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Gene expression changes in blood RNA after swimming in a pool

ABSTRACT: Trihalomethanes (THM) are a class of disinfection by-products in chlorinated waters linked to deleterious health effects in humans although biological mechanisms are unclear. We aimed to study short-term changes in blood gene expression of adult recreational swimmers associated with physical activity and THM exposure. Adult volunteers (18-50 years, non-smokers, non-asthmatics) swam 40 minutes in an indoor chlorinated pool in Barcelona. Blood samples and THM measurements in exhaled breath were collected before and 5 min/1h after swimming, respectively. Physical activity intensity was calculated as metabolic equivalents (METs). Gene expression in whole blood RNA was evaluated using Illumina HumanHT-12v3 Expression-BeadChip. Linear mixed models, Gene Set Enrichment Analyses-GSEA and mediation analyses were used. The study population comprised 37 before-after pairs, with mean age 31 years (SD: 6.0), 60% female, and average changes before-after swimming of 1.75 METs (SD: 1.36) and 0.23 µg/m3 of exhaled bromoform (SD: 0.23). Among THM, bromoform yielded the strongest effect on gene expression changes. Eighty eight probes were associated with bromoform, 326 probes with MET and 77 probes overlapped. In mutually adjusted models, 15 probes remained significant for MET after False Discovery Rate (FDR). Although not FDR significant, in 23 nominally significant probes (p-value <0.05), fulfilling criteria for exploring mediation, 29.5 to 53.4% of MET effect was mediated by exhaled bromoform. Individual genes in this subset and the GSEA of the mutually adjusted gene lists of bromoform and MET were associated with pathways related to inflammatory/immune response and to several cancers. In this first study evaluating short-term gene expression changes associated with swimming in a chlorinated pool, changes in gene expression were observed in association with physical activity with part of this effect mediated through bromoform exposure. Identified genes were correlated with inflammatory, immune response and cancer pathways. These results need replication in larger studies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE61225 | GEO | 2015/09/07

SECONDARY ACCESSION(S): PRJNA260538

REPOSITORIES: GEO

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Project description:Trihalomethanes (THM) are a class of disinfection by-products in chlorinated waters linked to deleterious health effects in humans although biological mechanisms are unclear. We aimed to study short-term changes in blood gene expression of adult recreational swimmers associated with physical activity and THM exposure. Adult volunteers (18-50 years, non-smokers, non-asthmatics) swam 40 minutes in an indoor chlorinated pool in Barcelona. Blood samples and THM measurements in exhaled breath were collected before and 5 min/1h after swimming, respectively. Physical activity intensity was calculated as metabolic equivalents (METs). Gene expression in whole blood RNA was evaluated using Illumina HumanHT-12v3 Expression-BeadChip. Linear mixed models, Gene Set Enrichment Analyses-GSEA and mediation analyses were used. The study population comprised 37 before-after pairs, with mean age 31 years (SD: 6.0), 60% female, and average changes before-after swimming of 1.75 METs (SD: 1.36) and 0.23 Âµg/m3 of exhaled bromoform (SD: 0.23). Among THM, bromoform yielded the strongest effect on gene expression changes. Eighty eight probes were associated with bromoform, 326 probes with MET and 77 probes overlapped. In mutually adjusted models, 15 probes remained significant for MET after False Discovery Rate (FDR). Although not FDR significant, in 23 nominally significant probes (p-value <0.05), fulfilling criteria for exploring mediation, 29.5 to 53.4% of MET effect was mediated by exhaled bromoform. Individual genes in this subset and the GSEA of the mutually adjusted gene lists of bromoform and MET were associated with pathways related to inflammatory/immune response and to several cancers. In this first study evaluating short-term gene expression changes associated with swimming in a chlorinated pool, changes in gene expression were observed in association with physical activity with part of this effect mediated through bromoform exposure. Identified genes were correlated with inflammatory, immune response and cancer pathways. These results need replication in larger studies. Expression profile differences were determined between total RNA extracted before and after exposure to trihalomethanes present in swimming pool water for 40 minute from whole blood samples from 33 healthy human individuals.

Project description:Skeletal muscle atrophy is dictated by the balance between protein synthesis and protein breakdown, known as proteostasis. With advanced age, muscle atrophy contributes to development of co-morbidities, loss of strength and independence, and all-cause mortality. Aging also coincides with the accumulation of senescent cells within skeletal muscle that produce inflammatory products, known as the senescence associated secretory phenotype. Previously, we found that a metformin + leucine (MET+LEU) combination treatment had synergistic effects in aged mice to improve skeletal muscle structure and function during disuse atrophy. Therefore, the objective of this study was to determine the mechanisms by which MET+LEU exhibits muscle atrophy protection in vitro and if this occurs through cellular senescence. C2C12 myoblasts differentiated into myotubes were used to determine MET+LEU mechanisms during serum-deprivation (SD) atrophy. Single myofibers were isolated from aged (22-23 mo) C57Bl6/J mice, and human primary myoblasts were extracted from a healthy older adult donor. 25 + 125 µM MET+LEU treatment increased differentiation of myotubes and prevented SD induced atrophy. Low concentration (0.1 + 0.5 µM) MET+LEU had unique effects to prevent myotube atrophy and cause transcriptional reprogramming compared to individual therapies. SD increased inflammatory and cellular senescence pathways that was reversed with MET+LEU treatment. SD resulted in dysregulated proteostasis that was rescued with MET+LEU, and proteasome inhibition with MG-132 also rescued myotube atrophy. Cellular senescence transcriptional pathways and markers increased by SD were reversed with MET+LEU treatment, and dasatinib + quercetin (D+Q) senolytic treatment prevented myotube atrophy similar to MET+LEU. In aged myofibers, MET+LEU prevented SD atrophy, and in human primary myotubes MET+LEU prevented reductions in myonuclei fusion. These data provide evidence that MET+LEU has muscle cell intrinsic properties to prevent atrophy by reversing senescence and improving proteostasis

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Gene expression changes in blood RNA after swimming in a pool

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