• Toxicological Research
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• v.21 no.2
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• pp.141-150
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• 2005

1,3-Dichloro-2-propanol (1,3-DCP) is known as chloride chemicals and causes severe hepatotoxic agent. The Ito cells and Kupffer's cells of the liver in the 5 old F344 Rats were exposed to 1,3-DCP gas chamber for 6 hours/ a day, 5 days/ a week, and 13 weeks, in the 0, 5, 20, 80 ppm, respectively. After then the body weights, liver weights, and relative liver weight to body weight were measured, and the hepatic tissues were prepared by the routine and Immunostain method, and observed by the LM, and EM. In the results, there were severe body weight decrease (p<0.05) in the 80 ppm of the male and female rats. The relative liver weights to the body weight were increased relate with exposed 1,3-DCP concentration (P<0.001). Inflammatory cells, infiltration was observed at the perivascular area in the 20 ppm exposed group, and bilirubin pigment infiltration, bile duct hyperplasia, inflammation hepatocytic necrosis, fibrosis were observed in the 80 ppm exposure group. In the 80 ppm exposure group, disarrangement of the endothelial cells, erythrocytes and hepatic cell fragment in the Disse space and numerous migration macrophages were observed in the necrotic area by EM observation. In the immunostained hepatic tissues positive stained ED1 cells were extremely increased (P<0.05) in central vein area, but ED2 was weakly positive immunostained in the 80 ppm exposed group. Immunostained desmin was observed in the Ito cell. It was no difference in the low and medium exposed group but it was typical increase in the necrotic area. In conclusion, These results suggest that NOAEL of 1,3-DCP may be 5 ppm in rats and the Immunostained of desmin, ED1 and ED2 positive cells activated in the inflammatory liver were related to the exposure volume and density. The increase of the Ito cells were related to the severe phagocytosis of the Kupffer's cells.

• Journal of Chest Surgery
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• v.20 no.1
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• pp.1-12
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• 1987

Respiratory care with oxygen inhalation is often a necessity to maintain life, and it is one of the important therapeutic adjuncts in respiratory disease and in intensive care after surgery. However, it has been reported that oxygen toxicity occurs after prolonged exposure to 100% 0, [Smith, 1899; Kistler et al. 1967; Schaffner et al. 1967; Rowland and Newman, 1969. Subjective symptoms of oxygen toxicity include tracheal irritation, frequent cough, some burning sensation in the trachea, tachypnea, severe dyspnea, etc. [Welch, 1963; Fisher et al, 1968; Milier et al, 1970; Clark and Lambertsen, 1971; Sackner, 1975]. Pathologic findings are atelectasis, injuries to the pulmonary capillaries and hemorrhage in the alveoli in gross specimens. There can be inflammation, proliferation of fibrin, thickening of alveolar membranes, degeneration of collagen fibers and interstitial edema in the microscopic findings. [Penrod, 1956; Cedergren, 1959; Bean, 1965; Schaffner, 1967]. Dubois and colleagues [1961] found that the amount of pulmonary surfactant was decreased in oxygen toxicity and atelectasis followed by the decreased pulmonary surfactant. Many authors reported that vital capacity, inspiratory force, pulmonary compliance, pulmonary capillary blood flow and pulmonary elasticity were deceased and arteriovenous shunting increased. [Comroe et al, 1945; Fuson et al, 1965; Kistler et al, 1966; Knowles and Blenner-hassett, 1967; Barber et al, 1978]. Many human volunteers were examined after prolonged exposure in a high oxygenated chamber and there were a few reports on animals with oxygen toxicity, subjects including rabbits. Gas partial pressures of alveoli and arteries were measured in rabbits exposed to 100% $O_2$ and the alveolar-arterial gas gradients were analyzed, which is the basis for the study of oxygen toxicity. These rabbits were divided into two groups; rabbits under natural respiration, and second group under artificial respiration with a respirator. The alveolar $PO_2$ [$P]AO_2$] and $PCO_2$ [$PACO_2$], and the arterial $PO_2$ [$PaO_2$] were measured under varying $O_2$ pressures; 15% $O_2$, 21% $O_2$ and 100% $O_2$.

• Journal of Korean Neurosurgical Society
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• v.53 no.3
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• pp.139-144
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• 2013

Objective : Transient anterograde amnesia is occasionally observed in a number of conditions, including migraine, focal ischemia, venous flow abnormalities, and after general anesthesia. The inhalation anesthetic, isoflurane, is known to induce transient anterograde amnesia. We examined the involvement of brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) in the underlying mechanisms of the isoflurane-induced transient anterograde amnesia. Methods : Adult male Sprague-Dawley rats were divided into three groups : the control group, the 10 minutes after recovery from isoflurane anesthesia group, and the 2 hours after recovery from isoflurane anesthesia group (n=8 in each group). The rats in the isoflurane-exposed groups were anesthetized with 1.2% isoflurane in 75% nitrous oxide and 25% oxygen for 2 hours in a Plexiglas anesthetizing chamber. Short-term memory was determined using the step-down avoidance task. BDNF and TrkB expressions in the hippocampus were evaluated by immunofluorescence staining and western blot analysis. Results : Latency in the step-down avoidance task was decreased 10 minutes after recovery from isoflurane anesthesia, whereas it recovered to the control level 2 hours after isoflurane anesthesia. The expressions of BDNF and TrkB in the hippocampus were decreased immediately after isoflurane anesthesia but were increased 2 hours after isoflurane anesthesia. Conclusion : In this study, isoflurane anesthesia induced transient anterograde amnesia, and the expressions of BDNF and TrkB in the hippocampus might be involved in the underlying mechanisms of this transient anterograde amnesia.

• Environmental Mutagens and Carcinogens
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• v.23 no.3
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• pp.85-93
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• 2003

Welders working in a confined space, like in the shipbuilding industry, are at risk of being exposed to high concentrations of welding fumes and developing pneumoconiosis or other welding-fume exposure related diseases. Among such diseases, manganism resulting from welding-fume exposure remains a controversial issue, as the movement of manganese into specific brain regions has not been clearly established. Accordingly, to investigate the distribution of manganese in the brain after welding-fume exposure, male Sprague Dawley rats were exposed to welding fumes generated from manual metal arc stainless steel (MMA-SS) at concentrations of $63.6{\pm}4.1$ $mg/m^3$ (low dose, containing 1.6 $mg/m^3$ Mn) and $107.1{\pm}6.3$ $mg/m^3$ (high dose, containing 3.5 $mg/m^3$ Mn) total suspended particulates for 2 hrs per day, in an inhalation chamber over a 60-day period. Blood, brain, lungs and liver samples were collected after 2 hr, 15, 30, and 60 days of exposure and the tissues analyzed for their manganese concentrations using an atomic absorption spectrophotometer. Although dose- and time-dependent increases in the manganese concentrations were found in the lungs and livers of the rats exposed for 60 days, only slight manganese increases were observed in the blood during this period. Major statistically significant increases in the brain manganese concentrations were detected in the cerebellum after 15 days of exposure and up until 60 days. Slight increases in the manganese concentrations were also found in the substantia nigra, basal ganglia (caudate nucleus, putamen, and globus pallidus), temporal cortex, and frontal cortex, thereby indicating that the pharmacokinetics and distribution of manganese inhaled from welding fumes would appear to be different from those resulting from manganese-only exposure.

• Journal of Life Science
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• v.18 no.11
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• pp.1543-1550
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• 2008

We studied the effects of smoking, which is one of indoor-environmental pollutants and related to various cancers, on glycoconjugates of rat sebaceous glands with the lectin histochemistry. To investigate the effects of smoking on glycoconjugates, male Sprague-Dawley rats were exposed to tabacco smoke for 10 minutes per day in an inhalation chamber for 1, 2, 3, and 5 days with active and passive exposure. For the structure of sebaceous glands we used PAS reaction, and for the glycoconjugates binding pattern 9 biotinylated lectins (DBA, SBA, PNA, BSL-1, WGA, RCA-1, UEA-1, Con A, and LCA) were used. Some remarkable changes, such as the decrease in the size of sebaceous glandular acini, the destruction of upper portion of sebaceous glands, vacuolation of central portion of sebocytes, and the immature sebaceous glandular acini were seen in the smoke-exposed rats. In the control rats, basal cells were stained with BSL-1, PNA and WGA, but the stronger reaction was founded in BSL-1 binding. Also, sebocytes were stained with PNA, WGA, Con A, BSL-1 and SBA, but stronger reactions were founded in PNA and Con A stainings. Specific changes in the lectin binding patterns were also observed in the smoke-exposed rats. In the basal cells of exposed rats, PNA binding increased, BSL-1 decreased but returned to control level, and WGA disappeared. Plus, immature glandular acini, which were not found in the control rats, were stained PNA, Con A and BSL-1, but the stronger reaction were founded in PNA and Con A binding. In conclusion, it was assumed that the tabacco smoke seriously effected on the structure and glycoconjugates metabolism of sebaceous glands.

• Journal of the Korean Institute of Gas
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• v.17 no.4
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• pp.18-25
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• 2013

It may occur health hazards or death by suffocation or acute poisoning in case of oxygen deficiency in ambient or exposure to harmful gas. As a part of accident prevention, we studied the change of activity and lethal dose by changing the concentration of several hazardous gas with inhalation exposure chamber and laboratory animals. We investigated the lethality and motility change during either the 4 hrs whole body exposure to oxygen, nitrogen, toluene, $H_2S$, CO and 48 recovery. As results, it is estimated that 5% oxygen concentration as lethal concentration and 5.5% as $LC_{50}$ (rat, 4 hrs) with statistics for dose-response. The results of lethality in oxygen deficient condition (approximately 6%), the lethalities were 40%, 20% with 20 ppm $H_2S$, 600 ppm CO respectively, and was not increased the lethality with 8% CO. Thus, it was confirmed that the $H_2S$, CO had influence to lethal dose, while toluene had low fluence.