Abstract
Better understanding of the physiological mechanisms and neurological symptoms involved in the development of decompression sickness could contribute to improvements of diving procedures. The main objective of the present study was to determine effects on the brain proteome of fast decompression (1 bar/20 s) compared to controls (1 bar/10 min) after heliox saturation diving, using rats in a model system. The protein S100B, considered a biomarker for brain injury, was not significantly different in serum samples from one week before, immediately after, and one week after the dive. Alterations in the rat brain proteome due to fast decompression were investigated using both iontrap and orbitrap LC-MS, and 967 and 1062 proteins were quantified, respectively. Based on the significantly regulated proteins in the iontrap (56) and orbitrap (128) datasets, the networks “synaptic vesicle fusion and recycling in nerve terminals” and “translation initiation” were significantly enriched in a system biological database analysis (Metacore). Ribosomal proteins (RLA2, RS10) and the proteins hippocalcin-like protein 4 and proteasome subunit beta type-7 were significantly upregulated in both datasets. The heat shock protein 105 kDa, Rho-associated protein kinase 2 and Dynamin-1 were significantly downregulated in both datasets. Another main effect of hyperbaric fast decompression in our experiment is inhibition of endocytosis and stimulation of exocytosis of vesicles in the presynaptic nerve terminal. In addition, fast decompression affected several proteins taking parts in these two main mechanisms of synaptic strength, especially alteration in CDK5/calcineurin are associated with a broad range of neurological disorders. In summary, fast decompression after heliox saturation affected the brain proteome in a rat model for diving, potentially disturbing protein homeostasis, e.g. in synaptic vesicles, and destabilizing cytoskeletal components. Data are available via ProteomeXchange with identifier PXD006349
Highlights
For many years it has been discussed whether professional divers are at risk of long-term health effects caused by their diving career [1,2,3]
In the present experiments 12 of 21 rats in the fast decompression rate group (FD, 1 bar/20 s) got decompression sickness (DCS) symptoms and, as expected, such symptoms were not observed in any rats from the slow decompression (SD) group (SD, 1 bar/10 min)
enzyme-linked immunosorbent assay (ELISA) analyses of serum S100B showed no significant differences in levels when comparing the FD groups from one week before, immediately after, and one week after the dive to the SD group one week after the dive (Fig 1)
Summary
For many years it has been discussed whether professional divers are at risk of long-term health effects caused by their diving career [1,2,3]. Increased prevalence of white matter changes is demonstrated in healthy individuals/divers without neurological decompression sickness [9,10]. This applies for recreational divers, and a minor decrease in neuro-cognitive performance has been demonstrated in some individuals [11,12]. Moen et al (2010) observed regional functional abnormalities in former saturation divers from diffusion- and perfusion-weighted MRI [13]. They found that the perfusion deficits in the watershed areas were consistent with arterial microemboli or some general dysfunction of cerebral microvascular function. The mean transition time was reduced which could be due to reduced flexibility of the microvascular system or reduced capillary complexity which they assumed to be long-term clinical symptoms reported by professional divers
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