자유 라디칼, lipid peroxidation
지질 과산화
脂質過酸化, lipid peroxidation
지질의 산화적 분해의 연쇄 반응이다. 지질 과산화는 자유 라디칼이 세포막의 지질로부터 전자를 빼앗아 세포를 손상시키는 과정이다. 이 과정은 자유 라디칼 연쇄 반응 메커니즘에 의해 진행된다. 이것은 특히 반응성 수소 원자를 가지고 있는 메틸렌 가교(-CH2-) 사이에 여러 이중 결합을 포함하기 때문에 다중불포화 지방산에 가장 자주 영향을 미친다.
과산화지질
피부에 유해한 대표적 물질로 불포화지방산이 산소를 흡수하여 산화되어 생긴다. 이것이 증가하면 피부의 섬유가 취약해져 주름살, 색소침착 등의 피부노화가 발생한다. 피부는 자외선을 비롯한 외기의 영향을 계속 받지만, 나이를 먹음에 따라 신진대사가 점차 쇠퇴하기 때문에 과산화지질의 대사가 일어나지 못하고 축적된다.
체내에 있는 불포화지방산이 산화되어 체내에 과산화지질이 증가하면 피부의 탄력을 좌우하는 섬유가 취약해져 주름살이 생기거나 색소침착을 일으키는 등의 노화현상을 촉진하고, 동맥경화 ·간질환 등이 진행하게 된다. 따라서 고기 ·생선 ·계란과 같은 산성식품 또는 과산화지질이 함유된 건어물(乾魚物)이나 기일이 지난 가공식품 등의 섭취를 가능한 줄인다.
Lipid peroxidation
metabolic process that causes oxidative deterioration of lipids by reactive oxygen species. This process can degrade the lipids within the cell membrane leading to cell damage and eventually, cell death.
Credit: Pavel Chagochkin/Shutterstock.com
Oxidative deterioration is caused by highly reactive free radical species. A free radical chain reaction occurs during lipid peroxidation as once a free radical is produced, it can react with another stable species to produce another free radical. The products of lipid peroxidation are useful indicators of oxidative stress in tissues and have been linked to the progression of cancer.
Mechanism of lipid peroxidation
The lipid peroxidation process has three steps that form a free radical chain reaction:
Initiation
Propagation
Termination
The initiation step involves production of a fatty acid radical when a reactive oxygen species, such as hydroxyl radical combines with a hydrogen atom to form water and a fatty acid radical. The unstable fatty acid radical quickly reacts with molecular oxygen in the propagation step to form a peroxyl-fatty acid radical.
This unstable radical further reacts with a free fatty acid to produce hydrogen peroxide or cyclic peroxide and another fatty acid radical. The chain reaction of free radical reactions continues until a non-radical species is formed by combination of two free radicals in the termination step. The free radical reactions can also be halted by antioxidant molecules within an organism. They can bind to the free radicals and prevent lipid peroxidation, often in the form of lipid-soluble vitamins.
Products of lipid peroxidation
Lipid peroxidation forms a number of oxidation products, including lipid hydroperoxides (LOOH) and aldehydes such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE). LOOH are the primary products of lipid peroxidation produced in the propagation step. After formation, LOOH can be reduced leading to inhibition of peroxidative damage or peroxidative damage induction.
Two electron reductions cause hydroperoxide decomposition that inhibits peroxidative damage, while one electron reduction induces new lipid hydroperoxides by contributing to the initiation and propagation steps. Studies have found that LOOH in serum can be used as an indicator of oxidative stress in tissues.
MDA is the most mutagenic product of lipid peroxidation and is commonly used as a biomarker for oxidative deterioration in omega-3 and omega-6 fatty acids. The thiobarbituric acid (TBA) test uses the reactivity of TBA towards MDA to measure autoxidative degradation within edible fats and oils.
4-HNE is the most toxic secondary product of lipid peroxidation, and it displays a dual role as a protective signaling molecule during gene expression and a cytotoxic promoter of pathological pathways.