Recovery from Acidification

1992 ◽  
pp. 467-494 ◽  
Author(s):  
A. O. Stuanes ◽  
H. Van Miegroet ◽  
D. W. Cole ◽  
G. Abrahamsen
Keyword(s):  
Recovery From Acidification

scholarly journals Inconsistent browning of northeastern U.S. lakes despite increased precipitation and recovery from acidification

Ecosphere ◽  
2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Jean‐Francois Lapierre ◽  
Sarah M. Collins ◽  
Samantha K. Oliver ◽  
Emily H. Stanley ◽  
Tyler Wagner
Keyword(s):  
Recovery From Acidification

Regulation of intracellular pH in J774 murine macrophage cells: H+ extrusion processes

1995 ◽  
Vol 268 (1) ◽  
pp. C210-C217 ◽  
Author(s):  
L. C. McKinney ◽  
A. Moran
Keyword(s):  
Intracellular Ph ◽  
Initial Rate ◽  
Adherent Cells ◽  
Murine Macrophage ◽  
Bafilomycin A1 ◽  
Macrophage Cell ◽  
Recovery From Acidification ◽  
J774 Cells ◽  
Acid Load ◽  
Rate Of Recovery

Mechanisms of intracellular pH (pHi) regulation were characterized in the murine macrophage cell line J774.1, using 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein to measure pHi. Under nominally HCO3(-)-free conditions, resting pHi of nonadherent J774.1 cells was 7.53 +/- 0.02 (n = 86), and of adherent cells was 7.59 +/- 0.02 (n = 97). In the presence of HCO3-/CO2, pHi values were reduced to 7.41 +/- 0.02 (n = 12) and 7.40 +/- 0.01 (n = 28), respectively. Amiloride, an inhibitor of Na+/H+ exchange, did not affect resting pHi. Inhibitors of a vacuolar type H(+)-ATPase [bafilomycin A1, N-ethylmaleimide (NEM), 7-chloro-4-nitrobenz-2-oxa-1,3-diazide (NBD), and p-chloromercuriphenylsulfonic acid (pCMBS)] reduced pHi by at least 0.2 pH units. Inhibitors of other classes of H(+)-ATPases (oligomycin, azide, vanadate, and ouabain) were without effect. Inhibition of H+ efflux, measured by the change in extracellular pH of a weakly buffered cell suspension, followed the same pharmacological profile, indicating that the reduction of pHi was due to inhibition of H+ extrusion. Mechanisms of recovery from an imposed intracellular acid load were also investigated. In NaCl-Hanks' solution, pHi recovered exponentially to normal within 2 min. The initial rate of recovery was inhibited > 90% by amiloride or by replacement of extracellular Na+ concentration by N-methyl-glucamine. Inhibitors of the vacuolar H(+)-ATPase also inhibited recovery. NEM and NBD nonspecifically inhibited all recovery. Bafilomycin A1 and pCMBS did not inhibit the initial amiloride-sensitive portion of recovery, but they did inhibit a late component of recovery when pHi was above 7.0. We conclude that the Na+/H+ exchanger is primarily responsible for recovery from an acid load but does not regulate resting pHi. Conversely, a vacuolar H(+)-ATPase regulates the resting pHi of J774 cells but contributes little to recovery from acidification.

scholarly journals Land use influences on acidification and recovery of freshwaters in Galloway, south-west Scotland

2001 ◽  
Vol 5 (3) ◽  
pp. 451-458 ◽  
Author(s):  
R. C. Helliwell ◽  
R. C. Ferrier ◽  
L. Johnston ◽  
J. Goodwin ◽  
R. Doughty
Keyword(s):  
Surface Waters ◽  
Chemical Recovery ◽  
Dry Period ◽  
Sulphur Deposition ◽  
South West ◽  
Recovery From Acidification ◽  
Long Term Trends ◽  
Acid Status ◽  
Annual Discharge

Abstract. The long term response of surface waters to changes in sulphur deposition and afforestation is investigated for three upland river systems in the Galloway region of south-west Scotland. From 1984-1999, these rivers exhibited a statistically significant decline in non-marine sulphate concentrations in response to reduced acid deposition. This reduction in non-marine sulphate was, however, insufficient to induce a pH recovery over the period. A statistically significant increase in river pH was observed between 1956-1970 (0.05 yr-1) when subsidised agricultural lime payments were at a maximum. In 1976, this subsidy ceased and surface waters have progressively acidified. In addition, climatic change is found to influence long-term trends in pH. Mean annual pH was greatest during a dry period between 1969-1973 when total annual discharge was low. Thereafter, pH declined gradually in response to higher rainfall and increased total annual discharge. Overall, surface waters draining the afforested catchments of the Rivers Cree and Bladnoch are more acid than those draining the moorland catchment of the Luce. These results indicate that in afforested catchments, current reductions in sulphur emissions have not led to an observed improvement in the acid status of surface waters. Forestry, therefore, represents a confounding factor with regard to chemical recovery from acidification in this region. Keywords: acidification, afforestation, deposition, rivers, lochs, non-marine sulphate, pH

scholarly journals Norwegian lakes show widespread recovery from acidification; results from national surveys of lakewater chemistry 1986-1997

1998 ◽  
Vol 2 (4) ◽  
pp. 555-562 ◽  
Author(s):  
B. L. Skjelkvåle ◽  
R. F. Wright ◽  
A. Henriksen
Keyword(s):  
Base Cations ◽  
Chemical Recovery ◽  
N Leaching ◽  
National Scale ◽  
Western Norway ◽  
Acid Neutralising Capacity ◽  
Recovery From Acidification ◽  
Lakewater Chemistry ◽  
Southern Norway ◽  
Eastern Norway

Abstract. Surveys of 485 lakes in Norway conducted in 1986 and again in 1995 reveal widespread chemical recovery from acidification. Sulphate concentrations in lakes have decreased by 40% in acidified areas in southern Norway. This decrease has been compensated about 25% by decreases in concentrations of base cations and of 75% by increased Acid Neutralising Capacity (ANC). The increased ANC in turn reflects lower concentrations of acidic cations Aluminum (ALn+) and Hydrogen (H+). A sub-set of 78 of the 485 lakes sampled yearly between 1986 and 1997 shows that, at first most of the decrease in non-marine sulphate (SO4*) was compensated by a decrease in base cations, such that ANC remained unchanged. Then as SO4* continued to decrease, the concentrations of non- marine calcium and magnesium ((Ca+Mg)*) levelled out. Consequently, ANC increased, and H+ and Aln+ started to decrease. In eastern Norway, this shift occurred in 1989–90, and came slightly later in southern and western Norway. Similar shifts in trends in about 1991–92 can also be seen in the non-acidified areas in central and northern Norway. This shift in trends is not as pronounced in western Norway, perhaps because of the confounding influence of sea-salt episodes on water chemistry. This is the first documented national-scale recovery from acidification due to reduced acid deposition. Future climate warming and potentially increased N-leaching can counteract the positive trends in recovery from acidification.

scholarly journals Predicting regional recovery from acidification; the MAGIC model applied to Scotland, England and Wales

1998 ◽  
Vol 2 (4) ◽  
pp. 543-554 ◽  
Author(s):  
C. D. Evans ◽  
A. Jenkins ◽  
R. C. Helliwell ◽  
R. Ferrier
Keyword(s):  
Surface Water ◽  
Significant Proportion ◽  
Chemical Properties ◽  
Regional Patterns ◽  
Surface Water Chemistry ◽  
Surface Water Acidification ◽  
Magic Model ◽  
Recovery From Acidification ◽  
The Uk ◽  
Physical And Chemical

Abstract. A dynamic, process-based model of surface water acidification, MAGIC, has been applied to over a thousand sites across the UK. The model is calibrated to surface water samples collected during a survey for the Critical Loads programme, and utilises the best available and consistent estimates of soil physical and chemical properties, rainfall and runoff volumes, and deposition chemistry. A total of 698 sites were calibrated successfully. At these sites, surface water chemistry was reconstructed from 1850 to the present day, and forecast to 2050 based on future decreases in sulphur (S) deposition in response to the Second S Protocol. Model outputs capture distinct regional patterns of acidification and recovery. the most acidic present-day conditions are found in acid-sensitive regions of Northern England (the Pennines, Lake District and North York Moors). Although a significant proportion of sites in these areas failed to calibrate, those that did are predicted to have experienced severe historic decreases in acidic neutralising capacity (ANC) in response to high levels of acidic deposition. The model also indicates significant acidification in the moderate deposition areas of Wales and Galloway, whereas in the low deposition region of northern Scotland, acidification has been minor even in areas of acid-sensitive geology. ANC is forecast to recover at virtually all sites, with the greatest recovery predicted for areas currently subject to high deposition. The model indicates that the Second S Protocol, however, will not be sufficient to produce full recovery, with average ANC increases to 2050 counteracting just 27% of the simulated decline from 1850 to present day. Acidic conditions (ANC < 0) are predicted to persist until 2050 at a significant number of sites in Northern England, Wales and Galloway.

scholarly journals Decoupled trophic responses to long‐term recovery from acidification and associated browning in lakes

2019 ◽  
Vol 25 (5) ◽  
pp. 1779-1792 ◽  
Author(s):  
Taylor H. Leach ◽  
Luke A. Winslow ◽  
Nicole M. Hayes ◽  
Kevin C. Rose
Keyword(s):  
Recovery From Acidification ◽  
Trophic Responses

Na-H exchange regulates intracellular pH in isolated rat hepatocyte couplets

1987 ◽  
Vol 252 (1) ◽  
pp. G109-G113
Author(s):  
R. M. Henderson ◽  
J. Graf ◽  
J. L. Boyer
Keyword(s):  
Carbon Dioxide ◽  
Intracellular Ph ◽  
Ph Regulation ◽  
Intracellular Acidification ◽  
Rat Hepatocyte ◽  
Buffering Power ◽  
Recovery From Acidification ◽  
Regulation Mechanisms ◽  
Phi Regulation ◽  
Isolated Rat

Intracellular pH (pHi) was measured directly in isolated rat hepatocyte couplets using pH sensitive microelectrodes. The hepatocytes were maintained in a minimal salt buffer without added hormones or serum. Values of pHi (6.99 +/- 0.12, mean +/- SE) were close to their Nernst equilibria. After intracellular acidification with ammonium chloride, pH regulation was inhibited with 1 mM amiloride or by omission of external sodium, consistent with a Na-H exchange mechanism. Mean intracellular buffering power, in the nominal absence of carbon dioxide, was 34.1 +/- 11.4 mM. In the presence of external bicarbonate, amiloride or omission of sodium slowed, but did not completely inhibit recovery from acidification, indicating that additional pHi regulation mechanisms may operate in this preparation. These studies provide a direct measurement of pHi in hepatocyte couplets and indicate that Na-H exchange, together with a bicarbonate dependent system are important mechanisms for pHi regulation in this preparation.

scholarly journals Intracellular pH regulation in neurons from chemosensitive and nonchemosensitive areas of the medulla

1998 ◽  
Vol 275 (4) ◽  
pp. R1152-R1163 ◽  
Author(s):  
Nick A. Ritucci ◽  
Laura Chambers-Kersh ◽  
Jay B. Dean ◽  
Robert W. Putnam
Keyword(s):  
Intracellular Ph ◽  
Inferior Olive ◽  
Ph Regulation ◽  
Ventrolateral Medulla ◽  
Solitary Tract ◽  
Intracellular Ph Regulation ◽  
Buffering Power ◽  
Recovery From Acidification ◽  
Central Chemoreception ◽  
Regulatory Properties

Intracellular pH (pHi) regulation was studied in neurons from two chemosensitive [nucleus of the solitary tract (NTS) and ventrolateral medulla (VLM)] and two nonchemosensitive [hypoglossal (Hyp) and inferior olive (IO)] areas of the medulla oblongata. Intrinsic buffering power (βint) was the same in neurons from all regions (46 mM/pH U). Na+/H+exchange mediated recovery from acidification in all neurons [Ritucci, N. A., J. B. Dean, and R. W. Putnam. Am. J. Physiol. 273 ( Regulatory Integrative Comp. Physiol.42): R433–R441, 1997]. Cl−/[Formula: see text]exchange mediated recovery from alkalinization in VLM, Hyp, and IO neurons but was absent from most NTS neurons. The Na+/H+exchanger from NTS and VLM neurons was fully inhibited when extracellular pH (pHo) <7.0, whereas the exchanger from Hyp and IO neurons was fully inhibited only when pHo <6.7. The Cl−/[Formula: see text]exchanger from VLM, but not Hyp and IO neurons, was inhibited by pHo of 7.9. These pH regulatory properties resulted in steeper pHi-pHorelationships in neurons from chemosensitive regions compared with those from nonchemosensitive regions. These differences are consistent with a role for changes of pHi as the proximate signal in central chemoreception and changes of pHo in modulating pHi changes.

pH regulatory transport systems in a smooth muscle-like cell line

1990 ◽  
Vol 258 (3) ◽  
pp. C470-C479 ◽  
Author(s):  
R. W. Putnam
Keyword(s):  
Prolonged Exposure ◽  
Ph Regulation ◽  
Transport Systems ◽  
Disulfonic Acid ◽  
High K ◽  
Recovery From Acidification ◽  
Ethanesulfonic Acid ◽  
Membrane Transport Systems ◽  
External Ph ◽  
External K

The membrane transport systems responsible for pH regulation in BC3H-1 cells were studied using the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF). In nominally CO2-free Na N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid buffer (NHB) recovery from acidification after an NH4Cl pulse was reversibly inhibited by 1 mM amiloride or by Na-free solutions. On exposure to 5% CO2-HCO3 (external pH constant at 7.4), BC3H-1 cells alkalinized by approximately 0.3-0.4 pH unit. This CO2-induced alkalinization was unaffected by 1 mM amiloride, markedly reduced by 0.5 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), and inhibited by Na-free solutions. On readdition of Na, cells rapidly alkalinized, even in the presence of 1 mM amiloride. Exposure to Cl-free CO2-HCO3 solutions caused a rapid alkalinization of nearly 1 pH unit that was abolished by SITS, largely independent of Na, unaffected by amiloride, and unchanged by membrane depolarization in high external K solutions. CO2-induced alkalinization was slowed by approximately 75% after prolonged exposure of cells to Cl-free NHB, but a distinct recovery from acidification remained in these Cl-depleted cells. This recovery was Na-dependent, SITS-inhibitable, and unaffected by depolarization in high-K solutions. In the presence of CO2, the acidification seen in response to NH4Cl-induced alkalinization was reduced 50% by 0.5 mM SITS. These data suggest that the regulation of pH in BC3H-1 cells is mediated by at least three transport systems: 1) Na-H exchange; 2) Cl-HCO3 exchange; and 3) electroneutral (Na + HCO3)-Cl exchange.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracellular pH homeostasis in cultured human placental syncytiotrophoblast cells: recovery from acidification

2005 ◽  
Vol 288 (4) ◽  
pp. C891-C898 ◽  
Author(s):  
Elizabeth A. Cowley ◽  
Mary C. Sellers ◽  
Nicholas P. Illsley
Keyword(s):  
Intracellular Ph ◽  
Driving Force ◽  
Progressive Decrease ◽  
Ph Homeostasis ◽  
Ion Substitution ◽  
Recovery From Acidification ◽  
Acid Load ◽  
Acidification Recovery ◽  
Intracellular Acid

Resting or basal intracellular pH (pHi) measured in cultured human syncytiotrophoblast cells was 7.26 ± 0.04 (without HCO3−) or 7.24 ± 0.03 (with HCO3−). Ion substitution and inhibitor experiments were performed to determine whether common H+-transporting species were operating to maintain basal pHi. Removal of extracellular Na+ or Cl− or addition of amiloride or dihydro-4,4′-diisothiocyanatostilbene-2,2′-disulfonate (H2DIDS) had no effect. Acidification with the K+/H+ exchanger nigericin reduced pHi to 6.25 ± 0.15 (without HCO3−) or 6.53 ± 0.10 (with HCO3−). In the presence of extracellular Na+, recovery to basal pHi was prompt and occurred at similar rates in the absence and presence of HCO3−. Ion substitution and inhibition experiments were also used to identify the species mediating the return to basal pHi after acidification. Recovery was inhibited by removal of Na+ or addition of amiloride, whereas removal of Cl− and addition of H2DIDS were ineffective. Addition of the Na+/H+ exchanger monensin to cells that had returned to basal pHi elicited a further increase in pHi to 7.48 ± 0.07. Analysis of recovery data showed that there was a progressive decrease in ΔpH per minute as pHi approached the basal level, despite the continued presence of a driving force for H+ extrusion. These data show that in cultured syncytial cells, in the absence of perturbation, basal pHi is preserved despite the absence of active, mediated pH maintenance. They also demonstrate that an Na+/H+ antiporter acts to defend the cells against acidification and that it is the sole transporter necessary for recovery from an intracellular acid load.

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