# The Impact of Recreational Diving to a Depth of 40 m on Selected Intracellular DAMPs

**Authors:** Anna Nowakowska, Małgorzata Marchelek-Myśliwiec, Marta Skórka-Majewicz, Wojciech Żwierełło, Konrad Grzeszczak, Izabela Gutowska

PMC · DOI: 10.3390/ijms26073061 · International Journal of Molecular Sciences · 2025-03-27

## TL;DR

This study examines how recreational diving to 40 meters affects certain proteins in the body that are linked to inflammation and stress.

## Contribution

This is the first study to analyze intracellular DAMPs in recreational divers under diving conditions.

## Key findings

- Diving caused a temporary decrease in HMGB1 expression at both mRNA and protein levels.
- S100A9 expression increased 1 hour after the dive compared to immediately after.
- Diving influenced genes related to glutathione synthesis and reduced plasma glutathione levels.

## Abstract

Increasingly popular, recreational diving is a physical activity that takes place under extreme environmental conditions, which include hyperoxia, hyperbaria and exposure to cold water. The effects of these factors on the human body induce increased levels of reactive oxygen and nitrogen species in divers’ bodies, which may modulate damage-associated molecular pattern (DAMPs), their receptors and the antioxidant response. This study involved 21 divers who descended to a depth of 40 metres. Determinations of selected intracellular DAMPs (high-mobility group box protein 1,HMGB1, S100 calcium-binding proteins A9 and A8, S100A8 and S100A9, heat shock protein family A member 1A, HSPA1A (Hsp70), heat shock protein family B, (small) member 1, HSPB1(Hsp27), thioredoxin, TXN), their receptors (Toll-like receptor 4, TLR4 and receptors for advanced glycation end products, RAGE), nuclear factor-κB (NF-κB) and antioxidant defence markers were performed before, after and 1 h after the dive. A significant transient reduction in HMGB1 expression was observed immediately after the dive at both the mRNA and protein levels. We noted an increase in S100A9 expression, which occurred 1 h post-dive compared to the post-dive time point, and a post-dive decrease in TLR4 expression only at the mRNA level. Diving also influenced the expression of genes encoding key enzymes associated with glutathione synthesis, (glutamate-cysteine ligase, catalytic subunit, GCLC and glutathione synthetase, GSS), and reduced plasma glutathione levels. However, no significant changes were observed in the expression of NF-κB, nitric oxide synthase 2 (NOS2) or circulating DAMP receptors (TLR4 and RAGE). The findings suggest an adaptive response to diving-induced oxidative stress, which appears to be a protective mechanism against an excessive inflammatory response. To our knowledge, this is the first study to analyse the role of intracellular DAMPs in recreational divers.

## Linked entities

- **Genes:** HMGB1 (high mobility group box 1) [NCBI Gene 3146], S100A9 (S100 calcium binding protein A9) [NCBI Gene 6280], S100A8 (S100 calcium binding protein A8) [NCBI Gene 6279], HSPA1A (heat shock protein family A (Hsp70) member 1A) [NCBI Gene 3303], HSPB1 (heat shock protein family B (small) member 1) [NCBI Gene 3315], TXN (thioredoxin) [NCBI Gene 7295], TLR4 (toll like receptor 4) [NCBI Gene 7099], AGER (advanced glycosylation end-product specific receptor) [NCBI Gene 177], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790], NOS2 (nitric oxide synthase 2) [NCBI Gene 4843], GCLC (glutamate-cysteine ligase catalytic subunit) [NCBI Gene 2729], GSS (glutathione synthetase) [NCBI Gene 2937]
- **Proteins:** HMGB1 (high mobility group box 1), S100A9 (S100 calcium binding protein A9), S100A8 (S100 calcium binding protein A8), HSPA1A (heat shock protein family A (Hsp70) member 1A), HSPB1 (heat shock protein family B (small) member 1), TXN (thioredoxin), TLR4 (toll like receptor 4), AGER (advanced glycosylation end-product specific receptor), NFKB1 (nuclear factor kappa B subunit 1), NOS2 (nitric oxide synthase 2)

## Full-text entities

- **Genes:** GCLC (glutamate-cysteine ligase catalytic subunit) [NCBI Gene 2729] {aka CNSHA7, GCL, GCS, GLCL, GLCLC}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, HSPA4 (heat shock protein family A (Hsp70) member 4) [NCBI Gene 3308] {aka APG-2, HEL-S-5a, HS24/P52, HSPH2, RY, hsp70}, HSPB1 (heat shock protein family B (small) member 1) [NCBI Gene 3315] {aka CMT2F, HEL-S-102, HMN2B, HMND3, HS.76067, HSP27}, TXN (thioredoxin) [NCBI Gene 7295] {aka TRDX, TRX, TRX1, TXN1, Trx80}, HMGB1 (high mobility group box 1) [NCBI Gene 3146] {aka HMG-1, HMG1, HMG3, SBP-1}, S100A8 (S100 calcium binding protein A8) [NCBI Gene 6279] {aka 60B8AG, CAGA, CFAG, CGLA, CP-10, L1Ag}, HSPA1A (heat shock protein family A (Hsp70) member 1A) [NCBI Gene 3303] {aka HEL-S-103, HSP70, HSP70-1, HSP70-1A, HSP70-2, HSP70.1}, AGER (advanced glycosylation end-product specific receptor) [NCBI Gene 177] {aka RAGE, SCARJ1, sRAGE}, S100A9 (S100 calcium binding protein A9) [NCBI Gene 6280] {aka 60B8AG, CAGB, CFAG, CGLB, L1AG, LIAG}, NOS2 (nitric oxide synthase 2) [NCBI Gene 4843] {aka HEP-NOS, INOS, NOS, NOS2A}, GSS (glutathione synthetase) [NCBI Gene 2937] {aka CNSHA6, GSHS, HEL-S-64p, HEL-S-88n}
- **Diseases:** hyperoxia (MESH:D018496), inflammatory (MESH:D007249)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11989067/full.md

## References

101 references — full list in the complete paper: https://tomesphere.com/paper/PMC11989067/full.md

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Source: https://tomesphere.com/paper/PMC11989067