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PubMed1975

Spongy degeneration in the central nervous system of domestic animals. Part III: Occurrence and pathogenesis hepatocerebral disease caused by hyperammonaemia.

Severe spongy degeneration of the central nervous system (CNS) was seen in 11 cattle, 19 sheep, 4 pigs and 1 goat, associated with a variety of hepatic diseases, particularly those caused by hepatotoxic pyrrolizidine alkaloids. It was also seen in a milder form in 2 of 8 horses examined, 1 dog of 5 dogs examined, and in 1 rabbit only of a large number of laboratory animals examined. This paper reports results of experiments which confirmed initially that the CNS disease cold be caused by pyrrolizidine alkaloid intoxication. This was done by poisoning lambs with lasiocarpine. As the disease was seen in hepatoses not caused by pyrrolizidine alkaloids, the hypothesis that CNS spongy degeneration in lambs could follow any hepatic disease irrespective of its cause, was tested by poisoning lambs with allyl formate, an hepatotoxin chemically unrelated to pyrrolizidine alkaloids. Three of 4 lambs poisoned by the allyl formate showed spongy degeneration in their brains. As the CNS spongy degeneration was an apparent form of hepatocerebral disease, an experiment was conducted to show that the neural disease in sheep was caused by hyperammonaemia. CNS spongy degeneration developed in the brains of all sheep infused intravenously with ammonium acetate, and advanced spongy changes developed in the sheep infused for more than 3 days. The cerebral changes were probably temporary, since sheep infused for 5 days and retained for 3 weeks showed marked regression of vacuolation. Hyperammonaemia caused by intravenous ammonium acetate infusion is a simple, rapid model of CNS spongy degeneration. The syndrome, CNS spongy degeneration caused by hepatic failure and hyperammonaemia, is probably one of the morphologic expressions of hepatocerebral disease in domestic animals and could be an analogue of similar congenital and hepatocerebral diseases in man.

Acetates↗
PubMed1981

The pathology of allyl chloride neurotoxicity in mice.

Allyl chloride is known to produce a neuropathy in man after occupational exposure to its vapour. The present study describes the neuropathy which develops in mice given allyl chloride by mouth. Mice were dosed three times weekly with 300 or 500 mg/kg allyl chloride for periods from 2-17 weeks. Functional disability was observed in some animals. Apart from evidence of focal kidney damage in 70% of dosed mice, pathological changes were restricted to the nervous system. Nerve fibre degeneration was found in many peripheral nerves and in roots, tending to be more marked distally and to affect more motor than sensory nerves. Degenerated fibres were also found in dorsal, ventral and lateral columns of the spinal cord. Males were more severely affected than females. Increased numbers of filaments were on early axonal change, occurring multifocally and apparently preceding axonal degeneration. No neuronal death was observed, but occasional anterior horn and dorsal root ganglion cells showed some morphological changes. Vacuolated lesions mainly due to swelling of astrocytes and their processes were found in the ventral horn in cervical and lumbar regions of spinal cord. Animals appeared to become tolerant to allyl chloride after continuous dosing. This neuropathy appears to be a central-peripheral distal type of axonopathy.

Allyl Compounds↗
PubMed1991

Access to fluorescent probes via allyl glycosides: the synthesis of a Brucella trisaccharide epitope linked to a coumarin.

Oligosaccharide allyl glycosides are demonstrated to provide a route to fluorescent probes and simple inhibitors. Ethyl 2-O-acetyl-4-azido-3-O-benzoyl-4,6-dideoxy-1-thio-alpha-D-mannopyranosid e (6) was used as glycosyl donor in the preparation of the trisaccharide [alpha-D-Rha p4NFo-(1----2)-]2-alpha-D-Rha p4NFo-O-allyl (16). Thioglycoside 6 was activated with N-iodosuccinimide and triflic acid or by bromine in the glycosylations and the inhibitor 16 was obtained after deprotection by transesterification, reduction of the azido groups with hydrogen sulfide, and N-formylation with ethyl formate. Ozonolysis of the allyl glycoside in 16 and reductive amination with 7-amino-4-methylcoumarin then gave the target fluorescent trisaccharide conjugate.

Allyl Compounds↗
PubMed1991

Inhalation exposure to 1,3-dichloropropene in the Dutch flower-bulb culture. Part II. Biological monitoring by measurement of urinary excretion of two mercapturic acid metabolites.

A biological monitoring study was carried out in the Dutch flower-bulb culture to determine the relationship between respiratory occupational exposure to Z- and E-1,3-dichloropropene (Z- and E-DCP) and urinary excretion of two mercapturic acid metabolites, N-acetyl-S-(Z- and E-3-chloropropenyl-2)-L- cysteine (Z- and E-DCP-MA). Urinary excretion of Z- and E-DCP-MA, either based on excretion rates or on creatinine excretion, followed first order elimination kinetics after exposure. Urinary half-lives of elimination were 5.0 +/- 1.2 hr for Z-DCP-MA and 4.7 +/- 1.3 hr for E-DCP-MA and were not statistically significantly different. Calculated coefficients of variation indicated that the half-lives of elimination of Z- and E-DCP-MA were quite consistent inter- and intra-individually. Strong correlations (r greater than or equal to 0.93) were observed between respiratory 8-hr time weighted average (TWA) exposure to Z- and E-DCP and complete cumulative urinary excretion of Z- and E-DCP-MA. Z-DCP yielded three times more mercapturic acid than E-DCP, probably due to differences in metabolism. Z- and E-DCP were excreted 45 and 14% as their respective mercapturic acid metabolites. A respiratory 8-hr TWA exposure to the Dutch occupational exposure limit of 5 mg.m-3 DCP would result in a complete cumulative excretion of 14.4 mg (95% confidence interval: 11.7-17.0 mg) Z-DCP-MA and 3.2 mg (95% confidence interval: 2.3-4.1 mg) E-DCP-MA.

Adult↗