• Toxicological Research
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• v.31 no.1
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• pp.49-59
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• 2015

Eye is a highly vascularised organ. There are chances that a foreign substance can enter the systemic circulation through the eye and cause oxidative stress and evoke immune response. Here the eyes of rabbits were exposed, for a period of 7 days, to 5 known ocular irritants: Cetyl pyridinium chloride (CPC), sodium salicylate (SS), imidazole (IMI), acetaminophen (ACT) and nicotinamide (NIC). The eyes were scored according to the draize scoring. Blood collected from the treated rabbit were analyzed for haematological and biochemical parameters. After sacrifice, histological analysis of the eye and analysis of pro-inflammatory biomarkers ($IL-1{\alpha}$, $IL-1{\beta}$, IL-8 and $TNF-{\alpha}$) in the cornea using ELISA was carried out. Spleen was collected and the proliferation capacities of spleenocytes were analyzed. Liver and brain were collected and assessed for oxidative stress. The eye irritation potential of the chemicals was evident from the redness and swelling of the conjunctiva and cornea. Histopathological analysis and ELISA assay showed signs of inflammation in the eye. However, the haematological and biochemical parameters showed no change. Spleenocyte proliferations showed only slight alterations which were not significant. Also oxidative stress in the brain and liver were negligible. In conclusion, chemicals which cause ocular irritation and inflammation did not show any systemic side-effects in the present scenario.

• Parasites, Hosts and Diseases
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• v.50 no.4
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• pp.371-374
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• 2012

Toxoplasma gondii is one of the major agents of infectious abortions and due to its worldwide distribution can threat healthy pregnant women who had no previous exposure to this parasite. The present study was designed to investigate the contribution of T. gondii to spontaneous abortions in Zanjan, Northwest of Iran, using ELISA method. Blood Samples were collected from 264 mothers referred to the provincial hospitals of Zanjan due to spontaneous abortion. The sera were isolated and subjected to evaluate the anti-Toxoplasma IgG, IgM and IgA antibodies. The results showed IgG positive ($IgG^+$) in 99 cases (37.5%). A total of 68 women (25.8%) showed seroconversion with IgM or IgA or both IgM and IgA. They included: $IgM^+$ in 21 (8.0%), $IgA^+$ in 23 (8.7%) and both $IgM^+$ and $IgA^+$ in 24 (9.1%) subjects. In 23 cases, positive titers of IgM and IgG were accompanied. In general, the analysis of anti-Toxoplasma antibody patterns, showed that about 17% of the spontaneous abortions were associated with serological patterns of acute infection. According to these findings, a considerable proportion of spontaneous abortions can be attributed to T. gondii in the study area.

• Korean Journal of Pharmacognosy
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• v.10 no.2
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• pp.61-67
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• 1979

Two pure saponin components, Panax saponin C (protopanaxatriol derivative, ginsenoside Re) and Panax saponin E (protopanaxadiol derivative, ginsenoside $Rb_l$) were isolated from Panax ginseng root and their acute toxicities in mice and antistress effects in rats were investigated. Average lethal doses $(LD_{50})$ of ginsenoside Re were 130mg/kg (i.v.), more than 1,000mg/kg (i.p.) and more than 1,500mg/kg (s.c.), respectively. Average lethal dose of ginsenoside $Rb_{1}$ was 243mg/kg intravenously. Adrenal ascorbic acid and cholesterol contents were significantly decreased when normal rats were exposed to heat $(40^{\circ}C)$ for 30 min. The reduction of the adrenal ascorbic acid and cholesterol contents in rats was partially prevented when the rats received the ginseng saponins prior to exposure to heat stress and most pronounced effects were observed in rats received ginsenoside Re. However, it was found that administration of ginseng alone, without stress, did not significantly change the ascorbic acid and cholesterol contents in adrenal glands. Eosinophil counts in the blood of the rats were elevated when the rats were exposed to the heat stress, and the elevation of the eosinophil counts were prevented with the ginseng saponins under the stress, but the changes were all insignificant statistically.

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.2
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• pp.249-257
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• 2010

Crataegii Fructus is commonly used as a improving digestion, removing retention of food, promoting blood circulation and resolving blood stasis agent in East Asia. Cadmium (Cd) is widely distributed in the environment due to its use in industry. An exposure to Cd causes dysuria, polyuria, chest pain, hepatic and renal tubular diseases. The liver is the most important target organ when considering Cd-induced toxicity because Cd primarily accumulates in the liver. This study investigated the protective effect of Crataegii Fructus water extract against cadmium ($CdCl_2$, Cd)-induced liver toxicity in H4IIE cells, a rat hepatocyte-derived cell line and in rats. Cell viability was significantly reduced in Cd-treated H4IIE cells in a time and concentration-dependent manner. However, Crataegii Fructus water extract (CFE) protected the cells from Cd-induced cytotoxicity via inhibition of PARP cleavage. To induce acute toxicity in rats, Cd (4 mg/kg body weight) was dissolved in normal saline and intravenously injected into rats. The rats then received either a vehicle or silymarin (as a positive control) or CFE (50, 100 mg/kg/day) for 3 days, and were subsequently exposed to a single injection of Cd. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were significantly increased by Cd treatment. In contrast, pretreatment with CFE reduced ALT, AST and LDH. In histopathological analysis, CFE reduced the hepatic degenerative regions and the number of degenerative hepatocytes. These are considered as direct evidences that Crataegii Fructus has favorable inhibitory effects on the Cd-intoxicated liver damages. The efficacy of Crataegii Fructus shows slight lower than that of silymarin in the present study.

• Toxicological Research
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• v.31 no.2
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• pp.97-104
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• 2015

The skin exposure to solar irradiation and photoreactive xenobiotics may produce abnormal skin reaction, phototoxicity. Phototoxicity is an acute light-induced response, which occurs when photoreacive chemicals are activated by solar lights and transformed into products cytotoxic against the skin cells. Multifarious symptoms of phototoxicity are identified, skin irritation, erythema, pruritis, and edema that are similar to those of the exaggerated sunburn. Diverse organic chemicals, especially drugs, are known to induce phototoxicity, which is probably from the common possession of UV-absorbing benzene or heterocyclic rings in their molecular structures. Both UVB (290~320 nm) and UVA (320~400 nm) are responsible for the manifestation of phototoxicity. Absorption of photons and absorbed energy (hv) by photoactive chemicals results in molecular changes or generates reactive oxygen species and depending on the way how endogenous molecules are affected by phototoxicants, mechanisms of phototoxcity is categorized into two modes of action: Direct when unstable species from excited state directly react with the endogenous molecules, and indirect when endogeneous molecules react with secondary photoproducts. In order to identify phototoxic potential of a chemical, various test methods have been introduced. Focus is given to animal alternative test methods, i.e., in vitro, and in chemico assays as well as in vivo. 3T3 neutral red uptake assay, erythrocyte photohemolysis test, and phototoxicity test using human 3-dimensional (3D) epidermis model are examples of in vitro assays. In chemico methods evaluate the generation of reactive oxygen species or DNA strand break activity employing plasmid for chemicals, or drugs with phototoxic potential.

• Toxicological Research
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• v.31 no.2
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• pp.203-211
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• 2015

Trichloroacetonitrile is used as an intermediate in insecticides, pesticides, and dyes. In Korea alone, over 10 tons are used annually. Its oral and dermal toxicity is classified as category 3 according to the globally harmonized system of classification and labelling of chemicals, and it is designated a toxic substance by the Ministry of Environment in Korea. There are no available inhalation toxicity data on trichloroacetonitrile. Thus, the present study performed inhalation tests to provide data for hazard and risk assessments. Sprague-Dawley rats were exposed to trichloroacetonitrile at concentrations of 4, 16, or 64 ppm for 6 hour per day 5 days per week for 13 weeks in a repeated study. As a result, salivation, shortness of breath, and wheezing were observed, and their body weights decreased significantly (p < 0.05) in the 16 and 64 ppm groups. All the rats in 64 ppm group were dead or moribund within 4 weeks of the exposure. Some significant changes were observed in blood hematology and serum biochemistry (e.g., prothrombin time, ratio of albumin and globulin, blood urea nitrogen, and triglycerides), but the values were within normal physiological ranges. The major target organs of trichloroacetonitrile were the nasal cavity, trachea, and lungs. The rats exposed to 16 ppm showed moderate histopathological changes in the transitional epithelium and olfactory epithelium of the nasal cavity. Nasal-associated lymphoid tissue (NALT) and respiratory epithelium were also changed. Respiratory lesions were common in the dead rats that had been exposed to the 64 ppm concentration. The dead animals also showed loss of cilia in the trachea, pneumonitis in the lung, and epithelial hyperplasia in the bronchi and bronchioles. In conclusion, the no-observed-adverse-effect level (NOAEL) was estimated to be 4 ppm. The main target organs of trichloroacetonitrile were the nasal cavity, trachea, and lungs.

• The Journal of the Korean Society for Microbiology
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• v.22 no.4
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• pp.393-402
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• 1987

The halophilic bacterium Vibrio vulnificus, previously called lactose-positive(L+) Vibrio and Beneckea vulnifica, causes acute, fulminating wound infections and septicemia in humans. Septicemia is very serious infection with a fatality rate of about 50%. Most patients with primary septicemia due to V. vulnificus have preexisting liver disease. V. vulnificus also cause severe wound infections usually after trauma and exposure to marine animals or the marine environment. The mortality rate is not nearly as high as in primary septicemia caused by this organism. In most cases human disease results from ingestion of contaminated seafood or from infection of a wound, frequently of seawater or crab origin. The author made an attempt to isolation of the V vulnificus from seawater, seamud, fish, shellfish, and algae on the southern sea of Korea from January to September in 1987, using for the purpose of vaccine preparation. The author investigated for bacteriological identification, hemolysis and determination of serotypes of isolated V. vulnificus strains. Eighty-five strains(5.9%) out of 1450 specimens collected of V. vulnificus were isolated. The distribution of the 85 isolates were as follows: 21 strains from seawater, 11 strains from seamud, 28 strains from fish, 19 strains from shellfish, and 6 strains from algae, respectively. All 85 isolates were positive reaction on human blood agar. The distribution of serotypes of V. vulnificus isolates were O1 to O8: 13 strains of O1, 6 strains of O2, 11 strains of O3, 9 strains of O4, 10 strains of O5, 7 strains of O6, 15 strains of O7, and 10 strains of O8, respectively. Eighty-one strains showed agglutination with O antisera, but 4 strains failed to show agglutination. In this study, the author suspected that serotypes of V. vulnificus isolates distributed also in the seaside of Korea as well as in most seaside of the world, and new serotypes were in existence in the seaside of Korea except reported up to now.

• Journal of Radiation Protection and Research
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• v.14 no.1
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• pp.1-7
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• 1989

In order to evalulate the cause of polyuric acute tubular necrosis, we measured electrolytes, $Na^{+}\;and\;K^{+}$ excreted in urine, and activities of $Na^{+}-K^{+}$adenosine triphosphatase ($Na^{+}-K^{+}$ATPase) Excretion of $Na^{+}\;and\;K^{+}$ significantly increased in 24hr exposure on the uranyl nitrate and then decreased below the normal level after 3 days. The concentration of $Na^{+}\;and\;K^{+}$ in urines of the rats treated uranyl nitrate was less than that of the normal rats. The activities of $Na^{+}-K^{+}$ATPase decreased only in the group treated with high dose group of uranyl nitrate (30mg/kg BW) on the 3rd day but were not changed in the low dose groups(5 mg/kg BW and 15mg/kg BW).

• Proceedings of the Korean Environmental Health Society Conference
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• 2004.06a
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• pp.173-177
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• 2004

The acute toxicities of two major anti-pathogenic veterinary medicines, i.e., ciprofloxacin and enrofloxacin, and six benzimidazole anthelmintics, i.e., albendazole, thiabendazole, flubendazole, febantel, fenbendazole, and oxfendazole, were evaluated with a marine bacterium, Vibrio fischeri, and invertebrate Daphnia magna. These veterinary medical products have been widely used for farm animals, but their impact on aquatic fauna has seldom been investigated. In general, daphnids responded as much as 3 orders of magnitude more sensitively to the tested pharmaceuticals than the microbes. For Daphnia, the most toxic product among the tested anthelmintics was fenbendazole, followed by flubendazole > albendazole ${\approx}$ febantel > thiabendazole > oxfendazole. Daphnids' EC50 values obtained from 48 to 96 hrs of fenbendazole exposure ranged from 2.7 to 6.3 ug/L. The mixture toxicity of the test pharmaceuticals was generally additive in nature and was well predicted by a concentration addition model. Using the predicted no effect concentrations (PNECs) of the benzimidazole derivatives estimated from this study, and predicted environmental concentrations (PECs) of these pharmaceuticals, the risk quotients of each anthelmintics were calculated. Most of the test anthelmintic compounds resulted in risk quotients greater than 1. Especially, risk quotient for fenbendazole was 2,791, which strongly indicates this compound might cause severe ecological consequences, should no future action be taken. This study is the first report on the aquatic toxicities and potential ecological risk of major anthelmintic and antimicrobial veterinary products in Korea. The result of this study provides information necessary for conducting more detailed ecological risk assessment of pharmaceutical products in ambient water and guiding proper management decision.

• Molecules and Cells
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• v.20 no.2
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• pp.189-195
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• 2005

Ethanol has long been implicated in triggering apoptotic neurodegeneration. We examined the effects of ethanol on the rat brain during synaptogenesis when a spurt in brain growth occurs. This period corresponds to the first 2 postnatal weeks in rats and is very sensitive to ethanol exposure. Ethanol was administered subcutaneously to 7-day- postnatal rat pups by a dosing regimen of 3 g/kg at 0 h and again at 2 h. Blood ethanol levels peaked ($677{\pm}16.4mg/dl$) at 4 h after the first ethanol administration. The cerebral cortexes of the ethanol-treated group showed several typical symptoms of apoptosis such as chromosome condensation and disintegration of cell bodies. Activated caspase-3 positive cells were found in the cortex within 2 h of the first injection, and reached a peak at 12 h. In addition, TUNEL staining revealed DNA fragmentation in the same regions. These results demonstrate that acute ethanol administration causes neuronal cell death via a caspase-3-dependent pathway within 24 h, suggesting that activation of caspase-3 is a marker of the developmental neurotoxicity of ethanol.