• Journal of Environmental Health Sciences
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• 제15권2호
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• pp.97-106
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• 1989

This experiment was performed to study the acute toxic effects of mereuric chloride(HgCl$_{2}$) in goldfish (Carassius aurams). In the study, Lc$_{50}$ values were determined for each 24, 48, 72 ,and 96-hr and mercury bioassay during the tests were performed. in five parts gill, kidney, liver, muscle and egg. The results isummarized were as follows 1. In the range of acute lethal toxicity for goldfish was 0.15-1.50 mg/l and the Lc$_{50}$ values decreased with exposure time. 2. The Lc$_{50}$ values of HgCl$_{2}$ for goldfish at 24, 48, 72 and 96 hour were 0.64, 0.53, 0.46, and 0.39 mg/l, respectively. 3. In the 400 $\mu$g/l treatment group, the average levels of mercury residues in the gill, kidey, liver, muscle and egg during 96 hour were 107.02 $\mu$g/g, 8.65 $\mu$g/g, 6.87 $\mu$g/g, 0.61 $\mu$g/g, and 0.82 $\mu$g/g, respectively. 4. The mercuny residues of gill was up to 12-175 times greater than mercury contents found in the other tissues.

• Toxicological Research
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• 제16권1호
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• pp.63-66
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• 2000

The effects of acute ethanol on the high K+ induced $Ca^{2+}}$ signals were examined from primary cultures of cerebellar granule neurons. $Ca^{2+}}$ signals were measured with Calcium Green-1 based microscopic video imaging. Because $Ca^{2+}}$ signal was low in most of granule neurons without stimuli, high KCI was used for depolarization. In most case, acute exposure to ethanol reduced the peak amplitude of the $Ca^{2+}}$ signals, induced by high K+, even though low concentration of ethanol(2~10mM) was used and the effects lasted more than 30min. In was also possible to see differences of ethanol inhibition, i.e. the temporal pattern of $Ca^{2+}}$ signal reductions and the strength of inhibition of $Ca^{2+}}$ signals in cerebellar granule neurons. These results indicate that low concentration of ethanol has diverse actions on the $Ca^{2+}}$ signals in cerebellar granule neurons.

• International journal of thyroidology
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• 제10권1호
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• pp.50-55
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• 2017

Sweet's syndrome, or acute febrile neutrophilic dermatosis, occurs in association with autoimmune diseases such as Hashimoto's thyroiditis but is rare in Graves' disease, in which all cases are induced by propylthiouracil (PTU). We report a case of Sweet's syndrome in a patient with Graves' disease treated with methimazole (MMI) during three weeks. A 34-year-old man presented with the acute onset of high fever, skin rashes on the whole body, arthralgia, and acroparesthesia. Laboratory results showed leukocytosis and elevated C-reactive protein. MMI first stopped and antibiotics and antihistamine therapy started, but his symptoms dramatically improved after oral prednisolone. Graves' disease has again been treated by MMI because of his aggravated ophthalmopathy. After one year of retreatment with MMI, there has been no recurrence of Sweet's syndrome, supporting that Sweet's syndrome in this case was not related to MMI exposure. To our knowledge, this is the first report of Sweet's syndrome associated with Graves' disease per se but not PTU or MMI use.

• Asian Pacific Journal of Cancer Prevention
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• 제17권2호
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• pp.877-877
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• 2016

• Proceedings of the Korean Society of Toxicology Conference
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• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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• pp.107-107
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• 2002

It has been reported that antinatriuresis is induced by acute cadmium intoxication. However, the mechanisms related to the increase in renal sodium reabsorption by cadmium exposure is not clear yet although it has been suggested that the elevated aldosterone might involve in this process.(omitted)

• The Korean Nurse
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• 제23권2호통권125호
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• pp.29-36
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• 1984

Bone marrow transplantation has been recognized as one of the best methods in the treatment of patients with severe aplastic anemia, acute leukemia, chronic myelocytic leukemia, congenital immune deficiency syndrome and radiation exposure. While there are

• Korean Journal of Fisheries and Aquatic Sciences
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• 제50권4호
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• pp.388-395
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• 2017

We investigated the toxicity of zinc and aluminum hot-dip galvanized sheet steel to abalone Haliotis discus hannai via changes in the gill and hepatopancreas using histological and transmission electron microscopy analysis. Experimental groups were composed of one control and four exposure conditions (direct or indirect exposure to zinc and aluminum hot-dip galvanized sheet steel). In the control group, aluminum exposure groups (direct and indirect), and indirect zinc exposure group, abalone mortality was not observed until the end of the experiment, and no histopathological changes were observed in the gill and hepatopancreas. However, the direct zinc exposure group exhibited 100% mortality. Ultrastructural analysis of the cytoplasm of ciliated and microvilli-bearing epithelial cells from gill filaments revealed electron-dense vesicles near the cell membrane and disruption of the nuclear membrane. We also observed swollen mitochondria and a loss of mitochondrial cristae. The hepatopancreas showed similar changes, and we detected highly electron-dense particles within the vesicles. These results suggest that abalone exposed directly to zinc hot-dip galvanized sheet steel experience acute toxicity, causing damage to cell organelles in the gill and hepatopancreas and, finally, inducing mortality.

• Journal of Environmental Health Sciences
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• 제22권4호
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• pp.91-101
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• 1996

Exposure indices are important tools which enable scientists to reliably predict and detect exposures to xenobiotics and resultant cell injury. Since the de novo synthesis of stress proteins can be detected early after exposure to some agents, analysis of toxicant-induced changes in gene expression, i.e. alterations in patterns of protein synthesis, may be useful to develop as biomarkers of exposure and toxicity. The acute and chronic effects of cadmium(Cd, $CdCl_2$ 20 mg/kg) on Wistar male rats were evaluated concerning cadmium contents, tissues enzyme activity, HSP expression. The results of the study were as follows: 1. Less cadmium was absorbed through the digestive tracts, but the ratio of contents in renal to hepatic cadmium was higher at 8 weeks after treatment. 2. ALT(alanine aminotransferase), AST(aspartate aminotransferase), glucose, BUN(blood urea nitrogen), creatinine, the key indices of the clinical changes in hepatic and renal function were significantly changed by the cadmium treatment after 1 week in liver, after 4 weeks in kidney. 3. Enhanced synthesis of 70 KDa relative molecular mass proteins were detected in 2 hours after cadmium exposure, with maximum activity occurring at 8~48 hours. Induction of $HSP_{70}$ was evident at proximal tubules and glomeruli in kidney. Testicular cells produced enough HSP to be detected normally. From the above results, it could be concluded that $HSP_{70}$ induction by the cadmium treatment was a rapid reaction to indicate the exposure of xenobiotics.

• Journal of fish pathology
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• 제36권2호
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• pp.349-360
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• 2023

Common carp (Cyprinus carpio) (Weight 23.05 ± 6.98 g, Length 12.65 ± 1.38 cm) were exposed to waterborne nitrite at 0, 50, 100, 200, 400 and 800 mg NO₂ ^-/L for 96 hours. The lethal concentration 50 (LC₅₀) of C. carpio exposed to waterborne nitrite was 398.6 mg NO₂ ^-/L. Hemoglobin, hematocrit and RBC count were significantly decreased by waterborne nitrite exposure. The MCV (mean mean corpuscular volume) (µl), MCH (mean corpuscular hemoglobin) (pg) and MCHC (mean corpuscular hemoglobin concentration) (%) were significantly increased. The inorganic component, plasma calcium, was significantly increased, and the organic components such as plasma cholesterol and total protein were significantly increased showing a similar tendency with calcium. In enzymatic components, the AST and ALT were also significantly increased by nitrite exposure. The results of this study indicate that exposure to nitrite can affect the survival and hematological physiology of C. carpio.

• Biomolecules & Therapeutics
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• 제25권3호
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• pp.239-248
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• 2017

Desensitization and acute tolerance are terms used to describe the attenuation of receptor responsiveness by prolonged or intermittent exposure to an agonist. Unlike desensitization of G protein-coupled receptors (GPCRs), which is commonly explained by steric hindrance caused by the ${\beta}$-arrestins that are translocated to the activated receptors, molecular mechanisms involved in the acute tolerance of GPCRs remain unclear. Our studies with several GPCRs and related mutants showed that the acute tolerance of GPCRs could occur independently of agonist-induced ${\beta}$-arrestin translocation. A series of co-immunoprecipitation experiments revealed a correlation between receptor tolerance and interactions among receptors, ${\beta}$-arrestin2, and $G{\beta}{\gamma}$. $G{\beta}{\gamma}$ displayed a stable interaction with receptors and ${\beta}$-arrestin2 in cells expressing GPCRs that were prone to undergo tolerance compared to the GPCRs that were resistant to acute tolerance. Strengthening the interaction between $G{\beta}{\gamma}$ and ${\beta}$-arrestin rendered the GPCRs to acquire the tendency of acute tolerance. Overall, stable interaction between the receptor and $G{\beta}{\gamma}$ complex is required for the formation of a complex with ${\beta}$-arrestin, and determines the potential of a particular GPCR to undergo acute tolerance. Rather than turning off the signal, ${\beta}$-arrestins seem to contribute on continuous signaling when they are in the context of complex with receptor and $G{\beta}{\gamma}$.