cellular response to lipid hydroperoxide

Definition

Target type: biologicalprocess

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a lipid hydroperoxide stimulus. Lipid hydroperoxide is the highly reactive primary oxygenated products of polyunsaturated fatty acids. [GOC:mah]

Cellular response to lipid hydroperoxide is a complex process involving a cascade of events that ultimately lead to the detoxification and repair of damaged cells. This process is crucial for protecting organisms from the damaging effects of oxidative stress.

Lipid hydroperoxides are reactive oxygen species (ROS) that can be generated by various cellular processes, such as mitochondrial respiration, inflammation, and exposure to environmental toxins. These molecules can damage cellular components, including lipids, proteins, and DNA, leading to cell death and disease.

To counter these damaging effects, cells have evolved sophisticated mechanisms to detect and respond to lipid hydroperoxides. The process begins with the recognition of lipid hydroperoxides by specific receptors or sensors. These receptors can be located on the cell surface or within the cytoplasm, and their activation triggers a signaling cascade that activates downstream effector molecules.

One important effector molecule is the transcription factor Nrf2. Nrf2 is normally sequestered in the cytoplasm by the Keap1 protein. However, upon exposure to lipid hydroperoxides, Keap1 undergoes conformational changes, leading to the release of Nrf2. Nrf2 then translocates to the nucleus, where it binds to antioxidant response elements (AREs) in the promoter regions of genes involved in detoxification and antioxidant defense.

These genes include those encoding enzymes such as glutathione S-transferases (GSTs), NAD(P)H quinone oxidoreductase 1 (NQO1), and heme oxygenase-1 (HO-1). GSTs catalyze the detoxification of electrophilic compounds, while NQO1 reduces quinones, and HO-1 degrades heme, producing bilirubin, an antioxidant. These enzymes work together to protect cells from oxidative stress.

Another important component of cellular response to lipid hydroperoxides is the activation of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx). SOD converts superoxide radicals into hydrogen peroxide, which is then degraded by catalase or GPx. GPx also reduces hydrogen peroxide, using glutathione as a reducing agent. These enzymes work in concert to remove ROS and protect cells from damage.

In addition to activating antioxidant defense mechanisms, cells can also repair damaged molecules. This repair process involves a variety of enzymes, including DNA repair enzymes, protein repair enzymes, and lipid repair enzymes.

Overall, the cellular response to lipid hydroperoxides is a complex and tightly regulated process that involves multiple signaling pathways, transcription factors, and effector molecules. This process is essential for maintaining cellular homeostasis and protecting organisms from the damaging effects of oxidative stress.'
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Proteins (1)

Compounds (4)