D-Lactate formation, D-LDH activity and glycolytic potential ofHelix pomatia L.

1978 ◽  
Vol 126 (3) ◽  
pp. 249-255 ◽  
Author(s):  
Wolfgang Wieser ◽  
Elizabeth Wright
2019 ◽  
Vol 76 (9) ◽  
pp. 1616-1623
Author(s):  
Nicholas B. Edmunds ◽  
Timothy J. Bartley ◽  
Amanda Caskenette ◽  
Frédéric Laberge ◽  
Kevin S. McCann

Piscivorous predators at the apex of aquatic food webs are thought to exhibit foraging behaviours that depend on environmental conditions. Walleye (Sander vitreus), for example, is a freshwater predator that is most active under low light conditions. This study examined walleye resource use and swimming activity across lakes located in northwestern Ontario representing a gradient of water transparency. Muscle glycolytic potential, an index of swimming activity, was estimated by the activity of the enzyme lactate dehydrogenase (LDH). We show that walleye white muscle LDH activity increased with lake water transparency, but that this relationship is not determined by the use of nearshore resources, estimated from δ13C stable isotope signatures, or by prey abundance. On the other hand, walleye muscle LDH activity decreased with increasing prey size, and prey size was larger in lakes of low water transparency. These results support a positive relationship between water transparency and swimming activity in walleye, with prey size as an important factor contributing to this effect.


Author(s):  
Kali M Horn ◽  
Michelle E Fournet ◽  
Kaitlin A Liautaud ◽  
Lynsey N Morton ◽  
Allie M Cyr ◽  
...  

Abstract The intertidal zone is characterized by persistent, tidally-driven fluctuations in both abiotic (e.g., temperature, [O2], salinity) and biotic (e.g., food availability, predation) factors, which make this a physiologically challenging habitat for resident organisms. The relative magnitude and degree of variability of environmental stress differs between intertidal zones, with the most extreme physiological stress often being experienced by organisms in the high intertidal. Given that so many of the constantly shifting parameters in this habitat are primary drivers of metabolic rate (e.g., temperature, [O2], food availability), we hypothesized that sessile conspecifics residing in different tidal zones would exhibit distinct ‘metabolic phenotypes,’ a term we use to collectively describe the organisms’ baseline metabolic performance and capacity. To investigate this hypothesis, we collected acorn barnacles (Balanus glandula) from low, mid, and high intertidal positions in San Luis Obispo Bay, CA and measured a suite of biochemical (whole-animal citrate synthase (CS) and lactate dehydrogenase (LDH) activity, aerial [D-lactate]), physiological (O2 consumption rates), morphological (body size) and behavioral (e.g., cirri beat frequency, % time operculum open) indices of metabolism. We found tidal zone-dependent differences in B. glandula metabolism that primarily related to anaerobic capacity, cirral activity patterns and body size. Barnacles from the low intertidal tended to have a greater capacity for anaerobic metabolism (i.e., increased LDH activity, increased baseline [D-lactate]), have reduced cirral beating activity—and presumably reduced feeding—when submerged, and be smaller in size compared to conspecifics in the high intertidal. We did not, however, see any D-lactate accumulation in barnacles from any tidal height throughout the 96 h of air exposure. This trend indicates that the enhanced capacity of low intertidal barnacles for anaerobic metabolism may have evolved to support metabolism during more prolonged episodes of emersion or during events other than emersion (e.g., coastal hypoxia, predation). There were also no significant differences in CS activity or baseline oxygen consumption rates (in air or seawater at 14˚C) across tidal heights, which implies that aerobic metabolic capacity may not be as sensitive to tidal position as anaerobic processes. Understanding how individuals occupying different shore heights differ in their metabolic capacity becomes increasingly interesting in the context of global climate change, given that the intertidal zone is predicted to experience even greater extremes in abiotic stress.


2005 ◽  
Vol 9 (5) ◽  
pp. 599-607 ◽  
Author(s):  
Navinchandra Asthana ◽  
Aspi Kolah ◽  
Dung T. Vu ◽  
Carl T. Lira ◽  
Dennis J. Miller

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Ulka Sachdev ◽  
Xiangdong Cui ◽  
Qian Sun ◽  
Edith Tzeng ◽  
Alex Chen ◽  
...  

Introduction: Millions of Americans are at risk for amputation from severe peripheral arterial disease (PAD) when surgery is not possible. Pro-regenerative and angiogenic agents may improve outcome in that setting. Chloroquine (CQ) promotes wound healing in scleroderma but has not been tested in PAD. CQ promotes healing of ischemic muscle, increases muscle high mobility group box 1 (HMGB1), an inflammatory, pro-angiogenic protein, and activates caspase-1 in myoblasts. We hypothesize that HMGB1 mediates protective effects of CQ and is regulated by caspase-1 in muscle. Controlled rather than indiscriminate release of HMGB1 from damaged muscle may be protective during ischemia. Methods: C2C12 myoblasts in low serum were treated with CQ (0-50μM) ± Ac-YVAD-cmk (10 μg/ml), a caspase-1 inhibitor. HMGB1 release in supernatants was measured using ELISA. Cytotoxicity was assessed by comparing spontaneous lactate dehydrogenase (LDH) activity in culture media from control, treated and maximally lysed cells. CQ (50μg/ml) or placebo treated wild-type and inducible HMGB1 knockout (iHMGB1KO) mice underwent unilateral femoral artery ligation (FAL). Laser Doppler perfusion imaging (LDPI) before and 1,7,14 and 21d after FAL was reported as % improvement over time. ANOVA was used to assess statistical significance among groups. Results: CQ (5-10uM) attenuated spontaneous LDH leak after 12h from serum-depleted myoblasts (p <0.01, N=3), and modestly increased HMGB1 release (p <0.001, N=3). Ac-YVAD-cmk reversed the cytoprotective effects of CQ, significantly raising both LDH activity to 55% of maximal activity and HMGB1 in the supernatant. Compared to d1 post FAL, CQ improved perfusion recovery in WT mice by 300-800% over 21 days (p<0.03, N=7/group), but not in iHMGB1KO mice. Conclusion: We present the novel finding that in nutrient-depleted myoblasts, caspase-1 mediates the survival benefits of CQ and regulates HMGB1 release. In turn, HMGB1 is critical for CQ’s beneficial effects on perfusion after FAL, another stress condition. Regulated HMGB1 release may be immunomodulatory, regenerative and modifiable with drugs like CQ. Altering survival and inflammatory pathways through CQ may present a novel therapeutic strategy in PAD.


PEDIATRICS ◽  
1974 ◽  
Vol 54 (1) ◽  
pp. 27-33
Author(s):  
David W. Powers ◽  
Elia M. Ayoub

Lactate dehydrogenase (LDH) was assayed in peripheral leukocytes of 32 children with bacterial meningitis, nine children with nonbacterial meningitis, and 24 age-matched, healthy controls. Leukocyte LDH activity in patients with bacterial meningitis was significantly higher than in patients with nonbacterial meningitis (p &lt; 0.01) and normal controls (p &lt; 0.001). Eighty-eight percent of the patients with bacterial meningitis had leukocyte LDH values exceeding, 150 units/106 WBC, the upper limit of normal value for controls. Nitroblue tetrazolium (NBT) dye tests performed on 23 patients with bacterial meningitis were elevated in ten patients (43%). The elevation of leukocyte LDH activity in patients with bacterial meningitis appears to be independent of the number of circulating granulocytes or the presence of bacteremia. A major factor which appeared to influence the leukocyte LDH activity was the duration of adequate antibiotic therapy. Sequential determinations showed a return of the LDH values to normal approximately ten days after the initiation of therapy. A rise in leukocyte LDH was encountered in two patients with subdural effusion. The finding of significantly elevated leukocyte LDH values in three newborn infants with neonatal meningitis and sepsis suggests that this test may be of value in the diagnosis of neonatal sepsis.


1998 ◽  
Vol 85 (2) ◽  
pp. 627-634 ◽  
Author(s):  
Russell S. Richardson ◽  
Elizabeth A. Noyszewski ◽  
John S. Leigh ◽  
Peter D. Wagner

It remains controversial whether lactate formation during progressive dynamic exercise from submaximal to maximal effort is due to muscle hypoxia. To study this question, we used direct measures of arterial and femoral venous lactate concentration, a thermodilution blood flow technique, phosphorus magnetic resonance spectroscopy (MRS), and myoglobin (Mb) saturation measured by 1H nuclear MRS in six trained subjects performing single-leg quadriceps exercise. We calculated net lactate efflux from the muscle and intracellular[Formula: see text] with subjects breathing room air and 12% O2. Data were obtained at 50, 75, 90, and 100% of quadriceps maximal O2 consumption at each fraction of inspired O2. Mb saturation was significantly lower in hypoxia than in normoxia [40 ± 3 vs. 49 ± 3% (SE)] throughout incremental exercise to maximal work rate. With the assumption of a[Formula: see text] at which 50% of Mb-binding sites are bound with O2 of 3.2 Torr, Mb-associated [Formula: see text] averaged 3.1 ± 0.3 and 2.3 ± 0.2 Torr in normoxia and hypoxia, respectively. Net blood lactate efflux was unrelated to intracellular[Formula: see text] across the range of incremental exercise to maximum ( r = 0.03 and 0.07 in normoxia and hypoxia, respectively) but linearly related to O2 consumption ( r = 0.97 and 0.99 in normoxia and hypoxia, respectively) with a greater slope in 12% O2. Net lactate efflux was also linearly related to intracellular pH ( r = 0.94 and 0.98 in normoxia and hypoxia, respectively). These data suggest that with increasing work rate, at a given fraction of inspired O2, lactate efflux is unrelated to muscle cytoplasmic [Formula: see text], yet the efflux is higher in hypoxia. Catecholamine values from comparable studies are included and indicate that lactate efflux in hypoxia may be due to systemic rather than intracellular hypoxia.


1990 ◽  
Vol 259 (3) ◽  
pp. C455-C461 ◽  
Author(s):  
M. J. Tang ◽  
R. L. Tannen

Primary cultures of rabbit proximal tubules, which revert to a glycolytic profile as reflected by increased activity of pyruvate kinase (PK) paralleled by increased glucose consumption and lactate formation, were utilized to explore the relationship between glycolytic metabolism and proliferation. Tubules placed in serum-free, hormonally defined Dulbecco's modified Eagle's medium with 5 mM glucose exhibited logarithmic growth beginning on day 3 in culture. The increase in PK activity lagged approximately 1 day behind, suggesting that the reversion to glycolysis is a consequence of rather than a prerequisite for cellular proliferation. Tubules cultured in 0.5 mM as contrasted with 25 mM glucose exhibited heightened proliferation reflected by an increase in protein content and cell number on day 5 in culture. The heightened proliferation was accompanied by increased PK activity. On day 9, after confluency had been achieved, no differences in protein content or PK activity were detected between tubules cultured in different glucose concentrations. These findings indicate that a low glucose concentration is mitogenic for renal proximal tubules and that the proliferative process in some fashion up-regulates the activity of the glycolytic enzyme PK. Furthermore, because accelerated growth proceeds in the presence of glucose restriction, the energy from glycolysis is not required for the proliferative process.


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