response to reactive oxygen species

Definition

Target type: biologicalprocess

Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a reactive oxygen species stimulus. Reactive oxygen species include singlet oxygen, superoxide, and oxygen free radicals. [GOC:krc]

Reactive oxygen species (ROS) are highly reactive molecules containing oxygen, often generated as byproducts of normal cellular metabolism. They are essential for certain cellular processes, such as signaling and immune responses, but excessive ROS production can lead to oxidative stress, damaging cellular components like proteins, lipids, and DNA. The cellular response to ROS involves complex mechanisms to detoxify ROS, repair oxidative damage, and activate signaling pathways that promote adaptation and survival.

1. **ROS Detoxification:** Cells possess various antioxidant enzymes and molecules that scavenge ROS. These include:
* **Superoxide dismutase (SOD):** Converts superoxide radicals (O2-) into hydrogen peroxide (H2O2).
* **Catalase:** Decomposes hydrogen peroxide into water and oxygen.
* **Glutathione peroxidase:** Reduces hydrogen peroxide and lipid hydroperoxides.
* **Glutathione reductase:** Reduces oxidized glutathione (GSSG) to its reduced form (GSH), replenishing the antioxidant glutathione pool.
* **Non-enzymatic antioxidants:** Vitamin C, vitamin E, and carotenoids directly scavenge ROS or protect other molecules from ROS damage.

2. **Repair of Oxidative Damage:** Cells have mechanisms to repair damage caused by ROS.
* **DNA repair:** DNA repair pathways, such as base excision repair (BER) and nucleotide excision repair (NER), remove damaged nucleotides and replace them with undamaged ones.
* **Protein repair:** Chaperone proteins assist in refolding damaged proteins, while proteasomes degrade irreversibly damaged proteins.
* **Lipid repair:** Lipids are repaired by enzymes that break down oxidized lipids and replace them with new lipids.

3. **Signaling Pathways:** ROS can act as signaling molecules, activating various pathways to promote cellular adaptation and survival.
* **MAPK pathways:** ROS can activate mitogen-activated protein kinases (MAPKs), such as ERK, JNK, and p38, which regulate gene expression, cell growth, and apoptosis.
* **NF-κB pathway:** ROS activate the transcription factor NF-κB, which regulates genes involved in inflammation, immune responses, and cell survival.
* **Nrf2 pathway:** ROS can activate the Nrf2 transcription factor, which induces the expression of antioxidant genes.

4. **Cellular Adaptation:** Chronic exposure to low levels of ROS can induce adaptive responses.
* **Increased antioxidant defenses:** Cells increase the production of antioxidant enzymes and molecules.
* **Enhanced repair mechanisms:** Cells increase the activity of DNA repair, protein repair, and lipid repair pathways.
* **Increased autophagy:** Cells increase autophagy, a process that removes damaged organelles and proteins.

5. **Cell Death:** If ROS levels become overwhelming, cells can undergo programmed cell death (apoptosis) or necrosis.
* **Apoptosis:** A programmed cell death process characterized by DNA fragmentation and cell shrinkage.
* **Necrosis:** A form of cell death caused by severe damage, leading to cell lysis and inflammation.

In summary, the response to ROS is a complex and multifaceted process involving detoxification, repair, signaling, adaptation, and cell death. This intricate network of cellular mechanisms aims to maintain redox homeostasis, protect cells from oxidative damage, and promote survival.'
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Proteins (5)

Compounds (167)