Fatty acid ethyl esters: toxic non-oxidative metabolites of ethanol and markers of ethanol intake.

This report describes the biochemistry of fatty acid ethyl esters (FAEE), non-oxidative metabolites of ethanol, and their clinical significance. We review information regarding the enzymes responsible for FAEE synthesis and degradation, and the mechanisms involved with the intracellular and extracellular transport of FAEE and FAEE-mediated cytotoxicity. Also a summary of reports on the emerging clinical significance and diagnostic utility of FAEE as short and long-term markers of alcohol consumption, and the methodological aspects of FAEE assessment is included.

Organophosphorus ester-induced chronic neurotoxicity.

Organophosphorus compounds are potent neurotoxic chemicals that are widely used in medicine, industry, and agriculture. The neurotoxicity of these chemicals has been documented in accidental human poisoning, epidemiological studies, and animal models. Organophosphorus compounds have 3 distinct neurotoxic actions. The primary action is the irreversible inhibition of acetylcholinesterase, resulting in the accumulation of acetylcholine and subsequent overstimulation of the nicotinic and muscarinic acetylcholine receptors, resulting in cholinergic effects. Another action of some of these compounds, arising from single or repeated exposure, is a delayed onset of ataxia, accompanied by a Wallerian-type degeneration of the axon and myelin in the most distal portion of the longest tracts in both the central and peripheral nervous systems, and is known as organophosphorus ester-induced delayed neurotoxicity (OPIDN). In addition, since the introduction and extensive use of synthetic organophosphorus compounds in agriculture and industry half a century ago, many studies have reported long-term, persistent, chronic neurotoxicity symptoms in individuals as a result of acute exposure to high doses that cause acute cholinergic toxicity, or from long-term, low-level, subclinical doses of these chemicals. The author attempts to define the neuronal disorder that results from organophosphorus ester-induced chronic neurotoxicity (OPICN), which leads to long-term neurological and neurobehavioral deficits. Although the mechanisms of this neurodegenerative disorder have yet to be established, the sparse available data suggest that large toxic doses of organophosphorus compounds cause acute necrotic neuronal cell death in the brain, whereas sublethal or subclinical doses produce apoptotic neuronal cell death and involve oxidative stress.

[Acute poisoning with ethylene glycol esters]. / Ostrye otravleniia éfirami étilenglikolia.

The study was performed of 13 acute oral poisonings with ethylene glycol ethers characterized as moderate or severe and resulting in poor outcome in 3 cases. Ethyl ether was responsible for 3 poisonings, methyl ether for 10 ones. It was found, that the intoxication had four stages or periods (initial, latent, clinical, recovery) and presented with CNS impairment, gastrointestinal, hepatic, renal disorders, decompensated metabolic acidosis, etc. The paper describes two clinical cases and experimental toxicity of cellosolves as well as the effect of the inhibitor of isovaleric acid amide alcohol dehydrogenase on animal lethality. The results obtained support the suggestion of ADH-participated metabolic activation of cellosolves in the body. The prospects of further studies into intoxication pathogenesis and new opportunities for relevant poisoning management are outlined.