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Related Concept Videos

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The color of the skin is influenced by a number of pigments, including melanin, carotene, and hemoglobin. Recall that melanin is produced by cells called melanocytes, which are found scattered throughout the stratum basale of the epidermis. The melanin is transferred to the keratinocytes via melanosomes.
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The skin is divided into epidermis, dermis, and hypodermis, the skin's outermost, middle, and inner layers. The human epidermal layer regularly undergoes renewal, where old, dead cells are replaced by new cells. Epidermal stem cells or EpiSCs divide and differentiate to restore the lost cells. For the renewal process, some EpiSCs continuously self-renew. In contrast, few others differentiate into transit-amplifying cells, which later form prickle or spinous cells, followed by granular...
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Changes in Skin Color: Clinical Perspectives01:14

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The first thing a clinician sees is the skin, so the examination of the skin should be part of any thorough physical examination. Most skin disorders are relatively benign, but a few, including melanomas, can be fatal if untreated. A couple of the more noticeable disorders, albinism and vitiligo, affect the appearance of the skin and its accessory organs.
Albinism
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Radical Autoxidation01:20

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The oxidation of an organic compound in the presence of air or oxygen is called autoxidation. For example, cumene reacts with oxygen to form hydroperoxide. Autoxidation involves initiation, propagation, and termination steps. Many organic compounds are susceptible to autoxidation—especially ethers in the presence of oxygen, which form hydroperoxides. Even though this reaction is slow, old ether bottles contain small amounts of peroxide, which leads to laboratory explosions during ether...
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Oxidation of Phenols to Quinones01:17

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In the presence of oxidizing agents, phenols are oxidized to quinones. Quinones can be easily reduced back to phenols using mild reducing agents. The electron-donating hydroxyl group enhances the reactivity of the aromatic ring, enabling oxidation of the ring even in the absence of an α hydrogen.
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Cutaneous Redox Senescence.

Mariáurea Matias Sarandy1,2, Reggiani Vilela Gonçalves2,3, Giuseppe Valacchi1,4,5

  • 1Department of Animal Science, Plants for Human Health Institute, North Carolina State University, North Carolina Research Campus, 600 Laureate Way, Kannapolis, NC 28081, USA.

Biomedicines
|February 24, 2024
PubMed
Summary

Environmental and lifestyle factors induce skin cell senescence by disrupting redox balance, leading to oxidative stress. This oxidative stress damages cellular components and activates key pathways, ultimately promoting senescence.

Keywords:
biochemistrycutaneous senescenceinflammationmolecular signalingreactive oxygen species

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Cellular Redox Profiling Using High-content Microscopy
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Area of Science:

  • Dermatology
  • Cell Biology
  • Oxidative Stress Research

Background:

  • Skin cell senescence is influenced by environmental, lifestyle, and genetic factors.
  • These factors commonly disrupt cellular redox balance, causing oxidative stress.
  • Oxidative stress arises from an imbalance between free radicals, reactive oxygen species (ROS), and antioxidant defenses.

Purpose of the Study:

  • To elucidate the redox mechanisms underlying skin cell senescence.
  • To identify the primary targets of ROS in skin cells.
  • To highlight the role of oxidative stress in activating senescence pathways and the senescence-associated secretory phenotype (SASP).

Main Methods:

  • Review and synthesis of current understanding of skin senescence mechanisms.
  • Identification of key molecular pathways involved in ROS-induced senescence.
  • Analysis of cellular targets and downstream effects of oxidative stress.

Main Results:

  • Key redox mechanisms include telomere shortening, proteome oxidation, DNA damage, increased lysosomal mass (e.g., SA-β-gal activity), and elevated SASP.
  • The skin proteome (oxi-proteome) is a primary target of ROS, followed by telomeres, nucleic acids, lipids, proteins, and organelles.
  • Oxidative stress activates cell cycle arrest pathways (p16INK4A, p53), promotes lipid peroxidation, lysosomal dysfunction, mitochondrial issues, and SASP, including NF-κB-regulated cytokines.

Conclusions:

  • Oxidative stress is a central driver of skin cell senescence through multiple molecular pathways.
  • Confirmation of senescence requires multiple analyses, as individual markers may be insufficient.
  • Further investigation into ox-inflammatory pathways is crucial for a comprehensive understanding of cutaneous redox senescence.