carbon disulfide/ضمور

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Carbon disulfide effects on the visual system. II. Retinogeniculate degeneration.

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We examined the morphological effects of carbon disulfide exposure on neurons and vasculature of the visual system of macaque monkeys. Five monkeys were exposed to 256 ppm carbon disulfide (CS2) by inhalation for 6 hr a day, 5 days a week. One monkey, sacrificed immediately after exposure, had

Multiple system atrophy following chronic carbon disulfide exposure.

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Carbon disulfide toxicity is well characterized. The principal target organ is the nervous system, although cardiovascular, reproductive, ophthalmologic, and other effects are also recognized. The neurotoxicity manifests in three ways: encephalopathy, peripheral and cranial nerve dysfunction, and

Cerebellar atrophy as a delayed manifestation of chronic carbon disulfide poisoning.

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A 70-year-old man developed a slowly progressive cerebellar syndrome after having been exposed to carbon disulfide (CS2) in a viscose rayon plant for 27 years. Ataxia, dysmetria, dysarthria and adiadochokinesia appeared 7 years after retirement from work (at age 54), and were later accompanied by

Femtosecond degenerate four-wave mixing of carbon disulfide: high-accuracy rotational constants.

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Femtosecond degenerate four-wave mixing (fs-DFWM) rotational coherence spectroscopy (RCS) has been used to determine the rotational and centrifugal distortion constants of the 00 (0)0 ground and 01 (1)0 vibrationally excited states of gas-phase CS(2). RCS transients were recorded over the 0-3300 ps

Carbon disulfide neuropathy in rats. A morphological and ultrastructural study of degeneration and regeneration.

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The aim of this study was to elucidate the site and detailed nature of peripheral nerve damage induced in the rat by chronic CS2 inhalation exposure in the light of the relationship between pathological and neurophysiological data. Adult male rats were exposed to 700 ppm of CS2 2 h/d, 5 d/week for

Degeneration of the basal ganglia in monkeys from chronic carbon disulfide poisoning.

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Carbon disulfide neurotoxicity in rats: VI. Electrophysiological examination of caudal tail nerve compound action potentials and nerve conduction velocity.

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The effects of subchronic exposure to carbon disulfide (CS2) on ventral caudal tail nerve compound nerve action potential (CNAP) amplitudes and latencies, and nerve conduction velocity (NCV) in rats were examined. Male and female Fischer 344 rats were exposed to 0, 50, 500, or 800 ppm CS2 for 6

Carbon disulfide neurotoxicity in rats: IV. Increased mRNA expression of low-affinity nerve growth factor receptor--a sensitive and early indicator of PNS damage.

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Expression of the low-affinity nerve growth factor receptor (NGF-R) in the peripheral nervous system is regulated by Schwann cell-axonal contact. Steady-state mRNA levels for NGF-R are very low in the mature peripheral nervous system, but are markedly upregulated in sciatic nerve during both primary

The morphology of carbon disulfide neurotoxicity.

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The morphology of carbon disulfide induced peripheral neuropathy was studied in rats exposed to three concentrations of carbon disulfide by inhalation for 90 days. Rats exposed to 800 ppm developed neurofilamentous axonal swellings in the distal portions of long fibers, including the dorsal

Acrylamide and carbon disulfide treatments increase the rate of rat brain tubulin polymerization.

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Acrylamide and carbon disulfide produce central-peripheral distal axonopathy in experimental animals and humans. The main feature of this disease is the focal swellings containing neurofilaments in distal axons, followed by nerve degeneration beyond these swellings. We studied the possible role of

Carbon disulfide effects on the visual system. I. Visual thresholds and ophthalmoscopy.

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The visual effects of carbon disulfide exposure were studied in macaque monkeys with measurements of visual thresholds, fluorescein angiography and fundus photography. Five monkeys were exposed by inhalation for 6 hr a day, 5 days a week to 256 ppm carbon disulfide (CS2). The motor dysfunction

Carbon disulfide exposure and neurotoxic sequelae among viscose rayon workers.

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In Norway's only viscose rayon plant, carbon disulfide (CS2) concentrations in ambient air usually were between 30 and 50 mg/m3 during the first 23 years of production. From 1970/1971 until the factory was closed in 1982, corresponding values were 10-25 mg/m3. Through all of these years, high peak

Pathogenetic studies of hexane and carbon disulfide neurotoxicity.

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Two commonly employed solvents, n-hexane and carbon disulfide (CS2), although chemically dissimilar, result in identical neurofilament-filled swellings of the distal axon in both the central and peripheral nervous systems. Whereas CS2 is itself a neurotoxicant, hexane requires metabolism to the

Histochemical and electron microscopic observations on the myoneural junctions of rats with carbon disulfide induced polyneuropathy.

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Myoneural junctions in the tibialis anterior muscle of rats with clinical signs of polyneuropathy induced with carbon disulfide were studied by light and electron microscopy. Histochemically demonstrable acetylcholinesterase (AChE; E.C. 3.1.1.7) activity was distributed similarly in the myoneural

Carbon disulfide induced polyneuropathy: sural nerve pathology, electrophysiology, and clinical correlation.

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We report the clinical features, electrophysiological studies, sural nerve pathology and recovery course of carbon disulfide-(CS2) induced polyneuropathy in a 48-year-old man who worked in a viscose rayon plant. Sural nerve biopsy 2 years later still showed degeneration of both axon and myelin with

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