Initiators of lipid peroxidation in living cells are reactive oxygen species (ROS), such as OH• and HO2. Ros triggers lipid peroxidation.Could the initiation be caused by a mechanical/physical stress? Or other kind of stress? Could lipid peroxidation, initiated by a stimulus different from ROS, trigger ROS formation?
I agree with Dr Lopez-Martinez lipid peroxidation is a chemical reaction in which free hydroxyl radicals or nitric oxide radicals react with lipids to form either lipid peroxides or nitroperoxides. Whilst mechanical stress can stimulate an inflammatory reaction which will result in ROS production and hence to lipid peroxidation - this is a secondary process to the actual mechanical stress. The mechanical stress itself does not directly cause peroxidation, but simply is the prelude to inflammation which is the cause of lipid peroxidation.
Lipid peroxidation is an oxidation process by definition, as its name indicates. Thus, in this strict sense some kind of free radical attack should happen to cell membrane lipid degradation take place. Maybe one can evade the implication of ROS in peroxidation by manipulating the final product of the lipid peroxidation cascade, i.e. malondialdehyde. In this way you stimulate peroxidation but getting round the acting of ROS. Unfortunately I have never heard about such treatment and I have no concrete advice on how could be this carried out, if it's feasible at all.
Mechanical/physical stressors could lead to lipid peroxidation via generation of ROS
Perhaps Yes ! Provided stressor generates heat. and in turn free radicals !
Mechanical/physical stress could lead to inflammation and consequently lipid peroxidation which in this case would be a secondary reaction. Lipid peroxidation is a free radical driven reaction so if your stressor could produce free radicals, then lipid peroxidation may ensue.
Thank you all for your answers. I understand that other type of stressors can generate lipid peroxidation only via ROS, which are the principal initiators of the process.
Any radical generator is able to initiate lipid peroxidation. Examples are nuclear particles alpha, beta etc.
You may stress your cells by applying stressors like PKC inhibitors or else; the primary stress is not ROS, however it results in subsequent ROS production which at the next step causes lipid peroxidation, like that of cardiolipin at the inner mito membrane...
Lipid peroxidation (LPO) is initiated when a hydrogen atom is abstracted from the backbone of a fatty acid, leaving a carbon based radical which quickly adds O2 to make a peroxy radical.
This can then abstract another hydrogen atom from a neighboring fatty acid or cause breakdown of the carbon backbone to produce dialdehydes which are very stable and react with DNA.
There are two ways to abstract that hydrogen:
1) Radicals (ROS, RNS…)
2) Enzymatically (during prostaglandin biosynthesis)
If mechanical/physical stress produces tissue injuries leading to inflammatory response, then yes (indirectly). Inflammation can be a double whammy – leading to macrophages producing ROS and activation of cyclooxygenases, both of which can cause LPO.
I would like to add particles as another type of stressors, such as asbestos and other types of mineral particles, as well as pollution-generated particulates. The former can act as inflammatory agents by inducing futile phagocytosis in macrophages and/or by adding molecular oxygen to the existing carbon-centered radicals, as suggested above, both of which would cause ROS generation and, subsequently, lipid peroxidation as well as oxidation of proteins and nucleic acids.
Of course, like the same in DM patient or hypertension that more shear stress induces ROS in vasculature and subsequently, induces LP.
I am working on the impact of sewage on antioxidant status of a teleost and according to my results, any external or internal factor can bring about alterations in antioxidant activity leading to oxidative stress. This results in ROS production and when ROS overwhelms antioxidant activity, lipid peroxidation occurs.
A very detailes description, how LPO leads to ROS you can find in: http://www.ncbi.nlm.nih.gov/pubmed/21273555
Kampfrath et al 2012 show, how particular fine matter leads to ROS via TLR4 activation.
We showed that protein-restriction during neonatal life is associated with increased oxidative stress of the offspring in adult age . It has been shown that low protein diets during gestation or gestation and lactation could predispose to pancreatic islet dysfunction later in life by unbalance between higher concentration of superoxide radical-inactivating enzymes (SOD) and very low concentration of hydrogen peroxide inactivating enzymes (CAT and GPX) in islets of the progeny at 3 months-old rats (Theys et al. 2009). In addition, protein-restricted diet given to mothers during late pregnancy and early postnatal periods induced oxidative stress in their pups on postnatal day 14 . These findings indicate that the time window of protein restriction seems to be of critical importance for modulation of antioxidant defense capacity in adult life.
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