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hexane/atrofi

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Testicular and germ cell line morphology in rats were studied 2 weeks, 10 months and 14 months after cessation of a 61-day inhalation exposure to 1000 ppm n-hexane. Androgen biosynthetic capacity of testis, testosterone blood concentration, vas deferens morphology and noradrenaline (NA)

Degeneration in central and peripheral nervous systems produced by pure n-hexane: an experimental study.

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Rats intoxicated with pure n-hexane, either by repetitive subcutaneous injection or by continuous inhalation, developed clinical and/or pathological evidence of peripheral neuropathy. Animals intoxicated by inhalation (400-600 ppm) developed clinical signs after forty-five days and displayed giant

2,5-Hexane diol induced thymic atrophy and lymphocytotoxicity in rats.

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Central and peripheral nervous system degeneration produced by pure n-hexane.

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Paramagnetic spin-lattice relaxation (SLR) in radical cations (RCs) of the cycloalkane series in liquid solution was studied and analyzed from the point of view of the correlation between the relaxation rate and the structure of the adiabatic potential energy surface (PES) of the RCs. SLR rates in

Degenerate electron exchange reaction of n-alkane radical cations in solution.

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The degenerate electron exchange (DEE) reaction involving radical cations (RCs) of n-nonane, n-dodecane, and n-hexadecane in n-hexane solution was studied over the temperature range 253-313 K using the method of time-resolved magnetic field effect in recombination fluorescence of spin-correlated

Toxic neurofilamentous axonopathies -- accumulation of neurofilaments and axonal degeneration.

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A number of neurotoxic chemicals induce accumulation of neurofilaments in axonal swellings that appear at varying distances from the cell body. This pathology is associated with axonal degeneration of different degrees. The clinical manifestation is most commonly that of a mixed motor-sensory

n-Hexane neuropathy caused by addictive inhalation: clinical and electrophysiological features.

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To assess the clinical and electrophysiological features of n-hexane neuropathy caused by addictive inhalation, 4 patients were studied in the progressive phase. The neurological manifestations were characterized by subacute predominantly motor polyneuropathy and disease progression despite

N-hexane neuropathy in offset printers.

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In an offset printing factory with 56 workers, 20 (36%) developed symptomatic peripheral neuropathy due to exposure to n-hexane. Another 26 workers (46%) were found to have subclinical neuropathy. The initial change in the nerve conduction study was reduced amplitude of the sensory action

Effects of chronic n-hexane exposure on nervous system-specific and muscle-specific proteins.

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Two kinds of nervous system-specific and muscle-specific proteins, enolase and S-100 protein, were quantitatively determined in peripheral nerves and skeletal muscles of rats chronically exposed to a neurotoxic solvent - n-hexane. Three groups of animals were exposed to n-hexane vapor at three

Biphasic recovery in n-hexane polyneuropathy. A clinical and electrophysiological study.

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We studied the course of recovery in n-hexane polyneuropathy in 4 patients by quantitatively assessing clinical and electrophysiological features. The electrophysiological study included measures of motor conduction of the median, ulnar, tibial and peroneal nerves and sensory conduction of the

NTP technical report on the toxicity studies of of n-Hexane in B6C3F1 Mice (Inhalation Studies) (CAS No. 110-54-3).

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Thirteen-week inhalation toxicity studies of n-hexane were conducted with B6C3F1 mice of each sex exposed to 0, 500, 1,000, 4,000, or 10,000 ppm, 6 hours per day, 5 days per week or to 1,000 ppm, 22 hours per day (referred to as 1,000c), 5 days per week. All mice lived to the end of the studies. The

Uncoupling of cerebral glucose supply and utilization after hexane-2,5-dione intoxication in the rat.

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Chronic administration of hexane-2,5-dione (2,5-HD) to rats causes an accumulation of neurofilaments within axons that may lead to their degeneration. This occurs in both the CNS and PNS. It has been suggested that one of the effects of 2,5-HD is an impairment of glucose utilization arising from an

Effects of respiratory treatment with N-hexane on rat testis morphology. I. A light microscopic study.

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Testicular damage was induced in rats by respiratory treatment with n-hexane at a concentration of 5000 ppm. The earliest lesions were observed immediately after 24 hr of continuous treatment, and involved primary spermatocytes from the leptotene to the middle pachitene stages and spermatids at late
The inhibitory effect of the Klebsiella pneumoniae ATCC 13883 strain caused by the hexane extract of Halimeda discoidea (Nor Afifah et al., 2010) was further evaluated by means of the microscopy view and its growth curves. The morphological changes of the K. pneumoniae ATCC 13883 cells were observed
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