Intracellular Cation Research Articles

To find association of socio-demographic factors of pregnant women with hypomagnesaemia

Magnesium is the second most common intracellular cation which is essential in metabolic processes, protein synthesis, membrane integrity, nervous tissue conduction, neuromuscular excitability, muscle contraction. In obstetrics magnesium has an important role in maternal and foetal wellbeing. Limited data is available in our state to find hypomagnesaemia during pregnancy and its association with socio-demographic profile of the women so the present study was done to find association of socio-demographic factors of the pregnant women with hypomagnesaemia. Methods: This was a hospital based cross-sectional study. 100 women in their third trimester of pregnancy and were included in the study after obtaining written informed consent. After detail history and examination, serum magnesium was measured. And data were analyzed. Results: Risk of hypomagnesaemia was 1.3 times in women who are ≥ 25 years, 1.5 times in urban women,3 times in obese women and 3 to 4 times in pre-eclamptic women. No significant association between hypomagnesaemia and gravid and parity. Women with gestational age <34 weeks are 2.7 times at risk of hypomagnesaemia. There was a weak positive correlation between gestational age and serum magnesium and a weak negative correlation between maternal serum magnesium and maternal age, systolic blood pressure and diastolic blood pressure. Conclusion: Magnesium should be measured in every pregnant women so that magnesium deficiency can be identified early and adequate measures and magnesium supplementation can be given to prevent untoward complications.

Mild early course of osteogenesis imperfecta type XIV - a case report

<p><strong>Introduction.</strong> Mutations in TMEM38B gene, which encodes the endoplasmatic reticulum membrane trimeric intracellular cation channel (TRIC) type B, cause osteogenesis imperfecta type XIV. So far there have been only four different pathogenic variants reported in TMEM38B. Clinical features of osteogenesis imperfecta type XIV described in scarce reports include osteopenia, femoral bowing, low trauma fractures, scoliosis, muscular hypotonia and cardiac pathology. </p><p><strong>Case report.</strong> A 2-month-old male infant was referred to a clinical geneticist office due to bone deformities. The shortening of the limbs was observed during the prenatal ultrasound examination in seventh month of pregnancy. Prenatal cytogenetic analysis was performed from a fetal blood sample and showed normal findings. Neither fetal fractures were observed prenatally, nor any occurred during vaginal labor. During the first clinical exam by the clinical geneticist, discrete rhizomelia and bluish sclerae were observed. Due to the suspicion of skeletal dysplasia, indication for genetic analysis was established. Next generation sequencing panel for skeletal dysplasia showed homozygous deletion of exons 1 and 2 in the TMEM38B gene, confirming osteogenesis imperfecta type XIV. At the follow-up visit performed at 12 months of age, no fractures were reported. Several skeletal deformities were observable: discrete frontal bossing, rhizomelic upper extremities, slightly bowed thighs and shins. The infant achieved normal psychomotor development. A radiographic examination showed bowing of long bones of the lower extremities, without significant osteopenia. </p><p><strong>Conclusion.</strong> Absence of early fractures is rare in osteogenesis imperfecta type XIV. Relatively mild clinical features of our patient therefore contribute to the understanding of the phenotype of osteogenesis imperfecta type XIV and its relation to the genotype.</p>

The intracellular cation channel TMEM176B as a dual immunoregulator.

Characterizing immune regulatory pathways is critical to understand physiological and pathophysiological processes as well as to identify novel immunotherapeutic targets. The cation channel TMEM176B has emerged in the last years as a potential new immunoregulatory player and pharmacological target. Here, we review how expression data, clinical associations of genetic variants and functional studies support a dual role for TMEM176B in regulating immune responses. Thus, TMEM176B can inhibit effector immune responses in some settings whereas it may also promote immunity by supporting antigen presentation in others. We also discuss a potential role for TMEM176B in regulating type 2 and 3 immunity and comment recent data on modulation of DC biology and inflammasome activation as well as CD8+ T cell responses. Understanding the role of TMEM176B in immunity is critical to propose rational pharmacological approaches targeting this channel.

Cellular and ultrastructural alterations of Arabidopsis thaliana roots in response to exogenous trans-aconitic acid

In this work, the responses of Arabidopsis thaliana (L.) Heynh to trans-aconitic acid (TAA) were investigated. A. thaliana was grown in the presence of TAA in a concentration range of 400–1200 µM for 7 or 15 days. Changes in the morphoanatomy, cellular ultrastructure, and micromorphology of the roots were evaluated by light and transmission electron (TEM) microscopy. At concentrations below 1000 µM, TAA reduced the length of the primary roots, but induced an early appearance of lateral roots and root hairs. At a concentration of 1200 µM, TAA suppressed the growth of seedlings. The images of longitudinal sections of root tips of seedlings treated with IC50 of TAA (684 µM) revealed a reduced elongation zone with an increased differentiation zone. TEM images showed an increase in the number and volume of vacuoles, an increase in vesicles containing electron-dense material derived from plasmalemma, and electron-dense granules attached to the cell wall. Trans-aconitic acid induced an early differentiation of A. thaliana seedlings suggesting an interference in the auxin action. Changes in the cellular ultrastructure may represent vacuolar and extracellular accumulation of TAA, to remove excess TAA in the cytosol and mitochondria. An inhibition of aconitase and the chelation of intracellular cations may have contributed to cytotoxicity of TAA at 1200 µM concentration.

The crosstalk effect between ferrous and other ions metabolism in ferroptosis for therapy of cancer.

Ferroptosis is an iron-dependent cell death process characterized by excessive accumulation of reactive oxygen species and lipid peroxidation. The elucidation of ferroptosis pathways may lead to novel cancer therapies. Current evidence suggests that the mechanism of ferroptosis can be summarized as oxidative stress and antioxidant defense mechanisms. During this process, ferrous ions play a crucial role in cellular oxidation, plasma membrane damage, reactive oxygen species removal imbalance and lipid peroxidation. Although, disregulation of intracellular cations (Fe2+, Ca2+, Zn2+, etc.) and anions (Cl-, etc.) have been widely reported to be involved in ferroptosis, their specific regulatory mechanisms have not been established. To further understand the crosstalk effect between ferrous and other ions in ferroptosis, we reviewed the ferroptosis process from the perspective of ions metabolism. In addition, the role of ferrous and other ions in tumor therapy is briefly summarized.

Channel Function of Polycystin-2 in the Endoplasmic Reticulum Protects against Autosomal Dominant Polycystic Kidney Disease.

Mutations of PKD2, which encodes polycystin-2, cause autosomal dominant polycystic kidney disease (ADPKD). The prevailing view is that defects in polycystin-2-mediated calcium ion influx in the primary cilia play a central role in the pathogenesis of cyst growth. However, polycystin-2 is predominantly expressed in the endoplasmic reticulum (ER) and more permeable to potassium ions than to calcium ions. The trimeric intracellular cation (TRIC) channel TRIC-B is an ER-resident potassium channel that mediates potassium-calcium counterion exchange for inositol trisphosphate-mediated calcium ion release. Using TRIC-B as a tool, we examined the function of ER-localized polycystin-2 and its role in ADPKD pathogenesis in cultured cells, zebrafish, and mouse models. Agonist-induced ER calcium ion release was defective in cells lacking polycystin-2 and reversed by exogenous expression of TRIC-B. Vice versa, exogenous polycystin-2 reversed an ER calcium-release defect in cells lacking TRIC-B. In a zebrafish model, expression of wild-type but not nonfunctional TRIC-B suppressed polycystin-2-deficient phenotypes. Similarly, these phenotypes were suppressed by targeting the ROMK potassium channel (normally expressed on the cell surface) to the ER. In cultured cells and polycystin-2-deficient zebrafish phenotypes, polycystin-2 remained capable of reversing the ER calcium release defect even when it was not present in the cilia. Transgenic expression of Tric-b ameliorated cystogenesis in the kidneys of conditional Pkd2-inactivated mice, whereas Tric-b deletion enhanced cystogenesis in Pkd2-heterozygous kidneys. Polycystin-2 in the ER appears to be critical for anticystogenesis and likely functions as a potassium ion channel to facilitate potassium-calcium counterion exchange for inositol trisphosphate-mediated calcium release. The results advance the understanding of ADPKD pathogenesis and provides proof of principle for pharmacotherapy by TRIC-B activators.

Protein nanoparticle-induced osmotic pressure gradients modify pulmonary edema through hyperpermeability in acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS), caused by noncardiogenic pulmonary edema (PE), contributes significantly to Coronavirus 2019 (COVID-19)-associated morbidity and mortality. We explored the effect of transmembrane osmotic pressure (OP) gradients in PE using a fluorescence resonance energy transfer-based Intermediate filament (IF) tension optical probe. Angiotensin-II- and bradykinin-induced increases in intracellular protein nanoparticle (PN)-OP were associated with inflammasome production and cytoskeletal depolymerization. Intracellular protein nanoparticle production also resulted in cytomembrane hyperpolarization and L-VGCC-induced calcium signals, which differed from diacylglycerol-induced calcium increment via TRPC6 activation. Both pathways involve voltage-dependent cation influx and OP upregulation via SUR1-TRPM4 channels. Meanwhile, intra/extracellular PN-induced OP gradients across membranes upregulated pulmonary endothelial and alveolar barrier permeability. Attenuation of intracellular PN, calcium signals, and cation influx by drug combinations effectively relieved intracellular OP and pulmonary endothelial nonselective permeability, and improved epithelial fluid absorption and PE. Thus, PN-OP is pivotal in pulmonary edema in ARDS and COVID-19, and transmembrane OP recovery could be used to treat pulmonary edema and develop new drug targets in pulmonary injury.Graphical

Correlation of Ionized Magnesium with the Parameters of Oxidative Stress as Potential Biomarkers in Patients with Anxiety and Depression: A Pilot Study.

BackgroundMagnesium (Mg) is the second most abundant intracellular cation. Ionized Mg is the only active form of Mg. The concentration of ionized Mg could be a potentially novel biomarker for anxiety and depression.AimThe aim of this study was to assess the serum concentration of ionized Mg and its correlation with biomarkers of oxidative stress and inflammation in patients with anxiety and depression.MethodsIn this study included 93 respondents were divided into 3 groups: C (control group—18 respondents); A (patients with anxiety disorder, dissociative/conversion disorders and somatoform disorders—36 patients); D (patients with depression—39 patients). Clinical diagnosis was based on ICD-10 criteria. Blood samples were used for standard laboratory analysis, ionized Mg analysis, oxidative stress, and inflammatory parameters.ResultsStatistical significance was recorded between healthy volunteers and patients (anxiety/depression) in ionized Mg values. In anxious patients, malondialdehyde (MDA) had a positive correlation between the parameters of oxidative stress with ionized Mg. In depressive patients, MDA had a positive correlation, and glutathione peroxidase 1 (GPX1) a negative correlation with the concentration of ionized Mg.ConclusionIonized Mg and its correlation with parameters of oxidative stress could be potential biomarkers in anxious and depressive patients.

Dysmagenesemia in critically ill patients: prevalence and nature of magnesium disorder.

Abstract: 
 Background: Magnesium, ranks on number four for its abundancy in the body. It is known as “the forgotten electrolyte” in the literature. It is second most abundant intracellular cation. Altered magnesium level is frequently encountered electrolyte imbalance in critically ill patients. It increases ICU related morbidity and mortality. Identification and prompt management of magnesium disorder helps in reducing ICU related mortality.
 Material and methods: we performed a prospective interventional study in which we collected data from intensive care unit of liaquat national hospital. We included only those patients who were having critical illness. We then measured serum magnesium level in all patients and reported the findings. 
 Results: A total of 107 patients from the Medical ICU were included in this study .56 were females (52%) and 51(47.7%) were males. The mean age was 59.6 years. We found that 63.3 % of patients had deranged levels of magnesium. 47.7 % of patients had hypermagnesemia whereas 15.9% of patients had hypomagnesemia.
 Conclusion: Dysmagenesemia is significantly common in critically ill patient.

Magnesium and Its Role in Primary Open Angle Glaucoma; A Novel Therapeutic?

Glaucoma is the leading cause of irreversible blindness globally, with Primary open angle glaucoma (POAG) being the commonest subtype. POAG is characterized by an increase in intraocular pressure (IOP), leading to optic nerve damage and subsequent visual field defects. Despite the clinical burden this disease poses, current therapies aim to reduce IOP rather than targeting the underling pathogenesis. Although the pathogenesis of POAG is complex, the culprit for this increase in IOP resides in the aqueous humour (AH) outflow pathway; the trabecular meshwork (TM) and Schlemm's canal. Dysfunction in these tissues is due to inherent mitochondrial dysfunction, calcium influx sensitivity, increase in reactive oxygen species (ROS) production, TGFβ-2 induction, leading to a sustained inflammatory response. Magnesium is the second most common intracellular cation, and is a major co-factor in over 300 reactions, being highly conserved within energy-dependent organelles such as the mitochondria. Magnesium deficiency has been observed in POAG and is linked to inflammatory and fibrotic responses, as well as increased oxidative stress (OS). Magnesium supplementation been shown to reduce cellular ROS, alleviate mitochondrial dysregulation and has further antifibrotic and anti-inflammatory properties within ocular tissues, and other soft tissues prone to fibrosis, suggesting that magnesium can improve visual fields in patients with POAG. The link between magnesium deficiency and glaucoma pathogenesis as well as the potential role of magnesium supplementation in the management of patients with POAG will be explored within this review.

Effect of intra-nasal nitrilotriacetic acid trisodium salt in lowering elevated calcium cations and improving olfactory dysfunction in COVID-19 patients

PurposeAn association between COVID-19 and olfactory dysfunction has been noted in many patients worldwide. The olfactory adaptation process leads to an increase in intracellular calcium cation levels. Nitrilotriacetic acid trisodium salt has high selective chelation for calcium cations from olfactory mucus. The aim of this work is to test the effect of an intranasal nitrilotriacetic acid trisodium salt to lower the elevated calcium cations in COVID-19 patients with relevant symptoms of olfactory dysfunction.MethodsFifty-eight COVID-19 adult patients with relevant symptoms of olfactory dysfunction were enrolled in a prospective randomized controlled trial. They received a nasal spray containing either 0.9% sodium chloride or 2% nitrilotriacetic acid trisodium salt. Olfactory function was assessed before and after treatment using the Sniffin’ Sticks test. Quantitative analysis of calcium cation concentration in nasal secretions was performed using a carbon paste ion-selective electrode.ResultsAfter the application of nitrilotriacetic acid trisodium salt compared to sodium chloride, a significant improvement from functional anosmia to healthy normosmia with significant decrease in calcium cation concentration was observed.ConclusionsFurther collaborative research is needed to fully investigate the effect of an intranasal nitrilotriacetic acid trisodium salt in the treatment of olfactory disorders.

Another Unique Feature of the Nociceptor-specific Sodium Channel NaV1.9

The voltage-gated Na+ channel NaV1.9 remains an important pain target because of its preferential expression in nociceptors, its involvement in rodent models of nociception, and the association between gain- or loss-of-function NaV1.9 mutations with the presence or absence of pain in humans. At room temperature, NaV1.9 has a low threshold for activation, carrying a persistent current that may influence the resting membrane potential, action potential threshold, and burst firing. We recently demonstrated that in the absence of extracellular Na+, NaV1.9 may also contribute to a transient outward current. Here, we used whole cell patch clamp recordings of human and rat dorsal root ganglion neurons to further characterize this outward current. We found that this current had pharmacological and biophysical properties consistent with a role for NaV1.9: insensitivity to K+, Na+, Cl-, and TRP channel blockers, sensitivity to internally-administered Na+ channel blocker QX-314, and an NaV1.9-like voltage-dependence of inactivation, steady-state inactivation, recovery from inactivation. Interestingly, in contrast to TTX- and A-803467-sensitive currents, the transient outward current persisted in the absence of intracellular Na+, suggesting that NaV1.9 is less selective than other voltage-gated Na+ channels in human and rat sensory neurons. Consistent with this suggestion, the reversal potential for persistent (NaV1.9) inward currents was left shifted relative to that of TTX- and A-803467-sensitive currents. Furthermore, the outward current persisted in the presence of even relatively large intracellular cations (Cs+ and TEA+). Our results suggest NaV1.9 is a relatively non-selective ion channel. Together, these observations have at least two important implications. First, NaV1.9-mediated currents may contaminate voltage-clamp recordings of voltage-gated K+, Ca2+, and Cl- channels in sensory neurons. Second, NaV1.9 may have a more significant impact on the action potential waveform than previously appreciated, including the attenuating the action potential overshoot. Grant support from NIH R01NS122784, NIH 4UH3TR003090.

Microelectrodes for measurement of intracellular [K+] and [Na+]in the choroid plexus epithelium and cerebrospinal fluid

The choroid plexus epithelium (CPE) has recently gained increasing interest as a potential target tissue to manipulating cerebrospinal fluid (CSF) production (1). It is therefore crucial to identify the basolateral Na+ transport mechanisms that are involved in CSF secretion, as it would be accessible from the blood side and thereby hold promise for pharmacological intervention. The sodium‐bicarbonate transporter Ncbe has been identified as a basolateral Na+ importer in the CPE (2,3). Currently, there is no direct intracellular cation measurements in choroid plexus and this information is needed to establish Ncbe as the main basolateral Na+ importer. The aim of this project is to measure the [Na+] and [K+] concentration in CSF and in CPE in vivo with double‐barreled microelectrodes. Ion selective double‐barreled microelectrodes are the tool to measure directly the different ion concentrations. The reference barreled was filled with 500 mM KCl solution and the tip of ion sensitive barrel was filled with Na+ or K+ionophore and then backfilled with KCl solution. In this ongoing project, we were able to estimate extracellular [K+] to 4.08 ± 1.06 mM in CSF of mice in vivo (n=7). The study is in progress.References1: Damkier HH, Brown PD, Praetorius J. Cerebrospinal fluid secretion by the choroid plexus. Physiol Rev. 2013;93:1847‐92.2: Praetorius J, Nejsum LN, Nielsen S. A SLC4A10 gene product maps selectively to the basolateral plasma membrane of choroid plexus epithelial cells. Am J Physiol Cell Physiol. 2004;286:C601‐10.3: Damkier HH, Nielsen S, Praetorius J. Molecular expression of SLC4‐derived Na+‐dependent anion transporters in selected human tissues. Am J Physiol Regul Integr Comp Physiol. 2007;293:R2136‐46.

Limiting Mitochondrial Magnesium Exacerbates Ketogenic Insufficiency and Alters Hepatic Lipid Metabolism

Mg2+ is an abundant intracellular cation and an important co‐factor in the machineries that replicate, transcribe and translate genomic information. Like Ca2+, Mg2+ is also compartmentalized to mitochondria, which are known to accumulate and release Mg2+ in response to metabolic stimuli and thus regulate the intracellular Mg2+ (iMg2+) levels. Mrs2, is the only known molecular machinery associated with mitochondrial Mg2+(mMg2+)influx. Though the core component of the mMg2+ influx is defined, our understanding of how mMg2+ homeostasis alters iMg2+ and the metabolic state of the cell remains incomplete. To begin elucidating the importance of mMg2+, we made a liver‐specific Mrs2 knockout mouse (KO) using the Cre‐loxP system. Liver being the central hub of lipid metabolism, we asked whether loss of mMg2+ alters hepatic lipid homeostasis. Our results show Mrs2 KO mice to accumulate intrahepatic lipid. To understand the molecular mechanism of the altered lipid accumulation, we performed a global proteome analysis in ad libitum fed state liver. We observed PPARα‐regulated targets to be differentially upregulated in Mrs2 KO. Our results show that in Mrs2 KO, Mg2+‐activated binding of AMPK/PPARα co‐activates PPARα to increase target gene expression. PPARα activation is known to increase the maximal fatty acid oxidization (FAO) in the liver but it is intriguing to observe intrahepatic lipid accumulation in Mrs2 KO. To understand this unusual relationship, we measured acetyl coA (AcCOA). In line with increased expression of FAO proteins, we observed AcCOA levels to be increased in Mrs2 KO. Since under homeostatic conditions, FAO derived AcCOA can be channeled to ketogenesis (Fig. 1 left panel), we anticipated robust ketogenesis in Mrs2 KO. Our results show no change in circulating ketone bodies (KB) in Mrs2 KO, however, revealing a state of ketogenic insufficiency. Additionally, our results show that in the setting of ketogenic insufficiency (Fig. 1 middle panel), the FAO‐derived AcCOA is exported to the cytoplasm as citrate. We also show the increased cytosolic citrate levels to positively correlate with increased de novo lipogenesis (DNL) via cataplerosis, resulting in excessive accumulation of diacyl glycerols (DAG) and triacyl glycerols (TAG). Though evidence exists on the regulation of lipid metabolism by Mg2+, the underlying molecular mechanism by which Mg2+ regulates lipid metabolism is an unanswered question for decades. Results from our study is the first of its kind to uncover new pathways through which Mg2+ regulates hepatic lipid metabolism. Future directions: Since increased DNL can trigger hepatic insulin resistance (IR) via DAG‐mediated activation of PKCε, for our future study we hypothesize Mrs2 KO to be insulin resistant in the extreme circumstance of ketogenic insufficiency and a high‐fat load (Fig. 1 right panel). We anticipate FAO‐derived acetyl‐CoA to sequester Coenzyme A and disrupt the tricarboxylic acid (TCA) cycle, resulting in excessive DNL, DAG/TAG accumulation, and hepatic IR through PKCε activation, thus iterating a triad relationship of mMg2+ homeostasis, hepatic lipid metabolism, and IR.

Zebrafish tmem38b Knock out unveils the in vivo role of Trimeric Intracellular Cation (TRIC) channel B on cell homeostasis

Zebrafish tmem38b Knock out unveils the in vivo role of Trimeric Intracellular Cation (TRIC) channel B on cell homeostasis

SERUM MAGNESIUM LEVEL IN TYPE2 DIABETES MELLITUS WITH SPECIAL REFERENCE TO DIABETIC RETINOPATHY

Background: Diabetes mellitus (DM) is a worldwide, growing epidemic, with an estimated 415 million adults globally. Patients with diabetes are at increased risk of death and a triad of serious diabetes-specific complications (neuropathy, nephropathy, and retinopathy) and other associated complications. Magnesium is an intracellular cation and co-enzyme for various reactions of glycolytic pathway. Hence, we evaluated serum magnesium level in type 2 DM with and without diabetic retinopathy. Materials and methods: The study is carried out on 40 patients of type 2 DM with retinopathy and 40 patients of type 2 DM without retinopathy. All patients are subjected to the detailed history taking, ocular examination, and investigations like serum magnesium, FBS, PPBS, glycated hemoglobin. Results: The study revealed that there is a significant decrease in serum magnesium level in diabetic patients with retinopathy than without retinopathy (t= -6.297, df= 58 p= <0.001).Similarly Fasting Blood sugar, post prandial blood sugar and duration of diabetes also show significant difference. Conclusion: As magnesium level decreases in patients with type 2 DM, the prevalence of retinopathy increases. Timely monitoring of serum magnesium levels and glycated hemoglobin as well as appropriate interventions would be beneficial in early detection and treatment of diabetic retinopathy.

Nitrogen-doped carbon dots as a highly selective and sensitive fluorescent probe for sensing Mg2+ ions in aqueous solution, and their application in the detection and imaging of intracellular Mg2+ ions

The magnesium (Mg2+) ion is the second most abundant intracellular cation after potassium, and it is involved in a variety of biological processes and physiological functions. Because of the different effects which are dependent on Mg2+ ion concentration, it is critical to monitor Mg2+ ion levels in biological systems. Here, we report the hydrothermal synthesis of photoluminescent N-doped carbon dots (NCDs) using 4-Hydroxybenzaldehyde and 1, 2, 4, 5-benzenetetramine tetrahydrochloride as carbon and nitrogen sources, respectively. The as-synthesized NCDs demonstrated excitation dependent photoluminescence (PL) with a quantum yield of 16.2%. Because of water dispersibility and chelating functional groups, NCDs were used for highly selective detection of Mg2+ ions using ratiometric PL enhancement with a detection limit of 60 μM. Following that, based on highly biocompatibility and sensing of Mg2+ ions in aqueous solutions, NCDs were employed as photoluminescent probe to detect the Mg2+ ions of mammalian cell lines such as J774, HeLa, and Hek293T, which is most likely due to effective complex formation between NCDs and the intracellular Mg2+ ions. As far as we could possibly know, this is the first report of aqueous solution dispersed carbon dots for intracellular sensing and imaging of Mg2+ ions based solely on an increase in NCDs PL intensity.

Pool size of microbial biomass potassium in various farmland soils

ABSTRACT Potassium (K) is the major intracellular cation in all kinds of organisms including soil microorganisms. This study for the first time presented the potassium pool size in microbial cells in various farmland soils and the effect of land use and organic matter application on the contents. Microbial biomass potassium was determined for several paddy field soils under various managements in different areas, together with some upland, orchard, and pasture field soils, to estimate the potassium pool size in microbial cells in the farmland soils. The contents of microbial biomass potassium ranged from 9 to 65 mg K kg−1 soil in the paddy field soils and showed no difference among soil groups of the paddy fields. The biomass potassium content was higher in the pasture field (183–187 mg K kg−1 soil) than that in the paddy, upland (8–51 mg K kg−1 soil) and orchard (25–50 mg K kg−1 soil) field soils. The average ratio of microbial biomass potassium to exchangeable potassium was 0.25 for all the soils and the average values for paddy field (0.31) and pasture field (0.53) soils were higher than those for upland field (0.06) and orchard field (0.08) soils. Positive correlations were found between the contents of microbial biomass potassium and microbial biomass carbon and nitrogen. Application of organic matter significantly increased microbial biomass potassium in the farmland soils. These findings indicate that microbial biomass potassium plays an important role in potassium supply to crops as a reservoir of potassium and also suggest that the contribution of microbial biomass potassium to the potassium source for crops could be relatively higher in paddy field and pasture field soils than upland field and orchard field soils.

Nucleic Acids Regulate Intracellular Ions and Membrane Potential

The positive charge on the major intracellular inorganic cations (K+, Na+, and Mg2+) significantly exceeds the combined negative charge on Cl- and HCO3-. This so-called anion gap must be balanced by organic anions. From the analysis of published data, we conclude that organic phosphorus-containing compounds (Po) are responsible for the neutralization of much of the anion gap. Importantly, many of them are large polymers, such as DNA, RNA, or polyphosphate, that undergo regular synthesis and degradation. That produces a variable average valency z associated with organic anions. It follows from theory that an increase in z should lead to membrane hyperpolarization and accumulation of cations: this result has been known before, and here we further confirm it by an analysis based on different cellular and computational models. Furthermore, we show that inhibition of potassium channels is expected to reduce the uptake of phosphorus through sodium-coupled transporters. This suggests a simple explanation to two long-established experimental facts about DNA synthesis: namely, that it is accompanied by cell hyperpolarization and that it requires functional potassium channels.

Ulmus davidiana var. japonica Extracts Suppress Lipopolysaccharide-Induced Apoptosis Through Intracellular Calcium Modulation in U937 Macrophages

This study was aimed to examine the antiapoptotic effect of Ulmus davidiana extracts through regulation of the intracellular cation mobilization in U937 human monocytic cells. To investigate the modulatory effects on lipopolysaccharide-induced apoptosis and the Ca2+ signaling pathway, we measured the levels of intracellular Ca2+ and various protein markers such as Bax, Bcl-2, and PARP. To isolate biopotent molecules, the branches of U. davidiana were processed sequentially using 60% ethanol, supercritical fluid extraction, and ethyl acetate extraction of the remaining samples to obtain single fractions and catechin-glycoside, which is one of the known bioeffector molecules of U. davidiana. Lipopolysaccharide increased intracellular Ca2+ mobilization in U937 cells by inducing transient oscillations and markedly increased Bax and PARP protein expression and decreased Bcl-2 expression. All U. davidiana and catechin-glycoside significantly reduced lipopolysaccharide-induced intracellular Ca2+ mobilization and downregulated apoptosis-related molecules. These results suggest that U. davidiana and catechin-glycoside may be useful for improving immune system function.