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Definition: How can apoptosis be triggered by oxidative stress?

Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify them or repair the resulting damage. Apoptosis, also known as programmed cell death, is a highly regulated process that eliminates damaged or unwanted cells. Under normal physiological conditions, apoptosis plays a crucial role in maintaining tissue homeostasis and eliminating potentially harmful cells.

However, excessive oxidative stress can disrupt the delicate balance of cellular processes and trigger apoptosis. This occurs through various mechanisms:

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1. Mitochondrial Dysfunction:

Oxidative stress can directly damage mitochondria, which are the powerhouse of the cell responsible for energy production. When mitochondria are impaired, they release ROS and other pro-apoptotic molecules, such as cytochrome c, into the cytoplasm. These molecules activate caspases, a group of enzymes that initiate the apoptotic cascade.

2. DNA Damage:

ROS can cause DNA damage by oxidizing nucleic acids. If the damage is severe and beyond repair, it can activate DNA damage response pathways, leading to apoptosis. This mechanism acts as a protective mechanism to prevent the propagation of cells with damaged DNA, which could potentially lead to mutations and cancer.

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3. Activation of Death Receptors:

Oxidative stress can also trigger apoptosis through the activation of death receptors on the cell surface. These receptors, such as Fas and tumor necrosis factor receptor 1 (TNFR1), transmit pro-apoptotic signals when bound by their respective ligands. Oxidative stress can enhance the expression of these ligands or sensitize cells to their effects, leading to apoptosis.

4. Inactivation of Anti-Apoptotic Proteins:

Oxidative stress can modify or inactivate anti-apoptotic proteins, such as Bcl-2 and Bcl-xL, which normally prevent apoptosis. When these proteins are compromised, the balance between pro-apoptotic and anti-apoptotic factors shifts towards apoptosis, resulting in cell death.

In summary, oxidative stress can trigger apoptosis through multiple mechanisms, including mitochondrial dysfunction, DNA damage, activation of death receptors, and inactivation of anti-apoptotic proteins. Understanding these processes is crucial for elucidating the role of oxidative stress in various diseases and developing therapeutic strategies to modulate apoptosis.

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