Narcosis

Narcosis is perhaps the most common mode of action of common industrial pollutants. A variety of compounds, especially those used as solvents, exhibit this mode of action during the typical toxicity test. Although a common mode of action from the point of view of symptomology, several different molecular mechanisms may be at play. 

Alteration of the interactions between the lipid bilayer and the associated proteins 

Schematic of cell membrane with associated protiens. 

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Short-term exposure. This is the maximum concentration to which workers can be exposed for a period of up to 15 minutes continuously without suffering from (a) intolerable irritation, (b) chronic or irreversible tissue change, or (c) narcosis of sufficient degree to increase accident proneness, impair self-rescue, or materially reduce efficiency, provided that no more than four excursions per day are permitted, with at least 60 minutes between exposure periods, and provided the daily time-weighted value is not exceeded. 

Full eye protection should be worn whenever handling acryhc monomers contact lenses must never be worn. Prolonged exposure to Hquid or vapor can result in permanent eye damage or blindness. Excessive exposure to vapors causes nose and throat irritation, headaches, nausea, vomiting, and dizziness or drowsiness (solvent narcosis). Overexposure may cause central nervous system depression. Both proper respiratory protection and good ventilation are necessary wherever the possibiHty of high vapor concentration arises. 

The threshold limit value (TLV) for cyclohexane is 300 ppm (1050 mg/m ). With prolonged exposure at 300 ppm and greater, cyclohexane may cause irritation to eyes, mucous membranes, and skin. At high concentrations, it is an anesthetic and narcosis may occur. Because of its relatively low chemical reactivity, toxicological research has not been concentrated on cyclohexane. 

Dichloroethylene is toxic by inhalation and ingestion and can be absorbed by the skin. It has a TLV of 200 ppm (10). The odor does not provide adequate warning of dangerously high vapor concentrations. Thorough ventilation is essential whenever the solvent is used for both worker exposure and flammabihty concerns. Symptoms of exposure include narcosis, dizziness, and drowsiness. Currently no data are available on the chronic effects of exposure to low vapor concentrations over extended periods of time. 

Inhalation is the most common means by which ethers enter the body. The effects of various ethers may include narcosis, irritation of the nose, throat, and mucous membranes, and chronic or acute poisoning. In general, ethers are central nervous system depressants, eg, ethyl ether and vinyl ether are used as general anesthetics. 

Signs and Symptoms Narcosis Behavioral changes decrease in motor functions ... 

Narcosis Narcosis is a state of deep stupor or unconsciousness, produced by a chemical substance, such as a drug or anesthesia. Inhalation of certain chemicals can lead to narcosis. For example, diethyl ether and chloroform, two common organic solvents, were among the first examples of anesthesia known. Many other chemicals that you would not suspect can also cause narcosis. For example, even though nitrogen gas comprises 80% of the air we breathe and is considered chemically inert (unreactive) it can cause narcosis under certain conditions. Always work with adequate inhalation and avoid inhaling chemical fumes, mists, dusts etc. whenever possible. Use fume hoods and respirators as necessary. 

Anhalonidine is not so active and resembles pellotine in action. In frogs it produces a type of narcosis or paresis, followed by a phase of increased excitability. Larger doses have a curare action. On mammals the action is slight. 

Peters s results for corycavine and corycavamine indicate that these two alkaloids produce narcosis in frogs followed by paralysis of the spinal cord, and in mammals increased secretion of tears and saliva and epileptiform convulsions without increase of reflex irritability they also adversely affect the heart. ... 

Arachis hypogcea L. Arachine, CgHj ONj, with choline and betaine. Yellowish-green syrup crystalline platinichloride, m.p. 216° and aurichloride produces transient narcosis in frogs and rabbits with partial paralysis (Mooser, Landw. Versuchs-Stat., 1904, 60, 321 Chem. Soc. Abstr., 1905, [i], 79)). 

Humans experience a wide range of acute adverse health effects, including irritation, narcosis, asphyxiation, sensitization, blindness, organ system damage, and death. In addition, the severity of many of these effects varies with intensity and duration of e.xposure. For example, exposure to a substance at an intensity that is sufficient to cause only mild throat irritation is of less concern than one that causes severe eye irritation, lacrimation, or dizziness, since the latter effects arc likely to impede escape from the area of contamination. 

Hurst (19) discusses the similarity in action of the pyrethrins and of DDT as indicated by a dispersant action on the lipids of insect cuticle and internal tissue. He has developed an elaborate theory of contact insecticidal action but provides no experimental data. Hurst believes that the susceptibility to insecticides depends partially on the cuticular permeability, but more fundamentally on the effects on internal tissue receptors which control oxidative metabolism or oxidative enzyme systems. The access of pyrethrins to insects, for example, is facilitated by adsorption and storage in the lipophilic layers of the epicuticle. The epicuticle is to be regarded as a lipoprotein mosaic consisting of alternating patches of lipid and protein receptors which are sites of oxidase activity. Such a condition exists in both the hydrophilic type of cuticle found in larvae of Calliphora and Phormia and in the waxy cuticle of Tenebrio larvae. Hurst explains pyrethrinization as a preliminary narcosis or knockdown phase in which oxidase action is blocked by adsorption of the insecticide on the lipoprotein tissue components, followed by death when further dispersant action of the insecticide results in an irreversible increase in the phenoloxidase activity as a result of the displacement of protective lipids. This increase in phenoloxidase activity is accompanied by the accumulation of toxic quinoid metabolites in the blood and tissues—for example, O-quinones which would block substrate access to normal enzyme systems. The varying degrees of susceptibility shown by different insect species to an insecticide may be explainable not only in terms of differences in cuticle make-up but also as internal factors associated with the stability of oxidase systems. 

Sections and all measurements after a single dose were carried out after 2, 4, 12, 24, 48, 72 and 120 hours following injection of the compounds. In the case of 3-7 fold administration, the animals were sacrificed 24 hours after the last dose. Rats were sacrificed under ether narcosis, mice - by dislocation of the spinal cord. Then livers and blood from heart were collected. 

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