Soluble and bound forms of intracellular acid carboxypeptidase inAspergillus saitoi

1980 ◽  
Vol 4 (2) ◽  
pp. 85-89 ◽  
Author(s):  
Eiji Ichishima ◽  
Yoshinori Tsuruda ◽  
Taro Ushijima ◽  
Takehiko Nomi ◽  
Shoji Suzuki ◽  
...  
Keyword(s):  
Acid Carboxypeptidase ◽  
Intracellular Acid

Intracellular acid carboxypeptidase ofPenicillium roqueforti isolated from blue cheese

1978 ◽  
Vol 1 (2) ◽  
pp. 95-98 ◽  
Author(s):  
Eiji Ichishima ◽  
Michio Takeuchi ◽  
Kazuo Yamamoto ◽  
Yoshiyuki Sano ◽  
toshihiko Kikuchi
Keyword(s):  
Blue Cheese ◽  
Acid Carboxypeptidase ◽  
Intracellular Acid

White Muscle Intracellular Acid-Base and Lactate Status Following Exhaustive Exercise: A Comparison between Freshwater- and Sea Water- Adapted Rainbow Trout

1991 ◽  
Vol 156 (1) ◽  
pp. 153-171 ◽  
Author(s):  
YONG TANG ◽  
ROBERT G. BOUTILIER
Keyword(s):  
Rainbow Trout ◽  
White Muscle ◽  
Sea Water ◽  
Ph Regulation ◽  
Recovery Period ◽  
Exhaustive Exercise ◽  
Acid Base ◽  
Post Exercise ◽  
Acid Base Status ◽  
Intracellular Acid

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.

Purification and Properties of Acid Carboxypeptidase I fromAspergillus oryzae

1972 ◽  
Vol 36 (8) ◽  
pp. 1343-1352 ◽  
Author(s):  
Tadanobu Nakadai ◽  
Seiichi Nasuno ◽  
Nobuyoshi Iguchi
Keyword(s):  
Acid Carboxypeptidase ◽  
Purification And Properties

Isolation and partial characterization of an acid carboxypeptidase from yeast

Biochemistry ◽  
1974 ◽  
Vol 13 (19) ◽  
pp. 3871-3877 ◽  
Author(s):  
Robert W. Kuhn ◽  
Kenneth A. Walsh ◽  
Hans Neurath
Keyword(s):  
Partial Characterization ◽  
Acid Carboxypeptidase

Contribution of a net transmembrane HCO3- flux to intracellular acid-base regulation

1977 ◽  
Vol 43 (6) ◽  
pp. 931-935 ◽  
Author(s):  
D. R. Strome ◽  
R. L. Clancy ◽  
N. C. Gonzalez
Keyword(s):  
Carbon Dioxide ◽  
Small Volume ◽  
Elevated Carbon Dioxide ◽  
Ringer Solution ◽  
Carbon Dioxide Tension ◽  
Acid Base ◽  
Initial Cell ◽  
Intracellular Acid

Experiments were performed to determine the relative effects of a net extracellular-to-intracellular HCO3- flux and of elevated carbon dioxide tension (PCO2) on cellular acid-base regulation. Isolated rabbit hearts were perfused by recirculating a small volume of Ringer solution in which the PCO2 and the HCO3- concentration could be independently altered. Net HCO3- flux was assessed by the disappearance of HCO3- from perfusate. Between 40 and 100 Torr PCO2, a HCO3- flux into the cell occurs only when perfusate HCO3- concentration is increased. Therefore, by selective manipulation of perfusate HCO3- and PCO2 it is possible to induce hypercapnia with or without an accompanying HCO3- flux. When perfusate HCO3- concentration was increased from 20 to 36 mM, cellular HCO3- concentration increased from 22.5 +/- 0.8 to 26.1 +/- 1.0 mM at 40 Torr PCO2 and from 27.8 +/- 0.7 to 34.1 +/- 1.4 mM at 98 Torr PCO2. These increases can be accounted for by the amount of HCO3- that disappeared from the perfusate. The results suggest that most of the initial cell CO2 buffering is provided by the net HCO3- flux in addition to the passive physicochemical buffering.

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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