ROS Flashcards
What are ROS?
Reactive Oxygen Species (ROS) are highly reactive molecules containing oxygen. Examples include superoxide anion (O2·-), hydrogen peroxide (H2O2), and hydroxyl radical (·OH). While ROS are byproducts of normal cellular metabolism, particularly in the mitochondria, their excessive accumulation can lead to oxidative stress, damaging proteins, lipids, and DNA.
What is redox balance?
The equilibrium between oxidants (such as ROS) and antioxidants in the cell. Antioxidative defense systems protect the cell from oxidative damage by neutralizing ROS.
Where do ROS come from?
ROS can come from external sources such as UV light, ionizing radiation, ozone, certain chemicals like quinones that promote superoxide formation, and smoke. Internally, ROS are produced in various parts of our cells, including mitochondria, peroxisomes, cytosol, plasma membrane, lysosomes, and the endoplasmic reticulum.
How are ROS produced in mitochondria?
In mitochondria, ROS are mainly produced during the process of cellular respiration. Electrons sometimes prematurely react with oxygen, forming superoxide anions. Peroxisomes generate ROS through the oxidation of fatty acids and other processes. In the cytosol, enzymes like xanthine oxidase contribute to ROS production. The plasma membrane also produces ROS through enzymes such as NADPH oxidase, which is crucial in immune response but can contribute to diseases if overactive.
How are ROS produced in the ER?
The ER produces ROS during protein folding, where the formation of disulfide bridges generates hydrogen peroxide. Prostaglandin and leukotriene biosynthesis in the ER also involves ROS formation through the actions of cyclooxygenases and lipoxygenases.
Explain what happens in over-existence and deficiency of NADPH oxidases.
NADPH oxidases (NOX) are enzymes found in both phagocytic (immune) cells and non-phagocytic cells. In immune cells, NOX enzymes play a role in what’s known as the “respiratory burst,” where they rapidly produce ROS to destroy pathogens. However, if these enzymes are overactive in blood vessels, they can contribute to arteriosclerosis by causing macrophages to adhere to arterial walls, absorb cholesterol, and form plaques. Conversely, a deficiency in NOX can lead to immune system problems, resulting in chronic infections due to impaired phagocytosis.
Superficially which cellular components is ROS damaging?
Damage by ROS can impact various cellular components, including proteins, lipids, and DNA.
Describe the protein damage that is caused by ROS.
ROS can oxidize amino acids, which alters protein structure and function. This can disrupt cellular processes and lead to cellular dysfunction.
Describe the lipid-damage that is caused by ROS.
ROS is causing lipid peroxidation. ROS attack lipids in cell membranes, starting a chain reaction of lipid oxidation.
The initial lipid radicals are unstable and transfer excess electrons to neighboring lipids, creating more radicals and leading to the formation of lipid peroxides and cyclic compounds.
Eventually, two lipid radicals combine to form a stable, but permanently altered, non-radical lipid. Antioxidants and enzymes can help detoxify these reactive lipid species, reducing damage.
Two reactions that form ROS:
Fenton: Fe2 + H2O2 → Fe3 + OH− + HO*
Haber-Weiss: O2− + H2O2 → O2 + HO− + HO
What is the oxidative stress?
Oxidative stress is a condition characterized by an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify these reactive intermediates or repair the resulting damage. Transition metals, such as iron (Fe) and copper (Cu), play a crucial role in the generation of ROS through redox cycling. The presence of excess free iron or copper in cells can exacerbate oxidative stress, leading to cellular damage and contributing to various diseases, including neurodegenerative disorders and cancer.
Name antioxidant enzymes:
Superoxide Dismutases (SODs), catalases, Glutathione Peroxidases (GPx), Peroxiredoxins (Prx). They maintain cellular redox balance and protect cells from oxidative damage.
