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Target Concepts:
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Query: UMLS:C0020440 (
hypercapnia
)
7,939
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Fish early life stages have been shown to react sensitive to simulated ocean acidification. In particular, acid-base disturbances elicited by altered seawater carbonate chemistry have been shown to induce pathologies in larval fish. However, the mechanisms underlying these disturbances are largely unknown. We used gene expression profiling of genes involved in acid-base regulation and metabolism to investigate the effects of seawater
hypercapnia
on developing Japanese ricefish (medaka; Oryzias latipes). Our results demonstrate that embryos respond with delayed development during the time window of 2-5 dpf when exposed to a seawater pCO(2) of 0.12 and 0.42 kPa. This developmental delay is associated with strong down-regulation of genes from major metabolic pathways including glycolysis (
G6PDH
), Krebs cycle (CS) and the electron transport chain (CytC). In a second step we identified acid-base relevant genes in different ontogenetic stages (embryos, hatchlings and adults) and tissues (gill and intestine) that are up regulated in response to
hypercapnia
, including NHE3, NBCa, NBCb, AE1a, AE1b, ATP1a1a.1, ATP1a1b, ATP1b1a, Rhag, Rhbg and Rhcg. Interestingly, NHE3 and Rhcg expressions were increased in response to environmental
hypercapnia
in all ontogenetic stages and tissues tested, indicating the central role of these proteins in acid-base regulation. Furthermore, the increased expression of genes from amino acid metabolism pathways (ALT1, ALT2, AST1a, AST1b, AST2 and GLUD) suggests that energetic demands of hatchlings are fueled by the breakdown of amino acids. The present study provides a first detailed gene expression analysis throughout the ontogeny of a euryhaline teleost in response to seawater
hypercapnia
, indicating highest sensitivity in early embryonic stages, when functional ion regulatory epithelia are not yet developed.
...
PMID:CO(2)-driven seawater acidification differentially affects development and molecular plasticity along life history of fish (Oryzias latipes). 2341 37
Seawater acidification due to anthropogenic release of CO2 as well as the potential leakage of pure CO2 from sub-seabed carbon capture storage (CCS) sites may impose a serious threat to marine organisms. Although infaunal organisms can be expected to be particularly impacted by decreases in seawater pH, as a result of naturally acidified conditions in benthic habitats, information regarding physiological and behavioral responses is still scarce. Determination of PO2 and P(CO2) gradients within burrows of the brittlestar Amphiura filiformis during environmental
hypercapnia
demonstrated that besides hypoxic conditions, increases of environmental P(CO2) are additive to the already high P(CO2) (up to 0.08 kPa) within the burrows. In response to up to 4 weeks exposure to pH 7.3 (0.3 kPa P(CO2)) and pH 7.0 (0.6 kPa P(CO2)), metabolic rates of A. filiformis were significantly reduced in pH 7.0 treatments, accompanied by increased ammonium excretion rates. Gene expression analyses demonstrated significant reductions of acid-base (NBCe and AQP9) and metabolic (
G6PDH
, LDH) genes. Determination of extracellular acid-base status indicated an uncompensated acidosis in CO2-treated animals, which could explain the depressed metabolic rates. Metabolic depression is associated with a retraction of filter feeding arms into sediment burrows. Regeneration of lost arm tissues following traumatic amputation is associated with significant increases in metabolic rate, and hypercapnic conditions (pH 7.0, 0.6 kPa) dramatically reduce the metabolic scope for regeneration, reflected in an 80% reduction in regeneration rate. Thus, the present work demonstrates that elevated seawater P(CO2) significantly affects the environment and the physiology of infaunal organisms like A. filiformis.
...
PMID:Energy metabolism and regeneration are impaired by seawater acidification in the infaunal brittlestar Amphiura filiformis. 2473 72