scholarly journals Elucidating the acid-base mechanisms underlying otolith overgrowth in fish exposed to ocean acidification

2021 ◽  
Author(s):  
Garfield Tsz Kwan ◽  
Martin Tresguerres

Over a decade ago, ocean acidification (OA) exposure was reported to induce otolith overgrowth in teleost fish. This phenomenon was subsequently confirmed in multiple species; however, the underlying physiological causes remain unknown. Here, we report that splitnose rockfish (Sebastes diploproa) exposed to ~1,600 μatm pCO2 (pH ~7.5) were able to fully regulated the pH of both blood and endolymph (the fluid that surrounds the otolith within the inner ear). However, while blood was regulated around pH 7.80, the endolymph was regulated around pH ~8.30. These different pH setpoints result in increased pCO2 diffusion into the endolymph, which in turn leads to proportional increases in endolymph [HCO3-] and [CO32-]. Endolymph pH regulation despite the increased pCO2 suggests enhanced H+ removal. However, a lack of differences in inner ear bulk and cell-specific Na+/K+-ATPase and vacuolar type H+-ATPase protein abundance localization pointed out to activation of preexisting ATPases, non-bicarbonate pH buffering, or both, as the mechanism for endolymph pH-regulation. These results provide the first direct evidence showcasing the acid-base chemistry of the endolymph of OA-exposed fish favors otolith overgrowth, and suggests that this phenomenon will be more pronounced in species that count with more robust blood and endolymph pH regulatory mechanisms.

2007 ◽  
Vol 293 (6) ◽  
pp. R2412-R2420 ◽  
Author(s):  
Li-Ming Chen ◽  
Inyeong Choi ◽  
Gabriel G. Haddad ◽  
Walter F. Boron

In the mammalian CNS, hypoxia causes a wide range of physiological effects, and these effects often depend on the stage of development. Among the effects are alterations in pH homeostasis. Na+-coupled HCO3− transporters can play critical roles in intracellular pH regulation and several, such as NCBE and NBCn1, are expressed abundantly in the central nervous system. In the present study, we examined the effect of chronic continuous hypoxia on the expression of two electroneutral Na-coupled HCO3− transporters, SLC4a7 (NBCn1) and SLC4a10 (NCBE), in mouse brain, the first such study on any acid-base transporter. We placed the mice in normobaric chambers and either maintained normoxia (21% inspired O2) or imposed continuous chronic hypoxia (11% O2) for a duration of either 14 days or 28 days, starting from ages of either postnatal age 2 days (P2) or P90. We assessed protein abundance by Western blot analysis, loading equal amounts of total protein for each condition. In most cases, hypoxia reduced NBCn1 levels by 20–50%, and NCBE levels by 15–40% in cerebral cortex, subcortex, cerebellum, and hippocampus, both after 14 and 28 days, and in both pups and adults. We hypothesize that these decreases, which are out of proportion to the expected overall decreases in brain protein levels, may especially be important for reducing energy consumption.


2017 ◽  
Vol 312 (5) ◽  
pp. R702-R717 ◽  
Author(s):  
Cian McGinley ◽  
David J. Bishop

The removal of protons (H+) produced during intense exercise is important for skeletal muscle function, yet it remains unclear how best to structure exercise training to improve muscle pH regulation. We investigated whether 4 wk of work-matched sprint-interval trining (SIT), performed 3 days/wk, with either 1 ( Rest-1; n = 7) or 5 ( Rest-5; n = 7) min of rest between sprints, influenced adaptations in acid/base transport protein content, nonbicarbonate muscle buffer capacity (βmin vitro), and exercise capacity in active women. Following 1 wk of posttesting, comprising a biopsy, a repeated-sprint ability (RSA) test, and a graded-exercise test, maintenance of adaptations was then studied by reducing SIT volume to 1 day/wk for a further 5 wk. After 4 wk of SIT, there was increased protein abundance of monocarboxylate transporter (MCT)-1, sodium/hydrogen exchanger (NHE)-1, and carbonic anhydrase (CA) XIV for both groups, but rest interval duration did not influence the adaptive response. In contrast, greater improvements in total work performed during the RSA test after 4 wk of SIT were evident for Rest-5 compared with Rest-1 (effect size: 0.51; 90% confidence limits ±0.37), whereas both groups had similarly modest improvements in V̇o2peak. When training volume was reduced to 1 day/wk, enhanced acid/base transport protein abundance was maintained, although NHE1 content increased further for Rest-5 only. Finally, our data support intracellular lactate as a signaling molecule for inducing MCT1 expression, but neither lactate nor H+ accumulation appears to be important signaling factors in MCT4 regulation.


2017 ◽  
Vol 284 (1864) ◽  
pp. 20171066 ◽  
Author(s):  
Marian Hu ◽  
Yung-Che Tseng ◽  
Yi-Hsien Su ◽  
Etienne Lein ◽  
Hae-Gyeong Lee ◽  
...  

The unusual rate and extent of environmental changes due to human activities may exceed the capacity of marine organisms to deal with this phenomenon. The identification of physiological systems that set the tolerance limits and their potential for phenotypic buffering in the most vulnerable ontogenetic stages become increasingly important to make large-scale projections. Here, we demonstrate that the differential sensitivity of non-calcifying Ambulacraria (echinoderms and hemichordates) larvae towards simulated ocean acidification is dictated by the physiology of their digestive systems. Gastric pH regulation upon experimental ocean acidification was compared in six species of the superphylum Ambulacraria. We observed a strong correlation between sensitivity to ocean acidification and the ability to regulate gut pH. Surprisingly, species with tightly regulated gastric pH were more sensitive to ocean acidification. This study provides evidence that strict maintenance of highly alkaline conditions in the larval gut of Ambulacraria early life stages may dictate their sensitivity to decreases in seawater pH. These findings highlight the importance of identifying and understanding pH regulatory systems in marine larval stages that may contribute to substantial energetic challenges under near-future ocean acidification scenarios.


1999 ◽  
Vol 277 (6) ◽  
pp. F841-F849 ◽  
Author(s):  
Saskia Huber ◽  
Esther Asan ◽  
Thomas Jöns ◽  
Christiane Kerscher ◽  
Bernd Püschel ◽  
...  

By enzyme-linked in situ hybridization (ISH), direct evidence is provided that acid-secreting intercalated cells (type A IC) of both the cortical and medullary collecting ducts of the rat kidney selectively express the mRNA of the kidney splice variant of anion exchanger 1 (kAE1) and no detectable levels of the erythrocyte AE1 (eAE1) mRNA. Using single-cell quantification by microphotometry of ISH enzyme reaction, medullary type A IC were found to contain twofold higher kAE1 mRNA levels compared with cortical type A IC. These differences correspond to the higher intensity of immunostaining in medullary versus cortical type A IC. Chronic changes of acid-base status induced by addition of NH4Cl (acidosis) or NaHCO3 (alkalosis) to the drinking water resulted in up to 35% changes of kAE1 mRNA levels in both cortical and medullary type A IC. These experiments provide direct evidence at the cellular level of kAE1 expression in type A IC and show moderate capacity of type A IC to respond to changes of acid-base status by modulation of kAE1 mRNA levels.


Physiology ◽  
2017 ◽  
Vol 32 (5) ◽  
pp. 367-379 ◽  
Author(s):  
Julian L. Seifter ◽  
Hsin-Yun Chang

Clinical assessment of acid-base disorders depends on measurements made in the blood, part of the extracellular compartment. Yet much of the metabolic importance of these disorders concerns intracellular events. Intracellular and interstitial compartment acid-base balance is complex and heterogeneous. This review considers the determinants of the extracellular fluid pH related to the ion transport processes at the interface of cells and the interstitial fluid, and between epithelial cells lining the transcellular contents of the gastrointestinal and urinary tracts that open to the external environment. The generation of acid-base disorders and the associated disruption of electrolyte balance are considered in the context of these membrane transporters. This review suggests a process of internal and external balance for pH regulation, similar to that of potassium. The role of secretory gastrointestinal epithelia and renal epithelia with respect to normal pH homeostasis and clinical disorders are considered. Electroneutrality of electrolytes in the ECF is discussed in the context of reciprocal changes in Cl−or non Cl−anions and [Formula: see text].


2020 ◽  
Author(s):  
Rossana Occhipinti ◽  
Soroush Safaei ◽  
Peter J. Hunter ◽  
Walter F. Boron

The classic Boron & De Weer (1976) paper provided the first evidence of active regulation of pH} in cells by an energy-dependent acid-base transporter. These authors also developed a quantitative model --- comprising passive fluxes of acid-base equivalents across the cell membrane, intracellular reactions, and an active transport mechanism in the cell membrane (modelled as a proton pump) --- to help interpret their measurements of intracellular pH under perturbations of both extracellular CO2/HCO3- and extracellular NH3/NH4+. This Physiome paper seeks to make that model, and the experimental conditions under which it was developed, available in a reproducible and well-documented form, along with a software implementation that makes the model easy to use and understand. We have also taken the opportunity to update some of the units used in the original paper, and to provide a few parameter values that were missing in the original paper. Finally, we provide an historical background to the Boron & De Weer (1976) proposal for active pH regulation and a commentary on subsequent work that has enriched our understanding of this most basic aspect of cellular physiology.


1991 ◽  
Vol 156 (1) ◽  
pp. 153-171 ◽  
Author(s):  
YONG TANG ◽  
ROBERT G. BOUTILIER

The intracellular acid-base status of white muscle of freshwater (FW) and seawater (SW) -adapted rainbow trout was examined before and after exhaustive exercise. Exhaustive exercise resulted in a pronounced intracellular acidosis with a greater pH drop in SW (0.82 pH units) than in FW (0.66 pH units) trout; this was accompanied by a marked rise in intracellular lactate levels, with more pronounced increases occurring in SW (54.4 mmoll−1) than in FW (45.7 mmoll−1) trout. Despite the more severe acidosis, recovery was faster in the SW animals, as indicated by a more rapid clearance of metabolic H+ and lactate loads. Compartmental analysis of the distribution of metabolic H+ and lactate loads showed that the more rapid recovery of pH in SW trout could be due to (1) their greater facility for excreting H+ equivalents to the environmental water [e.g. 15.5 % (SW) vs 5.0 % (FW) of the initial H+ load was stored in external water at 250 min post-exercise] and, to a greater extent, (2) the more rapid removal of H+, facilitated via lactate metabolism in situ (white muscle) and/or the Cori cycle (e.g. heart, liver). The slower pH recovery in FW trout may also be due in part to greater production of an ‘unmeasured acid’ [maximum approx. 8.5 mmol kg−1 fish (FW) vs approx. 6 mmol kg−1 fish (SW) at 70–130 min post-exercise] during the recovery period. Furthermore, the analysis revealed that H+-consuming metabolism is quantitatively the most important mechanism for the correction of an endogenously originating acidosis, and that extracellular pH normalization gains priority over intracellular pH regulation during recovery of acid-base status following exhaustive exercise.


2020 ◽  
Vol 21 (12) ◽  
pp. 4340 ◽  
Author(s):  
Juan Mao ◽  
Jianming Li

Brassinosteroids (BRs) are important plant growth hormones that regulate a wide range of plant growth and developmental processes. The BR signals are perceived by two cell surface-localized receptor kinases, Brassinosteroid-Insensitive1 (BRI1) and BRI1-Associated receptor Kinase (BAK1), and reach the nucleus through two master transcription factors, bri1-EMS suppressor1 (BES1) and Brassinazole-resistant1 (BZR1). The intracellular transmission of the BR signals from BRI1/BAK1 to BES1/BZR1 is inhibited by a constitutively active kinase Brassinosteroid-Insensitive2 (BIN2) that phosphorylates and negatively regulates BES1/BZR1. Since their initial discoveries, further studies have revealed a plethora of biochemical and cellular mechanisms that regulate their protein abundance, subcellular localizations, and signaling activities. In this review, we provide a critical analysis of the current literature concerning activation, inactivation, and other regulatory mechanisms of three key kinases of the BR signaling cascade, BRI1, BAK1, and BIN2, and discuss some unresolved controversies and outstanding questions that require further investigation.


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