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Updated: Jul 31, 2026

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
[Apoptosis and carcinogenesis in aging: oxygen-peroxide aspect]
Cellular dysfunction causes oxidative stress, leading to aging, cancer, and apoptosis. This imbalance in pro- and antioxidants, including active oxygen species and peroxides, drives these processes from initiation to execution.
Area of Science:
- Biochemistry
- Cell Biology
- Molecular Biology
Context:
- Aging, cancerogenesis, and apoptosis are complex biological processes with multifactorial origins.
- The role of oxidative stress and the oxygen-peroxide concept have been investigated as potential unifying mechanisms.
- Understanding the early cellular events is crucial for elucidating the progression of these conditions.
Purpose:
- To present new findings supporting the oxygen-peroxide concept of aging, cancerogenesis, and apoptosis.
- To elucidate the role of cellular respiration dysfunction and subsequent oxidative stress in initiating these processes.
- To highlight the function of signaling molecules, such as active oxygen forms and peroxides, in both the initiation and execution phases.
Summary:
- Cellular respiration dysfunction initiates oxidative stress, first in mitochondria, then in the cytoplasm and cell.
- Excessive formation of active oxygen forms and lipid/protein peroxides creates a pro- and antioxidant imbalance.
- This imbalance, particularly pronounced in aging, tumor, and apoptosis cells, is critical for initiating and executing aging, carcinogenesis, and apoptosis.
Impact:
- Provides a unified concept linking cellular dysfunction to major biological processes like aging and cancer.
- Identifies key signaling molecules (active oxygen, peroxides) that mediate these processes.
- Suggests potential therapeutic targets by influencing the balance of pro- and antioxidants and downstream effectors.
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