Studies of Triorthocresyl Phosphate Neuropathy, Morocco 1960

Svennilson, E.

doi:10.1111/j.1600-0447.1961.tb08416.x

Cited by 4 publications

(2 citation statements)

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“…In the 1920s about 20,000 persons in the United States developed "Ginger-Jake" paralysis after the consumption of an extract of ginger called "Jamaica Ginger" that had been adulterated with TOCP (13-21). Later this syndrome was recognized in Europe, South Africa, and India as a result of the deliberate or accidental use of TOCP-containing preparatio � ns (22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34). In 1951 three persons were poisoned with a then newly developed insecticide, mipafox, and developed symptoms of delayed neurotoxicity (35).…”

Section: Historymentioning

confidence: 99%

Organophosphorus Ester-Induced Delayed Neurotoxicity

Abou‐Donia¹

1981

Annu. Rev. Pharmacol. Toxicol.

395

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In certain animals, including humans, exposure to some organophosphorus esters causes delayed neurotoxicity (OPIDN). The clinical condition becomes manifest after a delay period, first as ataxia, followed by paralysis. Lesions are characterized by degeneration of axons with subsequent secondary degeneration of myelin in the peripheral and central nervous systems. Recovery is only likely in mild cases, whereas more severe cases show symptoms of an upper motor neuron lesion in the lower limbs. The risk of use of these chemicals is related not only to human sensitivity to this syndrome, but also to the fact that in most disasters involving OPIDN, humans were the prime victims. Therefore, the neurotoxic action of a chemical is of great significance, since pesticides with this property are not recommended for use. Although OPIDN has been recognized for over a half a century, its mechanism of action is still unknown. It is believed, however, that the initial target in OPIDN is the phosphorylation of a neurotoxicity target protein in the nervous system. Study of the relationship between the chemical structure of organophosphorus esters and their neurotoxic potencies suggests that two hydrophobic areas may be present in the vicinity of the active site of the neurotoxicity protein. This article attempts to present an up-to-date overview of OPIDN. Despite the difficulties attributed to experimental variations of the reported studies, I feel that several significant points have come forth from the data.

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Section: Historymentioning

confidence: 99%

Organophosphorus Ester-Induced Delayed Neurotoxicity

Abou‐Donia¹

1981

Annu. Rev. Pharmacol. Toxicol.

395

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show abstract

“…Besides, blood and urinary lead levels were normal in our patient. A causative role of TOCP is unlikely, as pyramidal signs, commonly observed in TOCP intoxication, were absent (Svennilson, 1961, Hopkins, 1975. Another hypothesis is that our patient's neu ropathy might be due to hydrocarbons.…”

Section: Discussionmentioning

confidence: 99%