ULTRAVIOLET RADIATION INDUCES A CHANGE IN CELL MEMBRANE POTENTIAL in vitro: A POSSIBLE SIGNAL FOR ULTRAVIOLET RADIATION INDUCED ALTERATION IN CELL ACTIVITY

1989 ◽  
Vol 49 (5) ◽  
pp. 655-662 ◽  
Author(s):  
RICHARD L. GALLO ◽  
IRENE E. KOCHEVAR ◽  
RICHARD D. GRANSTEIN
2021 ◽  
pp. 096032712110387
Author(s):  
Di Zhang ◽  
Fangfang Yu ◽  
Huanhuan Li ◽  
Qiuyue Wang ◽  
Meiya Wang ◽  
...  

Silver nanoparticles (AgNPs) are widely applied in the field of personal protection for their powerful toxic effects on cells, and recently, a new type of vaginal gel with AgNPs is used to protect the female reproductive tract from microbes and viruses. However, a high risk of AgNPs to the fetus and the underlying mechanism of AgNPs to interfere in embryo development still remain unclear. Thus, this study investigated the impact of two drugs of vaginal gel with AgNPs on reproductive capability of the female mouse by animal experiment. Then, kinetics of AgNPs affecting embryo development was investigated by in vitro embryos culturing, and cell membrane potential (CMP) of zygotes was analyzed by DiBAC4(3) staining. Results indicated that one of the drugs of vaginal gel certainly injured embryo development in spite of no apparent histological change found in ovaries and uteruses of drug-treated mice. In vitro embryo culturing discovered that the toxic effect of AgNPs on embryo development presented particle sizes and dose dependent, and AgNP treatment could rapidly trigger depolarization of the cell membrane of zygotes. Moreover, AgNPs changed the gene expression pattern of Oct-4 and Cdx2 in blastocysts. All these findings suggest that AgNPs can interfere with normal cellular status including cell membrane potential, which has not been noticed in previous studies on the impact of AgNPs on mammalian embryos. Thus, findings of this study alarm us the risk of applying vaginal gel with AgNPs in individual caring and protection of the female reproductive system.


1994 ◽  
Vol 81 (3) ◽  
pp. 437-442 ◽  
Author(s):  
Hans H. Dietrich ◽  
Ralph G. Dacey

✓ The relationship between cell membrane potential, vessel diameter, and pH in small cerebral arterioles is not completely understood. This study involved direct, simultaneous measurement of cell membrane potential and vessel diameter at various extracellular pH levels. Arterioles ranging from 44 to 91 µm in diameter were isolated, transferred to a temperature-controlled microscope chamber, which was used as an organ bath, and observed through an inverted videomicroscope. Two vessel cannulation procedures were used: a single-sided cannulation with the other side occluded, and a double-sided and perfused cannulation. After cannulation, the vessels were pressurized to 60 mm Hg intraluminally and the bath temperature was raised to 37°C. Cell membrane potentials of vessel wall cells were obtained after the bath temperature reached 37°C with the vessels partly constricted and again after spontaneous tone (constriction) of the healthy vessels had developed. The effect of extraluminal pH on cell membrane potentials was studied by changing the bath pH from 7.3 to either 7.65 or 6.8 in the single-sided cannulation. The average cell membrane potential for vessels at 37°C, with 60 mm Hg of intraluminal pressure and pH 7.3, was −37.5 mV. The cell membrane potential depolarized to −30.9 mV at pH 7.65 and hyperpolarized to −58.4 mV at pH 6.8, with a slope of 25.8 mV/pH unit. The effect of depolarizing extracellular potassium ions on the cell membrane potential was examined by perfusing two vessels with modified Ringer's solution containing 70 mM KCl. This perfusion method decreased the vessel diameter by 48% and depolarized the observed cell membrane potential from −41.9 to −19.8 mV, with a slope of −0.42 mV per percentage diameter change. These data provide the first measurements of membrane potentials of isolated penetrating arteriole wall cells in vitro. The results indicate that the cell membrane potential relates linearly to the vessel diameter. This new technique opens the possibility for studying vessel response to stimuli under controlled conditions and regulatory mechanisms such as the propagation of vasomotor responses.


2001 ◽  
Vol 281 (5) ◽  
pp. R1540-R1544
Author(s):  
Thomas A. Lutz ◽  
Alois Estermann ◽  
Nori Geary ◽  
Erwin Scharrer

The pancreatic hormone glucagon hyperpolarizes the liver cell membrane under various conditions. Here we investigated the physiological relevance of this effect by testing the influence of infusions of glucagon antiserum on the liver cell membrane potential in vivo. Intracellular microelectrode recordings of liver cells (up to 60/rat over 2 h) were done in anesthetized male rats. Livers were fixed in place, and recordings were done 10–30 min after intraperitoneal injections of glucagon or hepatic portal vein infusions of glucagon or specific polyclonal glucagon antibodies raised in rabbits. The isotonic lactose vehicle was used as a control for glucagon, and equal amounts of nonimmunized rabbit IgG were used as a control for glucagon antibodies. Intraperitoneal glucagon (400 μg/kg) hyperpolarized the liver cell membrane up to 12 mV, and intraportal glucagon (10 or 60 μg/kg) dose dependently hyperpolarized the liver cell membrane by 3–7 mV. Intraportal infusion of glucagon antiserum (in vitro binding capacity of 4 ng glucagon/rat) significantly depolarized the liver cell membrane by ∼2.5 mV. The effects of both glucagon and glucagon antiserum reversed after 60–90 min. We conclude that glucagon is a physiologically important modulator of the liver cell membrane potential.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Muhammad H. Khan ◽  
John J. Walsh ◽  
Jelena M. Mihailović ◽  
Sandeep K. Mishra ◽  
Daniel Coman ◽  
...  

AbstractUnder normal conditions, high sodium (Na+) in extracellular (Na+e) and blood (Na+b) compartments and low Na+ in intracellular milieu (Na+i) produce strong transmembrane (ΔNa+mem) and weak transendothelial (ΔNa+end) gradients respectively, and these manifest the cell membrane potential (Vm) as well as blood–brain barrier (BBB) integrity. We developed a sodium (23Na) magnetic resonance spectroscopic imaging (MRSI) method using an intravenously-administered paramagnetic polyanionic agent to measure ΔNa+mem and ΔNa+end. In vitro 23Na-MRSI established that the 23Na signal is intensely shifted by the agent compared to other biological factors (e.g., pH and temperature). In vivo 23Na-MRSI showed Na+i remained unshifted and Na+b was more shifted than Na+e, and these together revealed weakened ΔNa+mem and enhanced ΔNa+end in rat gliomas (vs. normal tissue). Compared to normal tissue, RG2 and U87 tumors maintained weakened ΔNa+mem (i.e., depolarized Vm) implying an aggressive state for proliferation, whereas RG2 tumors displayed elevated ∆Na+end suggesting altered BBB integrity. We anticipate that 23Na-MRSI will allow biomedical explorations of perturbed Na+ homeostasis in vivo.


2005 ◽  
Vol 98 (3) ◽  
pp. 1119-1124 ◽  
Author(s):  
Jay S. Naik ◽  
Scott Earley ◽  
Thomas C. Resta ◽  
Benjimen R. Walker

Chronic obstructive pulmonary diseases, as well as prolonged residence at high altitude, can result in generalized airway hypoxia, eliciting an increase in pulmonary vascular resistance. We hypothesized that a portion of the elevated pulmonary vascular resistance following chronic hypoxia (CH) is due to the development of myogenic tone. Isolated, pressurized small pulmonary arteries from control (barometric pressure ≅ 630 Torr) and CH (4 wk, barometric pressure = 380 Torr) rats were loaded with fura 2-AM and perfused with warm (37°C), aerated (21% O2-6% CO2-balance N2) physiological saline solution. Vascular smooth muscle (VSM) intracellular Ca2+ concentration ([Ca2+]i) and diameter responses to increasing intraluminal pressure were determined. Diameter and VSM cell [Ca2+]i responses to KCl were also determined. In a separate set of experiments, VSM cell membrane potential responses to increasing luminal pressure were determined in arteries from control and CH rats. VSM cell membrane potential in arteries from CH animals was depolarized relative to control at each pressure step. VSM cells from both groups exhibited a further depolarization in response to step increases in intraluminal pressure. However, arteries from both control and CH rats distended passively to increasing intraluminal pressure, and VSM cell [Ca2+]i was not affected. KCl elicited a dose-dependent vasoconstriction that was nearly identical between control and CH groups. Whereas KCl administration resulted in a dose-dependent increase in VSM cell [Ca2+]i in arteries taken from control animals, this stimulus elicited only a slight increase in VSM cell [Ca2+]i in arteries from CH animals. We conclude that the pulmonary circulation of the rat does not demonstrate pressure-induced vasoconstriction.


2012 ◽  
Vol 21 (6) ◽  
pp. 404-410 ◽  
Author(s):  
Tara L. Fernandez ◽  
Rebecca A. Dawson ◽  
Derek R. Van Lonkhuyzen ◽  
Michael G. Kimlin ◽  
Zee Upton

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