Paraldehyde poisoning

After 3 5 g of the hypnotic paraldehyde a qualitatively similar pattern of action was observed as with alcohol, although the stimulation phase was briefer and less pronounced and the paralysing action of the preparation was stronger. Following the intake of chloral hydrate and with the inhalation poisons the paralysing effect was still more pronounced. 

Ethanal (acetaldehyde) polymerizes under the influence of acids to the cyclic trimer, paraldehyde, and a cyclic tetramer, metaldehyde. Paraldehyde has been used as a relatively nontoxic sleep-producing drug (hypnotic). Metaldehyde is used as a poison for snails and slugs, Snarol. Ketones do not appear to form stable polymers like those of aldehydes. 

Acetaldehyde boils near room temperature, and it can be handled as a liquid. Acetaldehyde is also used as a trimer (paraldehyde) and a tetramer (metaldehyde), formed from acetaldehyde under acid catalysis. Heating either of these compounds provides dry acetaldehyde. Paraldehyde is used in medicines as a sedative, and metaldehyde is used as a bait and poison for snails and slugs. 

When cyclopentanecarbaldehyde is prepared, it is a colourless liquid. On standing, particularly with traces of acid, it forms the crystalline trimer. The trimer is a stable six-membered heterocycle with all substituents equatorial Acetaldehyde (ethanal) forms a liquid trimer called paraldehyde , which reverts to the monomer on distillation with catalytic acid. More interesting is metaldehyde , the common slug poison, which is an all-as tetramer (2,4,6,8-tetramethyl-l,3,5,7-tetroxocane) formed from acetaldehyde with dry HC1 at below 0°C. Metaldehyde is a white crystalline solid that has all the methyl groups pseudoequatorial, and it reverts to acetaldehyde on heating. 

Thiram and other dithiocarbamates are metabolic poisons. The acute effects of thiram are very similar to that of carbon disulfide, supporting the notion that the common metabolite of this compound is responsible for its toxic effects. The exact mechanism of toxicity is still unclear, however it has been postulated that the intracellular action of thiram involves metabolites of carbon disulfide, causing microsome injury and cytochrome P450 disruption, leading to increased heme-oxygenase activity. The intracellular mechanism of toxicity of thiram may include inhibition of monoamine oxidase, altered vitamin Bg and tryptophan metabolism, and cellular deprivation of zinc and copper. It induces accumulation of acetaldehyde in the bloodstream following ethanol or paraldehyde treatment. Thiram inhibits the in vitro conversion of dopamine to noradrenalin in cardiac and adrenal medulla cell preparations. It depresses some hepatic microsomal demethylation reactions, microsomal cytochrome P450 content and the synthesis of phospholipids. Thiram has also been shown to have moderate inhibitory action on decarboxylases and, in fish, on muscle acetylcholinesterases. 

Other Paraldehyde Class IV Exhaled via the lungs strong odor and disagreeable taste seldom used has been used to control delirium tremens (DTS) in alcoholics can be used for drug poisoning Status epilepticus and tetanus to control convulsions Pregnancy category C, PB UK half life 7.5 hours Sedative PO 5-10 mL q4—6h PRN in water or juice maximum dose of 30 mL Hypnotic PO 10-30 mL h.s. 

Coniine, 2-propylpiperidine the most important of the Conium alkaloids (see), and the toxic principle of the poison hemlock, Conium maculatum, which was used in ancient Athens to put Socrates to death. The lethal dose of C. in humans is 0.5-1 g. The largest quantities of C. are found in the unripe seeds The synthesis of C. from a-picoline and paraldehyde by Ladenburg in 1886 was the first laboratory synthesis of any alkaloid. M, 127.22, m.p. -2.5 C, b.p. 166 C, [a] 7 16°. 

Corresponding to the maximum acidity, the catalytic activities for paraldehyde depolymerization and m-2-butene isomerization show maxima at the composition of 10% M0O3. The active sites for butene isomerization are poisoned by ammonia but not by CO2, indicating that the acid sites are the active sites for the reaction. This is in contrast to the catalytic behavior of the single component oxide M0O3 in which the active sites are poisoned by CO2 but not by ammonia. 

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