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The enigma of in vivo oxidative stress assessment: isoprostanes as an emerging target

View Article: PubMed Central

ABSTRACT

Oxidative stress is believed to be one of the major factors behind several acute and chronic diseases, and may also be associated with ageing. Excess formation of free radicals in miscellaneous body environment may originate from endogenous response to cell injury, but also from exposure to a number of exogenous toxins. When the antioxidant defence system is overwhelmed, this leads to cell damage. However, the measurement of free radicals or their endproducts is tricky, since these compounds are reactive and short lived, and have diverse characteristics. Specific evidence for the involvement of free radicals in pathological situations has been difficult to obtain, partly owing to shortcomings in earlier described methods for the measurement of oxidative stress. Isoprostanes, which are prostaglandin-like bioactive compounds synthesized in vivo from oxidation of arachidonic acid, independently of cyclooxygenases, are involved in many human diseases, and their measurement therefore offers a way to assess oxidative stress. Elevated levels of F2-isoprostanes have also been seen in the normal human pregnancy, but their physiological role has not yet been defined. Large amounts of bioactive F2-isoprostanes are excreted in the urine in normal basal situations, with a wide interindividual variation. Their exact role in the regulation of normal physiological functions, however, needs to be explored further. Current understanding suggests that measurement of F2-isoprostanes in body fluids provides a reliable analytical tool to study oxidative stress-related diseases and experimental inflammatory conditions, and also in the evaluation of various dietary antioxidants, as well as drugs with radical-scavenging properties. However, assessment of isoprostanes in plasma or urine does not necessarily reflect any specific tissue damage, nor does it provide information on the oxidation of lipids other than arachidonic acid.

No MeSH data available.


Basic principle of non-enzymic lipid peroxidation involving polyunsaturated fatty acids.
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Figure 0001: Basic principle of non-enzymic lipid peroxidation involving polyunsaturated fatty acids.

Mentions: It is well acknowledged that polyunsaturated fatty acids (PUFAs) with two or more double bonds are more prone to oxidation than the saturated and monounsaturated fatty acids 8. This is largely due to the instability (weak energy of attachment) of the hydrogen atom adjoining the double bond. This means that the hydrogen atom can be abstracted easily through a reactive radical attack (Fig. 1). Lipid peroxidation in vivo requires a PUFA and an oxidant inducer, which form a free radical intermediate. The free radical intermediate reacts with oxygen to form a peroxyl radical (LOO·). The unpaired electrons of the peroxyl radicals further abstract a hydrogen atom from another PUFA to form a lipid hydroperoxide, which may decay to form alkoxyl or peroxyl radicals. These radicals may also attract adjoining diverse membrane proteins. The reaction of the peroxyl radical with other fatty acids generates a carbon-centred radical which, in turn, will be able to react with oxygen to form another peroxyl radical. This radical continues its reaction to the PUFAs, and a propagation reaction initiates a chain reaction that is maintained until a termination reaction starts by one or several endogenous chain-breaking antioxidants or by exogenously applied antioxidants, dietary radical scavengers or drugs 9. However, excess endogenous formation or exogenous administration of these biocombating factors may also lead to pro-oxidative effects in certain conditions which, so far, have been less studied.


The enigma of in vivo oxidative stress assessment: isoprostanes as an emerging target
Basic principle of non-enzymic lipid peroxidation involving polyunsaturated fatty acids.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2607004&req=5

Figure 0001: Basic principle of non-enzymic lipid peroxidation involving polyunsaturated fatty acids.
Mentions: It is well acknowledged that polyunsaturated fatty acids (PUFAs) with two or more double bonds are more prone to oxidation than the saturated and monounsaturated fatty acids 8. This is largely due to the instability (weak energy of attachment) of the hydrogen atom adjoining the double bond. This means that the hydrogen atom can be abstracted easily through a reactive radical attack (Fig. 1). Lipid peroxidation in vivo requires a PUFA and an oxidant inducer, which form a free radical intermediate. The free radical intermediate reacts with oxygen to form a peroxyl radical (LOO·). The unpaired electrons of the peroxyl radicals further abstract a hydrogen atom from another PUFA to form a lipid hydroperoxide, which may decay to form alkoxyl or peroxyl radicals. These radicals may also attract adjoining diverse membrane proteins. The reaction of the peroxyl radical with other fatty acids generates a carbon-centred radical which, in turn, will be able to react with oxygen to form another peroxyl radical. This radical continues its reaction to the PUFAs, and a propagation reaction initiates a chain reaction that is maintained until a termination reaction starts by one or several endogenous chain-breaking antioxidants or by exogenously applied antioxidants, dietary radical scavengers or drugs 9. However, excess endogenous formation or exogenous administration of these biocombating factors may also lead to pro-oxidative effects in certain conditions which, so far, have been less studied.

View Article: PubMed Central

ABSTRACT

Oxidative stress is believed to be one of the major factors behind several acute and chronic diseases, and may also be associated with ageing. Excess formation of free radicals in miscellaneous body environment may originate from endogenous response to cell injury, but also from exposure to a number of exogenous toxins. When the antioxidant defence system is overwhelmed, this leads to cell damage. However, the measurement of free radicals or their endproducts is tricky, since these compounds are reactive and short lived, and have diverse characteristics. Specific evidence for the involvement of free radicals in pathological situations has been difficult to obtain, partly owing to shortcomings in earlier described methods for the measurement of oxidative stress. Isoprostanes, which are prostaglandin-like bioactive compounds synthesized in vivo from oxidation of arachidonic acid, independently of cyclooxygenases, are involved in many human diseases, and their measurement therefore offers a way to assess oxidative stress. Elevated levels of F2-isoprostanes have also been seen in the normal human pregnancy, but their physiological role has not yet been defined. Large amounts of bioactive F2-isoprostanes are excreted in the urine in normal basal situations, with a wide interindividual variation. Their exact role in the regulation of normal physiological functions, however, needs to be explored further. Current understanding suggests that measurement of F2-isoprostanes in body fluids provides a reliable analytical tool to study oxidative stress-related diseases and experimental inflammatory conditions, and also in the evaluation of various dietary antioxidants, as well as drugs with radical-scavenging properties. However, assessment of isoprostanes in plasma or urine does not necessarily reflect any specific tissue damage, nor does it provide information on the oxidation of lipids other than arachidonic acid.

No MeSH data available.