Tissue Content Of Na Research Articles

Co adaptation of LiCl tolerant Solanum tuberosum L. callus cultures to NaCl stress

In this research, co-adaptation of the Calli of Solanum tuberosum , raised from petioles, to the presence of lithium (LiCl) and sodium chloride (NaCl) was studied. The cultures were adapted with LiCl in the absence of an osmotic stress and the response of adapted and unadapted calli to salinity was investigated. Undifferentiated callus growth was induced in S. tuberosum by the addition of 2 mg/l 2,4 dichlorophenoxy acetic acid (2,4-D), 0.25 mg/l kinetin to Murashige and Skoog medium. Subcultures were subjected to an incremental increase in LiCl to obtain adapted lines. Adapted and undapted calli were grown with LiCl and NaCl and the tissue content of Na + , K + , Ca 2+ , Mg 2+ and proline levels were determined. Either 40 mM LiCl or 100 mM NaCl inhibited unadapted calli by more than 50%, while adapted calli grew normally under these conditions. The adapted calli exhibited a lower K

Beyond the ionic and osmotic response to salinity in Chenopodium quinoa: functional elements of successful halophytism.

Chenopodium quinoa Willd. (quinoa) is a halophyte for which some parameters linked to salt tolerance have been investigated separately in different genotypes and under different growth conditions. In this study, several morphological and metabolic responses were analysed in parallel after exposure to salinity. In vitro seed germination was initially delayed by a 150mM NaCl treatment but eventually reached the same level as the control (0mM NaCl), whereas seedling root growth was enhanced; both parameters were moderately inhibited (~35-50%) by 300mM NaCl. In pot grown plants, plant size was reduced by increasing salinity (0-750mM NaCl). Transpiration and stomatal conductance were decreased at the highest salinity levels tested, consistent with reduced stomatal density and size. The density of epidermal bladder cells (EBCs) on the leaf surface remained unaffected up to 600mM NaCl. Tissue contents of Na+ and Cl- increased dramatically with salt treatment, but resulted in only a 50% increase in Na+ from 150 to 750mM NaCl. Internal K+ was unaffected up to 450mM NaCl but increased at the highest salinity levels tested. Excretion through sequestration into EBCs was limited (generally ≤20%) for all ions. A modest dose-dependent proline accumulation, and concomitant reduction in total polyamines and putrescine efflux occurred in NaCl-treated plants. Results confirm the importance of inorganic ions for osmotic adjustment, the plant's ability to maintain K+ levels and the involvement of putrescine efflux in maintaining ionic balance under high salinity conditions. Conversely, ion excretion and proline appear to play a minor role. Taken together these results indicate which parameters could be used for future comparison among different genotypes.

Effects of dietary intake of trace metals on tissue contents of sodium and calcium in mice ( Mus musculus)

Mice were given either cadmium (Cd), copper (Cu) or zinc (Zn) ad lib, and levels of the metals in the heart, kidneys and liver were measured together with organ contents of sodium (Na) and calcium (Ca). The contents of Cd increased more than 100-fold in all organs, whereas Zn increased by a factor of 2–4. Copper accumulated only in the liver. Cadmium exposure caused the Na and Ca contents in the kidneys to increase by a factor of 2–3, but caused a statistically significant reduction in the Na content of the liver. Cadmium also caused a reduction in the Ca content of the heart. Copper caused a statistically significant doubling of the Na content in the heart, but a significant reduction in the Ca content in this organ. Zinc caused a reduction in the Ca content of the heart. However, the mechanisms behind these effects are not clear. The accumulation of Cd in the kidneys and heart was associated with a gradual change in the Na and Ca levels in these organs, but trace metal accumulation was not associated with any conspicuous changes in the Na or Ca contents in any other organ. Copper was not accumulated in heart, but Cu intake still had marked effects on the Na and Ca contents in this organ. Since the tissue contents of Na and Ca are likely to be physiologically important, these ions may have potential as biomarkers for toxic stress. Since the effects of Cd and Cu differed markedly, the tissue contents of Na and Ca may also be used in a trace metal-specific system of fingerprint biomarkers.

SEED GERMINATION OF TWO WHEAT SPECIES DIFFERING IN THEIR SENSITIVITY TO NaCl, IN RESPONSE TO SALT STRESS

ABSTRACT The germination of two wheat species, Triticum aestivum var. Tanit and Triticum durum var. Ben Béchir, respectively, sensitive and tolerant to salt stress, were studied. In the presence of NaCl in the external medium, the tissue content of Na+ was increased much more than that of Cl−. Proline concentration was increased, and the overall peroxidase activity was decreased. These effects were more pronounced in the salt-sensitive than in the salt tolerant species, and they became apparent in the few hours following the beginning of germination. The PEPC activity was slightly decreased in the salt-sensitive species while it was slightly increased in the salt-tolerant species. Modelling the time course of seed germination and leaf sprouting with a sigmoidal equation, made it possible to distinguish the effect of NaCl on the three main parameters characteristic of the time courses of germination and of the sprouting of the first leaf: τ (the time lag before germination/leaf sprouting appreciably began), R (the rate of increase of the percentage of germination/leaf sprouting), and M (the maximal value of this percentage). The presence of external NaCl caused M and R to decrease and τ to increase. Again, the effect was more pronounced in the salt-sensitive than in the salt-tolerant species.

The spasmogenic effects of vanadate in human isolated bronchus.

1. Inhalation of vanadium compounds, particularly vanadate, is a cause of occupational bronchial asthma. We have now studied the action of vanadate on human isolated bronchus. Vanadate (0.1 microM-3 mM) produced concentration-dependent, well-sustained contraction. Its -logEC50 was 3.74 +/- 0.05 (mean +/- s.e.mean) and its maximal effect was equivalent to 97.5 +/- 4.2% of the response to acetylcholine (ACh, 1 mM). 2. Vanadate (200 microM)-induced contraction of human bronchus was epithelium-independent and was not inhibited by indomethacin (2.8 microM), zileuton (10 microM), a mixture of atropine, mepyramine and phentolamine (each at 1 microM), or by mast cell degranulation with compound 48/80. 3. Vanadate (200 microM)-induced contraction was unaltered by tissue exposure to verapamil or nifedipine (each 1 microM) or to a Ca2+-free, EGTA (0.1 mM)-containing physiological salt solution (PSS). However, tissue incubation with ryanodine (10 microM) in Ca2+-free, EGTA (0.1 mM)-containing PSS reduced vanadate-induced contraction. A series of vanadate challenges was made in tissues exposed to Ca2+-free EGTA (0.1 mM)-containing PSS with the object of depleting intracellular Ca2+ stores. In such tissues cyclopiazonic acid (CPA; 10 microM) prevented Ca2+-induced recovery of vanadate-induced contraction. 4. Tissue incubation in K+-rich (80 mM) PSS, K+-free PSS, or PSS containing ouabain (10 microM) did not alter vanadate (200 microM)-induced contraction. Ouabain (10 microM) abolished the K+-induced relaxation of human bronchus bathed in K+-free PSS. This action was not shared by vanadate (200 microM). The tissue content of Na+ was increased and the tissue content of K+ was decreased by ouabain (10 microM). In contrast, vanadate (200 microM) did not alter the tissue content of these ions. Tissue incubation in a Na+-deficient (25 mM) PSS or in PSS containing amiloride (0.1 mM) markedly inhibited the spasmogenic effect of vanadate (200 microM). 5. Vanadate (200 microM)-induced contractions were markedly reduced by tissue treatment with each of the protein kinase C (PKC) inhibitors H-7 (10 microM), staurosporine (1 microM) and calphostin C (1 microM). Genistein (100 microM), an inhibitor of protein tyrosine kinase, also reduced the response to vanadate. 6 Vanadate (0.1-3 mM) and ACh (1 microM- 3 mM) each increased inositol phosphate accumulation in bronchus. Such responses were unaffected by a Ca2+-free medium either alone or in combination with ryanodine (10 microM). 7. In human cultured tracheal smooth muscle cells, histamine (100 microM) and vanadate (200 microM) each produced a transient increase in intracellular Ca2+ concentration ([Ca2+]i). 8. Intracellular microelectrode recording showed that the contractile effect of vanadate (200 microM) in human bronchus was associated with cellular depolarization. 9. It is concluded that vanadate acts directly on human bronchial smooth muscle, promoting the release of Ca2+ from an intracellular store. The Ca2+ release mechanism involves both the production of inositol phosphate second messengers and inhibition of Ca-ATPase. The activation of PKC plays an important role in mediating vanadate-induced contraction at values of [Ca2+]i that are close to basal.

Germination of Selected Turfgrass Seeds under Saline Conditions

The influence of NaCl concentration on seed germination in blue grama grass (Bouteloua gracilis), salty alkaligrass (Puccinellia distans) and Kentucky bluegrass (Poa pratensis) were investigated. When seeds were germinated in petri dishes containing 0, 2.5, 5.0, 7.5, 10, 12.5, 15, 17.5, 20, 22.5, 25, 27.5, and 30 g·liter–1 NaCl at 22 C for 4 weeks, blue grama grass was most salt-tolerant with 50% germination at 17.5 g·liter–1. The salt concentrations that provided 50% germination for salty alkaligrass and Kentucky bluegrass were 5 and 1.5 g·liter–1, respectively. The upper limits of salinity that allowed any germination were 30 g·liter–1 (1%) for blue grama grass, 27.5 g·liter–1 (1%) for salty alkaligrass, and 5 g·liter–1 (2%) for Kentucky bluegrass. Germination was quickest in blue grama grass (90% germination in 1 week) followed by salty alkaligrass (50% in 3 weeks) and Kentucky bluegrass (50% in 4 weeks). The tissue contents of Na+ and Cl– as influenced by increasing levels of NaCl were also determined.

Regulation of intra- and extracellular pH in the rat brain in acute hypercapnia: a re-appraisal

Recent results have demonstrated that intracellular pH (pH i) in nerve and glial cells is not regulated back to normal during CO 2 exposure if extracellular pH (pH e) is reduced. This raises the question about regulation of pH i and pH e in vivo. In order to successively reduce pH e we exposed animals to incremental increases in CO 2 tension (11, 27.5, 42.5%) and studied regulation of pH i during the first 90 min of hypercapnia. Extracellular pH, as well as Na +, K +, and Cl − concentrations, were also measured, as were whole tissue contents of Na +, K +, and Cl −. At all CO 2 tensions studied, pH e slowly increased during CO 2 exposure. In animals breathing 11% CO 2 (ΔpH e ∼ 0.2 units), pH i increased slowly. However, in animals exposed to 27.5% CO 2 or 42.5% CO 2 ( ΔpH e > 0.4 units), no regulation of pH i was observed. Extracellular HCO 3 − concentrations increased substantially already during the first 15 min of hypercapnia (not significant in animals breathing 42.5% CO 2), and then gradually rose. These increases were accompanied by a decrease in Cl − and an increase in Na + concentration, K + concentration remaining constant. The total tissue content of these ions remained constant, suggesting that extracellular HCO 3 − concentration increases by Cl −/HCO 3 − antiport and/or by Na +·2HCO 3 − symport, the HCO 3 − emanating from intracellular sources. The results challenge the dogma of the supremacy of mechanisms regulating pH i, and suggest that brain cells, possibly astrocytes, regulate pH e at the expense of their own pH homeostasis. By inference, we further conclude that regulation of pH i normally occurs only if pH e is first regulated back close to normal value.

The influence of mono- and divalent cations on the cardiac metabolism of arachidonic acid

Our previous study indicated that, in the isolated rabbit heart, perfusion with Ca 2+ free Krebs Henseleit buffer (KHB) results in increased conversion of exogenous arachidonic acid to PGE 2 and 6-keto-PGF 1α, probably as the result of increased availability of substrate to cuclooxygenase. Since perfusion with Ca 2+ free buffer is known to cause alterations in the cardiac content of various mono- and divalent cations, the present study was performed to determine: a) The relationship between the conversion of exogenous arachidonic acid to prostaglandins and cardiac content of Na +, K +, Ca 2+ and Mg 2+; and b) Whether enhanced arachidonic acid conversion to prostaglandins during Caa 2+ free perfusion is due to reduced incorporation of this fatty acid into tissue lipids. Perfusion of the rabbit heart with Ca 2+ free buffer produced a significant reduction in the tissue content of Na +, K +, Ca 2+ and Mg 2+. However, the production of 6-keto-PGF 1α from exogenous arachidonic acid was linearly correlated with tissue Mg 2+. These observations, together with our finding that perfusion with Ca 2+ free KHB reduced the incorporation of [ 3H] arachidonic acid into tissue lipids, suggests that Ca 2+ free perfusion may, by reducing the activity of arachidonyl CoA synthetase (a Mg 2+ dependent enzyme), decrease the acylation of arachidonic acid into lipids, thus increasing the availability of arachidonic acid to cyclooxygenase.

Perinatal changes of transport systems for amino acids in slices of mouse brain

Perinatal changes in the uptake of amino acids were measured in slices of fetal (15- and 19-day) and newborn (4-, 24-, and 48-hr-old) mouse brain. Uptake increased with age; smaller changes occurred with basic and neutral amino acid transport systems, and the largest changes occurred in fetal brain with amino acids of putative neurotransmitter function (taurine, glycine, GABA, and the acidic amino acids). The pattern of increase in uptake was similar at high and at low external amino acid concentrations. Developmental changes in tissue content of Na(+), K(+), or ATP were small during this period, and so are unlikely to be responsible for the observed changes in uptake. It appears that by the 15th day of fetal life, the transport systems for essential amino acids are fairly well developed in the brain, and the transport systems for neurotransmitter amino acids are not so well developed, but undergo a rapid increase in the 15-19-day period. From birth to adulthood, the concentrative capacity of slices of mouse brain for nonessential (putative neurotransmitter) amino acids is much greater than for essential amino acids.