Calcium membrane permeability

The synthetic and plasmid DNAs are mixed and join their sticky ends spontaneously. They are covalently bound together by DNA ligases, when the resulting hybrid plasmid is inserted into bacterial cells. Dilute calcium chloride solutions render the bacterial membranes permeable and allow the passage of ONA into the cells. 

For compounds not metabolized by the gut wall, liver, or affected by transporters, a direct relationship between oral absorption and bioavailability should be observed. The calculated oral absorption, using PSA as a measure for passive membrane permeability reflecting the absorption step, relates to the in vivo observed bioavailability for three classes of compounds - angiotensin-converting enzymes (ACE) inhibitors, P-blockers, and calcium antagonists - is shown below [25],... 

Fas ligand and interleukin-ip), the neurotransmitter glutamate and thrombin. Like tumor necrosis factor (TNF) receptors, Fas is coupled to downstream death effector proteins that ultimately induce caspase activation (Ch. 22). Fas and TNF receptors recruit proteins called FADD and TRADD respectively FADD and TRADD then activate caspase-8, which, in turn, activates caspase-3 (Fig. 35-4). Calcium ion influx mediates neuronal apoptosis induced by glutamate receptor activation calcium induces mitochondrial membrane permeability transition pore opening, release of cytochrome c and caspase activation. Interestingly, in the absence of neurotrophic factors some neurotrophic factor receptors can activate apoptotic cascades, the low-affinity NGF receptor being one example of such a death receptor mechanism [23],... 

Once apoptosis is triggered, a stereotyped sequence of premitochondrial events occurs that executes the cell death process. In many cases proteins and/or lipid mediators that induce changes in mitochondrial membrane permeability and calcium regulation are produced or activated. For example, the pro-apoptotic Bcl-2 family members Bax, Bad and Bid may associate with the mitochondrial membrane and modify its permeability. Membrane-derived lipid mediators such as ceramide and 4-hydroxynonenal can also induce mitochondrial membrane alterations that are critical for the execution of apoptosis. 

Several different changes in mitochondria occur during apoptosis. These include a change in membrane potential (usually depolarization), increased production of reactive oxygen species, potassium channel activation, calcium ion uptake, increased membrane permeability and release of cytochrome c and apoptosis inducing factor (AIF) [25]. Increased permeability of the mitochondrial membranes is a pivotal event in apoptosis and appears to result from the formation of pores in the membrane the proteins that form such permeability transition pores (PTP) may include a voltage-dependent anion channel (VDAC), the adenine nucleotide translocator, cyclophilin D, the peripheral benzodiazepine receptor, hexokinase and... 

Living cells visualization of membranes, lipids, proteins, DNA, RNA, surface antigens, surface glycoconjugates membrane dynamics membrane permeability membrane potential intracellular pH cytoplasmic calcium, sodium, chloride, proton concentration redox state enzyme activities cell-cell and cell-virus interactions membrane fusion endocytosis viability, cell cycle cytotoxic activity... 

The occurrence and timing of effects on intracellular ionized calcium concentration, lysosomal mass, oxidative stress or plasma membrane permeability frequently provide additional information indicative of mechanism of toxicity (Table 14.5). 

Hormesis, in which compensatory adaptive changes precede and occur at lower doses than degenerative changes, was detected for half of the toxic drugs for cell proliferation, cell morphology and mitochondria [4, 33]. Hormesis could not be assessed for parameters that normally have low values, such as intracellular calcium measured by fluo4 or membrane permeability measured by toto-3, because assay methods were not sufficiently sensitive. However, for calcium, more sensitive dyes. 

Calcium ions are essential in a variety of physiological processes including blood clotting, release of neurotransmitter at the synapse, cell division, cell adhesion, secretion, bioluminescence, membrane permeability, muscle contraction, and bio-mineralization35,174 176. In most of these systems, the disposition and functions of membrane proteins are a key in transport and regulation of calcium. Thus in order to understand the functionality of calcium one should look at a membrane system where the biochemical interplay of calcium is known in detail. 

NaCIO is an acknowledged novel absorption enhancer for ampicillin sodium [99], glycyr-rhizin [100,101], gentamicin [102], phenoxymethyl penicillin [103], cefoxitin sodium [104,105], and acyclovir [106], Takahashi et al. [107] reported that the enhanced membrane permeability of phenolsulfonphthalein depends on the disappearance kinetics of CIO from the loop and its calcium ion sequestration capacity. The enhancing mechanisms of NaCIO are proposed to be involved in (1) Ca2+ sequestration, (2) increase in pore size and solvent drag, (3) interaction with membrane proteins and lipids, and (4) increase in the intracellular calcium level [104,105,108-111],... 

There is a delicate balance between cellular membrane permeability and intracellular calcium homeostasis during CVB3 infection. It has been well-documented that sustained elevation of calcium levels in the cytosol precedes Cyt c release from the mitochondria, and that the small amount of released Cyt c interacts with the inositol triphosphate receptor (IP3R) on the endoplasmic reticulum (ER) and prevents inhibition of ER calcium release. The overall increase of calcium leads to a massive release of Cyt c to maintain ER calcium release through interaction with the IP3Rs in a positive feedback loop, and to activate downstream caspases to execute apoptosis of damaged cells. 

The depolarization that accompanies the action potential induces an increase in membrane permeability to calcium ions. A large inward electrochemical gradient exists for calcium and it moves into the terminal. The calcium that enters the terminal activates enzymes that cause the attachment of some of the vesicles to releasing sites on the terminal membrane, membrane fusion, and the release of the vesicular contents into the synaptic cleft. Transmitter release is terminated by the removal of calcium from the terminal cytoplasm, either via a calcium pump, which pumps it out of the cell, or by uptake into the endoplasmic reticulum or into mitochondria. 

We found that a GSH deficit reversed the direction of DA modulation of NMDA responses (Steullet et al., 2008). In control neurons, DA enhanced NMDA responses. But in neurons with a BSO-induced GSH deficit, DA decreased NMDA responses via activation of D2-type receptors. This decrease disappeared when normal GSH levels were restored by GSH-ethyl ester, a membrane-permeable GSH analog. The difference in dopamine modulation of NMDA responses in control neurons and in neurons with a GSH deficit was mostly explained by a differential modulation of L-type calcium channels. DA enhanced the function of these channels in control neurons, but decreased it in BSO-treated neurons. The redox-sensitive ryanodine receptors (RyRs), which were enhanced in BSO-treated neurons, played an essential role in altering DA signaling in neurons with a GSH deficit. These data suggest that enhancement of the function of RyRs in neurons with low GSH levels favors D2-type receptor-mediated and calcium-dependent pathways, causing a change in DA modulation of L-type calcium channels and ultimately in DA modulation of NMDA responses. 

Cardiac troponin complex consists of three parts. Troponin T facilitates contraction, troponin I (cTnl) inhibits actin-myosin interactions and troponin C binds to calcium ions. Troponin I and T are specific to the heart. In the course of cell damage, cardiac troponin is released Irom myocytes, facilitated by increased membrane permeability that allows smaller troponin fragments to traverse the membrane. 

Malignant hyperthermia is probably due to the inability of certain individuals to control calcium concentrations in the muscle fiber and may involve a generalized alteration in cellular or subcellular membrane permeability, as suggested from research on pigs. This anomaly is genetically determined, but pre-anesthetic evaluation of susceptibility to malignant hyperthermia is a matter of controversy measurement of blood creatine kinase, ATP muscle depletion, or myophosphorylase A, histological... 

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