Cation and total macroelement concentrations influence Ca uptake in micropropagated potato plantlets

1998 ◽  
Vol 161 (6) ◽  
pp. 613-617 ◽  
Author(s):  
Jihad E. Abdulnour ◽  
Danielle J. Donnelly ◽  
Nayana N. Barthakur
Keyword(s):  
1973 ◽  
Vol 9 (3) ◽  
pp. 249-255
Author(s):  
H. R. Chheda ◽  
M. A. Mohamed Saleem

SUMMARYCynodon IB.8 was subjected to (i) various levels of N under cutting management, and (ii) various levels of K under grazing management. The results indicated significantly higher DM and CP production with 168 kg./ha. of N under cutting management, with resultant significant reduction in exchangeable and non-exchangeable soil K. Under grazing management, increased K application increased K content in the herbage, but showed a negative correlation with Ca uptake. Results indicated that the initial soil K status was adequate to supply the requirements of Cynodon, and that under grazing management the soil K status could be maintained at adequate levels to support lengthy cropping.


1988 ◽  
Vol 59 (1) ◽  
pp. 57-62 ◽  
Author(s):  
W. Keith Harvey ◽  
Tetsuo Nakamoto

1. The purpose of the present study was to determine the effects of diet on the mandibles and growth centres of the long bones in the fetuses of diabetic rat dams given a normal diet compared with those given a high-protein, low-carbohydrate diet.2. On the 9th day of gestation, the controls, groups 1 and 3, were injected with citrate buffer and given 200 and 600 g protein/kg diets respectively. Groups 2 and 4 were injected with 40 mg streptozotocin/kg body-weight and pair-fed with groups I and 3 respectively on the 200 and 600 g protein/kg diets.3. On day 22, some dams were injected with either 45Ca or [14C]proline. Mandibles and long bones were removed and weighed and analysed for Ca content, 45Ca uptake, collagen and collagen synthesis.4. The body-weights, and mandibular and long-bone weights of the fetuses in the diabetic 200 g protein/kg group were smaller than those of the non-diabetic 200 g protein/kg group, whereas those of the diabetic 600 g protein/kg group showed no difference from the non-diabetic 600 g protein/kg group.5. The rate of collagen synthesis was higher in the fetuses of the diabetic 600 g protein/kg group than those of the non-diabetic group. Bones of the diabetic 200 g protein/kg group were lower in collagen content when compared with the non-diabetic group, whereas there was no difference between the diabetic and non-diabetic 600 g protein/kg groups.6. Ca uptake and total Ca contents in the mandibles and long bones showed no difference between diabetic and non-diabetic groups fed on both diets.7. A high-protein, low-carbohydrate diet appeared to have a certain beneficial effect on bone development of the growing fetuses from diabetic dams.


1999 ◽  
Vol 18 (5) ◽  
pp. 327-332 ◽  
Author(s):  
J V Calderón-Salinas ◽  
M A Quintanar-Escorcia ◽  
M T González-Martínez ◽  
C E Hernández-Luna

In this paper we report the lead (Pb) and calcium (Ca) uptake by erythrocyte ghosts. In both cases the transport was carried out by a passive transport system with two kinetic components (Michaelis-Menten and Hill). Pb and Ca were capable of inhibiting the transport of the other metal in a non-competitive way. Under hyperpolarization, the uptakes of Ca and Pb were enhanced and the Michaelis-Menten component prevailed. Both Ca and Pb uptakes were inhibited by N-ethyl-maleimide to the same extent. These results indicate that Pb and Ca share the same permeability pathway in human erythrocytes and that this transport system is electrogenic.


1987 ◽  
Vol 252 (6) ◽  
pp. C595-C603 ◽  
Author(s):  
S. Sanchez-Armass ◽  
M. P. Blaustein

Ca efflux from rat brain presynaptic nerve terminals (synaptosomes) was examined after loading the terminals with 45Ca during a brief depolarization, usually in media containing 20 microM Ca labeled with 45Ca, to assure a small (physiological) load. Efflux of 45Ca was very slow in the absence of external Na and Ca (approximately 0.5% of the load/s) and was greatly accelerated by Na and/or Ca (presumably Na+-Ca2+ and Ca2+-Ca2+ exchange, respectively). The dependence of 45Ca efflux on external Na was sigmoid, with a Hill coefficient of approximately 2.5; this implies that more than two external Na ions are required to activate the efflux of one Ca ion. The external Na (Nao)-dependent Ca efflux was inhibited by 1 mM external La, by low temperature (Q10 congruent to 2.3), and by raising external K (to depolarize the synaptosomes). With small Ca loads, the mitochondrial uncoupler, carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP), had negligible effect on either Ca uptake or efflux; with large loads (greater than or equal to 5 nmol/mg protein), however, FCCP reduced the depolarization-stimulated Ca uptake and increased the Nao-dependent Ca efflux. These effects may be attributed to reduction of mitochondrial Ca sequestration. Mitochondria do not appear to sequester much Ca when the loads are smaller (and more physiological). Estimations of Ca efflux indicate that approximately 20% of a small 45Ca load (approximately 0.75 nmol Ca/mg protein) may be extruded via Na+-Ca2+ exchange within 1 s; this corresponds to a net Ca efflux of approximately 110 pmol Ca X mg protein-1 X s-1.(ABSTRACT TRUNCATED AT 250 WORDS)


1995 ◽  
Vol 268 (5) ◽  
pp. C1313-C1319 ◽  
Author(s):  
J. W. Bassani ◽  
W. Yuan ◽  
D. M. Bers

The release of sarcoplasmic reticulum (SR) Ca in cardiac muscle during excitation-contraction coupling is known to be graded by the amount of activating Ca outside the SR (i.e., Ca-induced Ca release). However, little is known about how intra-SR Ca affects the release process. In this study we assessed how the fractional SR Ca release as described by Bassani et al. [Am. J. Physiol. 265 (Cell Physiol. 34): C533-C540, 1993] is affected by alteration of trigger Ca and of SR Ca content. Experiments were done with isolated ferret ventricular myocytes using indo 1 to measure Ca concentration, perforated patch to measure Ca current (ICa), caffeine application to release SR Ca, and thapsigargin to completely block SR Ca uptake. For what we consider a Normal SR Ca load and trigger Ca [action potential at 0.5 Hz with 2 mM extracellular Ca concentration ([Ca]o)], 35 +/- 3% of the SR Ca content was released at a twitch. Changing trigger Ca by altering [Ca]o (to 0.5 and 8 mM) at a test twitch changed this fractional SR Ca release to 10 +/- 2 and 59 +/- 6%, with the same SR Ca load (and peak ICa changed in a parallel manner in separate voltage-clamp experiments). Three different levels of SR Ca load were studied (Low, Normal, and High; by action potential stimulation at different frequencies from 0.05 to 0.8 Hz) using the same standard test trigger Ca (2 mM). Surprisingly, the High-load condition only increased SR Ca content by approximately 4% but appeared to be very close to the limiting SR Ca capacity.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
H Hagiwara ◽  
M Watanabe ◽  
Y Fujioka ◽  
T Koya ◽  
M Nakao ◽  
...  

Abstract Background In heart failure (HF), diastolic calcium (Ca) leak from sarcoplasmic reticulum (SR) via ryanodine receptor (RyR) causes delayed after depolarization (DAD), leading ventricular arrhythmias (VAs). Recent study reported that Ca uptake into mitochondria via mitochondrial calcium uniporter (MCU) suppress Ca waves (CaWs) and DAD in catecholaminergic polymorphic ventricular tachycardia, in which diastolic Ca leak is thought to be a major cause of VAs as in HF. However, such anti-arrhythmic effect of mitochondrial Ca uptake via MCU remains unclear in HF. Purpose We sought to investigate whether mitochondrial Ca uptake via MCU decreases CAWs and VAs incidence in ischemic HF mice. Methods Ten-week-old male C57BL/6J mice were divided into 2 groups; sham operation mice (Sham) or HF mice (HF) in which myocardial infarction was induced by left coronary artery ligation. After 4–6 weeks, cardiomyocyte or mitochondria was isolated respectively from the myocardium of Sham and the non-infarct myocardium of HF. Influence of MCU activation on Ca dynamics, VA inducibility and left ventricular hemodynamics were evaluated using Kaemenpferol, a MCU activator. Intracellular Ca dynamics and mitochondrial Ca uptake were measured in isolated cardiomyocytes loaded with Fluo-4 AM on an epifluorescence microscopy and by estimating the extra-mitochondrial Ca reduction with Fluo-5N on a spectrofluoro-photometer, respectively. VAs was induced by programmed stimulation in the Langendorff perfused hearts. Left ventricular (LV) pressure was measured using a microtip transducer catheter. Finally, the effect of intravenous administration of Kaempferol (5mg/kg) on hemodynamic parameters was examined 30 minutes after administration in Sham and HF. Results HF mice showed left ventricular dysfunction, as well as the increased heart and lung weights compared to Sham. MCU protein expression in cardiomyocytes did not differ between Sham and HF. Kaempferol increased mitochondrial Ca uptake in the isolated mitochondria both in Sham and HF. The number of the diastolic CaWs was higher in HF compared to Sham. Such increased number of CaWs in HF was attenuated by 10 μM Kaempferol, which was, however, abolished by a MCU blocker Ruthenium Red. The incidence of induced VA was significantly higher in HF than Sham, which was suppressed by Kaempferol. In vivo measurements, intravenous administration of Kaempferol did not show significant changes in hemodynamic parameters in Sham and HF mice. Conclusions Mitochondrial Ca uptake via MCU suppresses CaWs and VAs, but did not change LV hemodynamics in HF. Whereas traditional antiarrhythmic drugs have limited use in heart failure patients, a novel strategy that promotes Ca uptake into mitochondria might be a new and safer option for treating VAs in HF. Funding Acknowledgement Type of funding source: None


1985 ◽  
Vol 40 (1-2) ◽  
pp. 102-108 ◽  
Author(s):  
Ana R. de Boland ◽  
Ricardo Boland

Cultures of vitamin D-deficient chick soleus muscle and 12 day-old chick embryo myoblasts were used to characterize the effects of 1,25-dihydroxy-vitamin D3 and 25-hydroxy-vitamin D3 on muscle cell Ca metabolism. Physiological amounts of both sterols increased the rate and extent of 45Ca uptake by cultures. However. 1.25(OH)2D3 was significantly more effective than 25 OHD3. The greater potency of 1,25(OH)2D3 to increase Ca uptake could be shown after various treatment intervals of cultures and using a wide concentration range of both derivatives. Information about Ca pools affected by vitamin D3 metabolites was obtained through kinetic analysis of Ca efflux in cultured myoblasts. Cytoplasmic and mitochondria Ca pools were identified on the basis of their half-times of desaturation and by selective inhibition of plasma membrane and mitochondrial Ca transport with LaCl3 and Ruthenium Red, respectively. The data suggests that 1,25(OH)2D3 acts on muscle cellular Ca by increasing Ca efflux and influx through mitochondrial and plasma membranes whereas the predominant effect of 25 OHD3 is to increase Ca influx into mitochondria.


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