# Cell type-dependent modulation of senescence features using Weo electrolyzed water

**Authors:** Brenda L. Court-Vazquez, Shirley A. Arroyo-Vizcarrondo, Jonathan A. Poli, Lara Nyman, Kelly Halderman, Anthony Ginter, Pierre-Yves Desprez

PMC · DOI: 10.18632/aging.205789 · Aging (Albany NY) · 2024-04-30

## TL;DR

This study shows that Weo electrolyzed water can reduce signs of aging in normal cells while making cancer cells more vulnerable to stress.

## Contribution

The study reveals that WEW has cell type-dependent senomorphic effects, modulating senescence and stress responses differently in normal and cancer cells.

## Key findings

- WEW reduced senescence markers and SASP factors in normal lung fibroblasts.
- WEW increased SASP factors and stress response genes in breast cancer cells.
- WEW's differential effects suggest potential for promoting longevity and reducing age-related diseases.

## Abstract

Electrolyzed-reduced water has powerful antioxidant properties with constituents that scavenge reactive oxygen species (ROS), which are known to be produced by several intrinsic and extrinsic processes. When there is an imbalance between ROS production and antioxidant defenses, oxidative stress occurs. Persistent oxidative stress leads to cellular senescence, an important hallmark of aging, and is involved in several age-related conditions and illnesses. This study aims to investigate whether Weo electrolyzed water (WEW) could modulate the phenotype of senescent cells. We compared normal human lung fibroblasts (BJ) and breast cancer cells (T47D) treated with hydrogen peroxide (H2O2) to induce senescence. We assessed the molecular impact of WEW on markers of cellular senescence, senescence-associated secretory phenotype (SASP) factors, and stress response genes. Treatment with WEW modulated markers of cellular senescence, such as the senescence-associated β-galactosidase (SA-β-gal) activity, EdU incorporation and p21 expression, similarly in both cell types. However, WEW modulated the expression of SASP factors and stress response genes in a cell type-dependent and opposite fashion, significantly decreasing them in BJ cells, while stimulating their expression in T47D cells. Reduction in the expression of SASP factors and stress-related genes in BJ cells suggests that WEW acts as a protective factor, thereby reducing oxidative stress in normal cells, while making cancer cells more sensitive to the effects of cellular stress, thus increasing their elimination and consequently reducing their deleterious effects. These findings suggest that, due to its differential effects as a senomorphic factor, WEW could have a positive impact on longevity and age-related diseases.

## Linked entities

- **Genes:** CDKN1A (cyclin dependent kinase inhibitor 1A) [NCBI Gene 1026]
- **Chemicals:** hydrogen peroxide (PubChem CID 784)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** H3P16 (H3 histone pseudogene 16) [NCBI Gene 644914] {aka H3.6, H3F3AP6, p21}
- **Diseases:** age-related diseases (MESH:D010024), cancer (MESH:D009369), breast cancer (MESH:D001943)
- **Chemicals:** ROS (MESH:D017382), EdU (MESH:C022811), H2O2 (MESH:D006861), water (MESH:D014867), WEW (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** T47D — Homo sapiens (Human), Invasive breast carcinoma of no special type, Cancer cell line (CVCL_0553), BJ — Homo sapiens (Human), Telomerase immortalized cell line (CVCL_6573)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11131983/full.md

## References

27 references — full list in the complete paper: https://tomesphere.com/paper/PMC11131983/full.md

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Source: https://tomesphere.com/paper/PMC11131983