High concentrations of H2O2, Fe2+ and ascorbic
acid increase lipid peroxidation in pig liver
homogenate
Assessor: Dr. Guus van den Akker
Faculty of Health, Medicine and Life Sciences (FHML)
Maastricht University
Scientific writing
First version: 3rd December 2021
Second version: 7th January 2022
Introduction
1
, Lipid peroxidation is oxidative damage to lipids that contain carbon-carbon double bonds, in
particular polyunsaturated fats (PUFAs). It is a process with many applications, which can be
both crucial and detrimental, and this is highly dependent on the levels of oxidation. It can be
used in both pathogenesis, phagocyte activity as well regulatory mechanisms. The main
factors leading to oxidative stress are free radicals and reactive oxygen species (ROS) (1).
Exogenous sources of ROS include ultraviolet rays, tobacco, pathogenic infections and
ionizing radiation. Though high levels can be dangerous, low levels are naturally produced by
the mitochondria in the electron transport chain, the plasma membrane, the endoplasmic
reticulum and peroxisomes (1).
One of the most chemically reactive species is the hydroxyl radical ( •OH). They are unstable
molecules synthesized from O2 as well as through the Fenton reaction, where free iron (Fe 2+)
and hydrogen peroxide (H2O2) react and form water (H2O) and an OH. This reaction works
alongside the Haber-Weiss reaction where the Fe2+ is produced from ferric iron (Fe3+) and
superoxide (O2-). These reactions are most common with iron, however, they can occur with
other transition metals such as Cu2+ (1).
Due to the reactiveness of •OH, they are short-lived and attack molecules in their close
proximity causing oxidative stress (1). Primary targets include lipids that are unsaturated,
glycolipids and cholesterol in cell membranes. When the •OH is formed through the
respective processes, it will abstract the allylic hydrogen of the unsaturated fats. This is
known as the initiation of lipid peroxidation (1). The propagation phase will then commence,
where the lipid radicals (L•) formed react with oxygen and form a peroxyl radical (LOO •). By
reacting with a PUFA, lipid hydroperoxide (LOOH) and another L•. The newly produced L•
can undergo the same process to form a LOO • followed by LOOH. The chain reaction will be
terminated when all the PUFA have reacted and when antioxidants donate a hydrogen to the
LOO• to render it stable and unreactive (1).
Lipid peroxidation is a self-propagating chain reaction, due to the highly chemically reactive
nature. This can lead to a large amount of damage from a low level of initial oxidation. There
are mechanisms present in the cell to counter lipid peroxidation, these include enzymes and
nonenzymatic inhibitors. The nonenzymatic inhibitors include vitamins, which are naturally
occurring antioxidants. An important one is vitamin c, otherwise known as ascorbic acid
(AA). It can react with ROS and reduce them, preventing them from initiating the lipid
peroxidation chain reaction.
2
acid increase lipid peroxidation in pig liver
homogenate
Assessor: Dr. Guus van den Akker
Faculty of Health, Medicine and Life Sciences (FHML)
Maastricht University
Scientific writing
First version: 3rd December 2021
Second version: 7th January 2022
Introduction
1
, Lipid peroxidation is oxidative damage to lipids that contain carbon-carbon double bonds, in
particular polyunsaturated fats (PUFAs). It is a process with many applications, which can be
both crucial and detrimental, and this is highly dependent on the levels of oxidation. It can be
used in both pathogenesis, phagocyte activity as well regulatory mechanisms. The main
factors leading to oxidative stress are free radicals and reactive oxygen species (ROS) (1).
Exogenous sources of ROS include ultraviolet rays, tobacco, pathogenic infections and
ionizing radiation. Though high levels can be dangerous, low levels are naturally produced by
the mitochondria in the electron transport chain, the plasma membrane, the endoplasmic
reticulum and peroxisomes (1).
One of the most chemically reactive species is the hydroxyl radical ( •OH). They are unstable
molecules synthesized from O2 as well as through the Fenton reaction, where free iron (Fe 2+)
and hydrogen peroxide (H2O2) react and form water (H2O) and an OH. This reaction works
alongside the Haber-Weiss reaction where the Fe2+ is produced from ferric iron (Fe3+) and
superoxide (O2-). These reactions are most common with iron, however, they can occur with
other transition metals such as Cu2+ (1).
Due to the reactiveness of •OH, they are short-lived and attack molecules in their close
proximity causing oxidative stress (1). Primary targets include lipids that are unsaturated,
glycolipids and cholesterol in cell membranes. When the •OH is formed through the
respective processes, it will abstract the allylic hydrogen of the unsaturated fats. This is
known as the initiation of lipid peroxidation (1). The propagation phase will then commence,
where the lipid radicals (L•) formed react with oxygen and form a peroxyl radical (LOO •). By
reacting with a PUFA, lipid hydroperoxide (LOOH) and another L•. The newly produced L•
can undergo the same process to form a LOO • followed by LOOH. The chain reaction will be
terminated when all the PUFA have reacted and when antioxidants donate a hydrogen to the
LOO• to render it stable and unreactive (1).
Lipid peroxidation is a self-propagating chain reaction, due to the highly chemically reactive
nature. This can lead to a large amount of damage from a low level of initial oxidation. There
are mechanisms present in the cell to counter lipid peroxidation, these include enzymes and
nonenzymatic inhibitors. The nonenzymatic inhibitors include vitamins, which are naturally
occurring antioxidants. An important one is vitamin c, otherwise known as ascorbic acid
(AA). It can react with ROS and reduce them, preventing them from initiating the lipid
peroxidation chain reaction.
2
