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Chemically induced release

Smith, D. K., Tender. L. M., Lane, G. A., Licht, S., Wiighton, M. S. (1989). Chemically induced release of charge from a rectifying polymer based on viologen and quinone subunits, /. Am. Chem. Soc, 111 1099. [Pg.563]

Activation of CXCR4 Induces Release of Chemical Transmitters (Gliotransmitters) from Glial Cells... [Pg.275]

B-NOD is a new NO donor compound. It has a chemical NO-releasing group similar to that of NTG, however, it releases NO in vitro and in vivo. After administration of B-NOD in vivo its activity persists for more than 7 h. In vitro, the release of NO from B-NOD was augmented by the presence ofliving cells (blood platelets). B-NOD increased cGMP levels and prevented thrombin-induced platelet aggregation in vitro in the same manner as SNP. In vivo, administration of B-NOD in rabbits did not cause a fall in blood pressure or an increase in heart rate [97]. [Pg.246]

Cyclodiene insecticides produce intense nerve excitation in both vertebrate and invertebrate species (Matsumura 1985 Matsumura and Tanaka 1984). It has been suggested that the biochemical mechanisms by which these chemicals induce hyperexcitation in the central nervous system are due to the release of neurotransmitters caused by the interactions of the insecticide with the picrotoxinin receptor. [Pg.55]

The formation and release of interferon by viral and other pathological stimulation has resulted in a search for chemical inducers of endogenous interferon. Administration of a wide range of compounds has resulted in induction of interferon production. However, no clinically useful compounds have been found for humans, although tilorone is effective in inducing interferon in mice. [Pg.157]

No information was located regarding the mechanism by which tetryl enters the blood stream from the lungs, skin, or gastrointestinal tract, the mechanism by which tetryl is transported in the blood stream, or the mechanism of toxicity for tetryl. Earlier studies suggested that the cause of tetryl-induced dermatitis, which is the most common and widely studied adverse effect, may be both physical (direct irritation by sharp tetryl crystals) and chemical (by reacting with components of the skin) (Ruxton 1917). The chemical hypothesis was later advanced by others as well (Bain and Thompson 1954 Brownlie and Cumming 1946). Bain and Thompson (1954) specifically suggested that histamine release may result from a tetryl-induced sensitization reaction or from direct tetryl-induced release from mast cells. [Pg.28]

Figure 4.10. Overview of nerve impulse transmission in chemical synapses. The action potential in the presynaptic nerve cell induces release of the nemotransmitter (e.g., acetylcholine) into the synaptic cleft. The transmitter binds to its receptor, e.g. the nicotinic acetylcholine receptor (NAR). The NAR is a hgand-gated channel it will open and become permeable to both and Na. This will move the membrane potential toward the average of the two respective equilibrium potentials however, in the process, the firing level of adjacent voltage-gated sodium charmels will be exceeded, and a full action potential will be triggered (inset). Figure 4.10. Overview of nerve impulse transmission in chemical synapses. The action potential in the presynaptic nerve cell induces release of the nemotransmitter (e.g., acetylcholine) into the synaptic cleft. The transmitter binds to its receptor, e.g. the nicotinic acetylcholine receptor (NAR). The NAR is a hgand-gated channel it will open and become permeable to both and Na. This will move the membrane potential toward the average of the two respective equilibrium potentials however, in the process, the firing level of adjacent voltage-gated sodium charmels will be exceeded, and a full action potential will be triggered (inset).
The list of countries which have released crop varieties developed through induced mutations is impressive. There are more than 40 countries with over 1500 released mutants of which less than 10% are chemically induced and more than 90% are induced by radiation. [Pg.69]

It is now recognized that GSH conjugation plays a critical role in chemical-induced nephrotoxicity and, in many cases, may be responsible for selective targeting and damage to the kidney versus other organ systems (Table 1). The capacity of the kidney to process and activate GSH conjugates is extensive and results in the release of toxic species within the proximal tubular cells. For example, haloalkenes and quinones are con-... [Pg.75]


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Chemical releases

Chemically induced

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