scholarly journals Exogenous Potassium (K+) Positively Regulates Na+/H+ Antiport System, Carbohydrate Metabolism, and Ascorbate–Glutathione Cycle in H2S-Dependent Manner in NaCl-Stressed Tomato Seedling Roots

Plants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 948
Author(s):  
M. Nasir Khan ◽  
Soumya Mukherjee ◽  
Asma A. Al-Huqail ◽  
Riyadh A. Basahi ◽  
Hayssam M. Ali ◽  
...  
Keyword(s):  
Carbohydrate Metabolism ◽  
Reactive Oxygen Species Generation ◽  
Nacl Stress ◽  
K Channel ◽  
Dependent Manner ◽  
Defense System ◽  
Tomato Seedling ◽  
Seedling Roots ◽  
Glutathione Cycle

Potassium (K+) is one of the vital macronutrients required by plants for proper growth and blossoming harvest. In addition, K+ also plays a decisive role in promoting tolerance to various stresses. Under stressful conditions, plants deploy their defense system through various signaling molecules, including hydrogen sulfide (H2S). The present investigation was carried out to unravel the role of K+ and H2S in plants under NaCl stress. The results of the study show that NaCl stress caused a reduction in K+ and an increase in Na+ content in the tomato seedling roots which coincided with a lower H+-ATPase activity and K+/Na+ ratio. However, application of 5 mM K+, in association with endogenous H2S, positively regulated the Na+/H+ antiport system that accelerated K+ influx and Na+ efflux, resulting in the maintenance of a higher K+/Na+ ratio. The role of K+ and H2S in the regulation of the Na+/H+ antiport system was validated by applying sodium orthovanadate (plasma membrane H+-ATPase inhibitor), tetraethylammonium chloride (K+ channel blocker), amiloride (Na+/H+ antiporter inhibitor), and hypotaurine (HT, H2S scavenger). Application of 5 mM K+ positively regulated the ascorbate–glutathione cycle and activity of antioxidant enzymes that resulted in a reduction in reactive oxygen species generation and associated damage. Under NaCl stress, K+ also activated carbohydrate metabolism and proline accumulation that caused improvement in osmotic tolerance and enhanced the hydration level of the stressed seedlings. However, inclusion of the H2S scavenger HT reversed the effect of K+, suggesting H2S-dependent functioning of K+ under NaCl stress. Therefore, the present findings report that K+, in association with H2S, alleviates NaCl-induced impairments by regulating the Na+/H+ antiport system, carbohydrate metabolism, and antioxidative defense system.

scholarly journals Inhibition of light-induced stomatal opening by allyl isothiocyanate does not require guard cell cytosolic Ca2+ signaling

2020 ◽  
Vol 71 (10) ◽  
pp. 2922-2932 ◽  
Author(s):  
Wenxiu Ye ◽  
Eigo Ando ◽  
Mohammad Saidur Rhaman ◽  
Md Tahjib-Ul-Arif ◽  
Eiji Okuma ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Stomatal Closure ◽  
Allyl Isothiocyanate ◽  
Stomatal Opening ◽  
Cation Channels ◽  
Dependent Manner ◽  
Defense System ◽  
Independent Manner ◽  
Dose Dependent

Abstract The glucosinolate–myrosinase system is a well-known defense system that has been shown to induce stomatal closure in Brassicales. Isothiocyanates are highly reactive hydrolysates of glucosinolates, and an isothiocyanate, allyl isothiocyanate (AITC), induces stomatal closure accompanied by elevation of free cytosolic Ca2+ concentration ([Ca2+]cyt) in Arabidopsis. It remains unknown whether AITC inhibits light-induced stomatal opening. This study investigated the role of Ca2+ in AITC-induced stomatal closure and inhibition of light-induced stomatal opening. AITC induced stomatal closure and inhibited light-induced stomatal opening in a dose-dependent manner. A Ca2+ channel inhibitor, La3+, a Ca2+chelator, EGTA, and an inhibitor of Ca2+ release from internal stores, nicotinamide, inhibited AITC-induced [Ca2+]cyt elevation and stomatal closure, but did not affect inhibition of light-induced stomatal opening. AITC activated non-selective Ca2+-permeable cation channels and inhibited inward-rectifying K+ (K+in) channels in a Ca2+-independent manner. AITC also inhibited stomatal opening induced by fusicoccin, a plasma membrane H+-ATPase activator, but had no significant effect on fusicoccin-induced phosphorylation of the penultimate threonine of H+-ATPase. Taken together, these results suggest that AITC induces Ca2+ influx and Ca2+ release to elevate [Ca2+]cyt, which is essential for AITC-induced stomatal closure but not for inhibition of K+in channels and light-induced stomatal opening.

Evidence for presence of functional beta-adrenoceptor in rabbit S2 proximal straight tubules

1991 ◽  
Vol 261 (3) ◽  
pp. F393-F399 ◽  
Author(s):  
K. Kudo ◽  
Y. Kondo ◽  
K. Abe ◽  
Y. Igarashi ◽  
K. Tada ◽  
...  
Keyword(s):  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
K Channel ◽  
Dependent Manner ◽  
Electrophysiological Properties ◽  
Beta Adrenoceptor ◽  
Organic Solute ◽  
Cell Depolarization ◽  
Dose Dependent

The effect of isoproterenol on the electrophysiological properties of the S2 proximal segment of the rabbit was examined. Isoproterenol at 10(-8) to 10(-4) M depolarized the basolateral membrane voltage (Vb) in a dose-dependent manner. Propranolol attenuated the isoproterenol-induced depolarization. These possible mechanisms of cell depolarization were explored. The role of luminal Na(+)-organic solute cotransport was negligible, since the removal of organic solute did not change the depolarization. Basolateral Na(+)-(HCO3-) cotransport was supported by the finding that 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid inhibited isoproterenol-induced depolarization. Basolateral K+ conductance was suggested by the finding that the application of Ba2+ blocked the isoproterenol-induced depolarization. Na(+)-K(+)-adenosine-triphosphatase (ATPase) was questionable. Although ouabain blocked isoproterenol-induced depolarization, the removal of Na+ did not inhibit the depolarization. Further experiment revealed that dibutylyl-adenosine 3',5'-cyclic monophosphate (cAMP), 8-bromo cAMP, and forskolin did not mimic the response of isoproterenol. These results demonstrate: 1) there is a functional beta-adrenoceptor that depolarizes Vb; 2) isoproterenol-induced depolarization is due to an inhibition of basolateral K+ channel or the activation of basolateral Na(+)-(HCO3-)n cotransport; 3) isoproteronol-induced depolarization is independent of cAMP in the rabbit proximal tubule.

Copper doping enhanced the oxidative stress–mediated cytotoxicity of TiO2 nanoparticles in A549 cells

2017 ◽  
Vol 37 (5) ◽  
pp. 496-507 ◽  
Author(s):  
J Ahmad ◽  
MA Siddiqui ◽  
MJ Akhtar ◽  
HA Alhadlaq ◽  
A Alshamsan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Environmental Remediation ◽  
Titanium Dioxide Nanoparticles ◽  
Reactive Oxygen Species Generation ◽  
A549 Cells ◽  
Glutathione Depletion ◽  
Dependent Manner ◽  
Cu Doping ◽  
And Oxidative Stress

Physicochemical properties of titanium dioxide nanoparticles (TiO2 NPs) can be tuned by doping with metals or nonmetals. Copper (Cu) doping improved the photocatalytic behavior of TiO2 NPs that can be applied in various fields such as environmental remediation and nanomedicine. However, interaction of Cu-doped TiO2 NPs with human cells is scarce. This study was designed to explore the role of Cu doping in cytotoxic response of TiO2 NPs in human lung epithelial (A549) cells. Characterization data demonstrated the presence of both TiO2 and Cu in Cu-doped TiO2 NPs with high-quality lattice fringes without any distortion. The size of Cu-doped TiO2 NPs (24 nm) was lower than pure TiO2 NPs (30 nm). Biological results showed that both pure and Cu-doped TiO2 NPs induced cytotoxicity and oxidative stress in a dose-dependent manner. Low mitochondrial membrane potential and higher caspase-3 enzyme (apoptotic markers) activity were also observed in A549 cells exposed to pure and Cu-doped TiO2 NPs. We further observed that cytotoxicity caused by Cu-doped TiO2 NPs was higher than pure TiO2 NPs. Moreover, antioxidant N-acetyl cysteine effectively prevented the reactive oxygen species generation, glutathione depletion, and cell viability reduction caused by Cu-doped TiO2 NPs. This is the first report showing that Cu-doped TiO2 NPs induced cytotoxicity and oxidative stress in A549 cells. This study warranted further research to explore the role of Cu doping in toxicity mechanisms of TiO2 NPs.

scholarly journals Maintenance of K+/Na+ Balance in the Roots of Nitraria sibirica Pall. in Response to NaCl Stress

Forests ◽  
2018 ◽  
Vol 9 (10) ◽  
pp. 601 ◽  
Author(s):  
Xiaoqian Tang ◽  
Xiuyan Yang ◽  
Huanyong Li ◽  
Huaxin Zhang
Keyword(s):  
Plasma Membrane ◽  
Nacl Stress ◽  
K Channel ◽  
Sodium Vanadate ◽  
Atpase Inhibitor ◽  
K Channels ◽  
Non Invasive ◽  
Na Efflux ◽  
Seedling Roots ◽  
Nitraria Sibirica

Using Non-invasive Micro-test Technology (NMT), the Na+, K+ and H+ flux profiles in the root meristem regions were investigated in Nitraria sibirica Pall. seedlings under different NaCl concentrations. NaCl stress increased the K+ and Na+ contents in the roots of N. sibirica seedlings. NaCl stress significantly increased the steady Na+ efflux from the N. sibirica seedling roots. Steady K+ effluxes were measured in the control roots (without NaCl) and in the roots treated with 200 mM NaCl, and no significant differences were observed between the two treatments. The steady K+ efflux from roots treated with 400 mM NaCl decreased gradually. NaCl treatment significantly increased the H+ influx. Pharmacological experiments showed that amiloride and sodium vanadate significantly inhibited the Na+ efflux and H+ influx, suggesting that the Na+ efflux was mediated by a Na+/H+ antiporter using energy provided by plasma membrane H+-ATPase. The NaCl-induced root K+ efflux was inhibited by the K+ channel inhibitor tetraethylammonium chloride (TEA), and was significantly increased by the H+-ATPase inhibitor sodium vanadate. The NaCl-induced K+ efflux was mediated by depolarization-activated outward-rectifying K+ channels and nonselective cation channels (NSCCs). Under salt stress, N. sibirica seedlings showed increased Na+ efflux due to increased plasma membrane H+-ATPase and Na+/H+ antiporter activity. High H+ pump activity not only restricts the Na+ influx through NSCCs, but also limits K+ leakage through outward-rectifying K+ channels and NSCCs, leading to maintenance of the K+/Na+ balance and higher salt tolerance.

scholarly journals The Role of K+, Ca2+ channels and Endothelial Hyperpolarizing Factors in Vasorelaxation Induced by Tribulus terrestris

2021 ◽  
Vol 2 (1) ◽  
pp. 94-100
Author(s):  
Thamer M. Bashir ◽  
Omar A.M. Al-Habib
Keyword(s):  
Methanolic Extract ◽  
K Channel ◽  
Tribulus Terrestris ◽  
Channel Blockers ◽  
Dependent Manner ◽  
The Novel ◽  
Concentration Dependent Manner ◽  
Relaxant Effect ◽  
Calcium Ion Channels

The present study focused on the relaxant effect of themethanolic extract (ME) of Tribulus terristris on rats’ thoracic aortae and included the study of underlying vasorelaxation mechanisms. The methanolic extract produced concentration-dependent relaxation in rats’ aorta. The methanolic extract produced concentration-dependent relaxation in the aortic rings. The use of different K+ channel blockers (BaCl2, 4-AP, GLIB, and TEA) indicated that Kv, KATP, KIR, and KCa and L-type Ca channels played no role in the methanolic extractinduced relaxation. However, with respect to endothelium-derived hyperpolarizing factors, PGI2 and sGC produced a mild inhibition in the relaxation response to ME while NO produced no effect at all. Based on the novel results of the current study, it can be concluded that T. terrestris methanolic extract (ME) mediated relaxation in isolated rat aortic tissues in a concentration-dependent manner. Moreover, we discovered that ME-mediated relaxation is endothelium-dependent and that potassium and calcium ion channels play no role in this relaxation with a limited role of PGI2 and sGC.

scholarly journals Adrenomedullin Reduces Gender-Dependent Loss of Hypotensive Cerebrovasodilation after Newborn Brain Injury through Activation of ATP-Dependent K Channels

2007 ◽  
Vol 27 (10) ◽  
pp. 1702-1709 ◽  
Author(s):  
William M Armstead ◽  
Monica S Vavilala
Keyword(s):  
Brain Injury ◽  
Clinical Intervention ◽  
K Channel ◽  
Dependent Manner ◽  
Channel Activation ◽  
Cranial Window ◽  
Pial Artery ◽  
Newborn Brain ◽  
Newborn Pigs

Cerebrovascular dysregulation during hypotension occurs after fluid percussion brain injury (FPI) in the newborn pig owing to impaired K channel function. This study was designed to (1) determine the role of gender and K channel activation in adrenomedullin (ADM) cerebrovasodilation, (2) characterize the role of gender in the loss of hypotensive cerebrovasodilation after FPI, and (3) determine the role of gender in the ability of exogenous ADM to modulate hypotensive dysregulation after FPI. Lateral FPI (2 atm) was induced in newborn male and female newborn pigs (1 to 5 days old) equipped with a closed cranial window, n = 6 for each protocol. Adrenomedullin-induced pial artery dilation was significantly greater in female than male piglets and blocked by the KATP channel antagonist glibenclamide, but not by the Kca channel antagonist iberiotoxin. Cerebrospinal fluid ADM was increased from 3.8 ± 0.7 to 14.6 ± 3.0 fmol/mL after FPI in female but was unchanged in male piglets. Hypotensive pial artery dilation was blunted to a significantly greater degree in male versus female piglets after FPI. Topical pretreatment with a subthreshold vascular concentration of ADM (10−10 mol/L) before FPI reduced the loss of hypotensive pial artery dilation in both genders, but protection was significantly greater in male versus female piglets. These data show that hypotensive pial artery dilation is impaired after FPI in a gender-dependent manner. By unmasking a gender-dependent endogenous protectant, these data suggest novel gender-dependent approaches for clinical intervention in the treatment of perinatal traumatic brain injury.

Amelioration of Carbon Tetrachloride-Induced Liver Injury by Citrus Leaf Extract

2019 ◽  
Vol 17 (4) ◽  
pp. 426-431
Author(s):  
Jin Xuezhu ◽  
Li Jitong ◽  
Nie Leigang ◽  
Xue Junlai
Keyword(s):  
Carbon Tetrachloride ◽  
Leaf Extract ◽  
Hepatic Injury ◽  
The Body ◽  
Dependent Manner ◽  
Weight Changes ◽  
Citrus Leaf ◽  
Dose Dependent ◽  
And Oxidative Stress

The main purpose of this study is to investigate the role of citrus leaf extract in carbon tetrachloride-induced hepatic injury and its potential molecular mechanism. Carbon tetrachloride was used to construct hepatic injury animal model. To this end, rats were randomly divided into 4 groups: control, carbon tetrachloride-treated, and two carbon tetrachloride + citrus leaf extract-treated groups. The results show that citrus leaf extract treatment significantly reversed the effects of carbon tetrachloride on the body weight changes and liver index. Besides, treatment with citrus leaf extract also reduced the levels of serum liver enzymes and oxidative stress in a dose-dependent manner. H&E staining and western blotting suggested that citrus leaf extract could repair liver histological damage by regulating AMPK and Nrf-2.

The Role of Human T-Lymphotropic Virus Type 1 (HTLV-1)-Infected Dendritic Cells in the Development of HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis

1999 ◽  
Vol 73 (6) ◽  
pp. 4575-4581 ◽  
Author(s):  
Masahiko Makino ◽  
Satoshi Shimokubo ◽  
Shin-Ichi Wakamatsu ◽  
Shuji Izumo ◽  
Masanori Baba
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Virus Type ◽  
Spastic Paraparesis ◽  
Tropical Spastic Paraparesis ◽  
Normal Donor ◽  
Dependent Manner ◽  
T Lymphotropic Virus

ABSTRACT The development of human T-lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is closely associated with the activation of T cells which are HTLV-1 specific but may cross-react with neural antigens (Ags). Immature dendritic cells (DCs), differentiated from normal donor monocytes by using recombinant granulocyte-macrophage colony-stimulating factor and recombinant interleukin-4, were pulsed with HTLV-1 in vitro. The pulsed DCs contained HTLV-1 proviral DNA and expressed HTLV-1 Gag Ag on their surface 6 days after infection. The DCs matured by lipopolysaccharides stimulated autologous CD4+ T cells and CD8+ T cells in a viral dose-dependent manner. However, the proliferation level of CD4+ T cells was five- to sixfold higher than that of CD8+ T cells. In contrast to virus-infected DCs, DCs pulsed with heat-inactivated virions activated only CD4+ T cells. To clarify the role of DCs in HAM/TSP development, monocytes from patients were cultured for 4 days in the presence of the cytokines. The expression of CD86 Ag on DCs was higher and that of CD1a Ag was more down-regulated than in DCs generated from normal monocytes. DCs from two of five patients expressed HTLV-1 Gag Ag. Furthermore, both CD4+ and CD8+ T cells from the patients were greatly stimulated by contact with autologous DCs pulsed with inactivated viral Ag as well as HTLV-1-infected DCs. These results suggest that DCs are susceptible to HTLV-1 infection and that their cognate interaction with T cells may contribute to the development of HAM/TSP.

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