• Journal of environmental and Sanitary engineering
• /
• v.14 no.2
• /
• pp.8-17
• /
• 1999

This research employed a senescence-accelerated mouse(SAM) to explore the possibility that differences exist among the major antioxidatns, lipid peroxidation in terms of ability to protect such animal treatment PQ, SAM-R/1 and SAM-P/8 were administered with PQ(200ppm/Kg) orally. The toxicity of PQ on SAM was determined as a bioassays of SOD, catalase and lipid peroxidation in the mouse liver. The data show that the SOD activity was induced by paraqwuat terement in both SAM-R/1 and SAM-P/8. The degree of lipid peroxidation was increased with PQ treatment. This means that SOD rather than catalase may protect against oxygen radical toxicity. Finally, over data lead to the toxicity of PQ and its function may efect to the antioxidants including SOD, catalase and lipid peroxidation in both SAM-R/1 and SAM-P/8 .

• YAKHAK HOEJI
• /
• v.23 no.3_4
• /
• pp.173-179
• /
• 1979

A dose, 1g/kg of ethanol produced experimental hyperuricemia in mouse. Ginseng saponins were tested for their ability to alter the hepatic xanthine oxidase activity and the blood level of uric acid in the ethanol-treated mouse. Intraperitoneal injection of ginseng saponin 4mg/kg markedly decreased the xanthine oxidase activity in the ethanol-treated mouse liver. It was also observed that ginseng saponin reduced the blood concentration of uric acid in experimentally induced hyperuricemia by alcohol treatment. In vitro, it was found that a low concentration of ginseng saponin in the reaction mixture incresed the hepatic xanthine oxidase activity, while a high concentration inhibited both enzyme preparations of normal and ethanol treated mice. In contrast with the xanthine oxidase, uricase activity was not influenced by ginseng saponin as well as in vivo. These results suggest there is a possibility that ginseng saponin may have some therapeutic effect on gout and other hyperuricemia syndrome.

• Biomolecules & Therapeutics
• /
• v.3 no.3
• /
• pp.229-232
• /
• 1995

In order to study if Glycyrrhizae Radix (GR) has protective effects on hepatotoxicity of acetaminophen in mouse, one of the species which are sensitive to acetaminophen-induced hepatotoxicity, effects of GR on liver weight to body weight ratio, serum alanine and aspartate transaminase (ALT and AST) activities, hepatic UDP-GT2 activity, and histopathologic changes were determined in acetaminophen-treated mice. Liver weight to body weight ratio and UDP-GT2 activity in mouse liver were not altered by GR. However, GR pretreatment lowered serum ALT and AST activities by 77% and 90% respectively, and diminished the degree of centrilobular necrosis caused by acetaminophen in liver as determined by histopathologic observation. These results suggest a possible protective effect of GR against the acetaminophen-induced hepatotoxicity in mice.

• Journal of Sasang Constitutional Medicine
• /
• v.8 no.2
• /
• pp.219-238
• /
• 1996

Effects of Taeyeumjoweetang on the obestity of mouse induced by gold thioglucose. It is researched to elucidate the effects of Taeyeumjoweetang on the obesity of mouse induced by gold thioglucose and the differentiation and growth of preadipocyte, 3T3-L1 cell. The result were as follows. 1. Taeyeumjoweetang extract improved the blood level of transaminase changed by the obesity of mouse induced by gold thioglucose. 2. Taeyeumjoweetang extract inhibited the increase of liver fat and body fat induced by the obesity of mouse induced by gold thioglucose. 3. Taeyeumjoweetang extract inhibited the increase of body weight induced by the obesity of mouse induced by gold thioglucose. 4. Taeyeumjoweetang extract inhibited the growth of undifferentiate preadipocyte 3T3-L1. 5. Taeyeumjoweetang extract showed the effects of inhibition on the differentiation of preadipocyte 3T3-L1. The above results suggested that the Taeyeumjoweetang extract may be used on the obesity induced by the overgrowth and differentiation of adipocyte, and the accumulation of fat in liver and body.

• Toxicological Research
• /
• v.22 no.4
• /
• pp.365-373
• /
• 2006

The present study was designed to characterize the effects of estrogen receptor agonist (4,4',4'-(4-Propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol, PPT) on liver and kidney in male mouse using a light microscopic analysis. PPT was subcutaneously given to adult male mice at a weekly dosage of 178.6mg/kg in a volume 0.08 ml of vehicle for 3, 5 and 8 weeks. There were differences in body and organ weights between control and the treated groups. Body and kidney weights were decreased in treated group whereas, liver weight was increased. In microscopic observations, sinusoidal diameter in liver of treated group was increased 156%, 216% and 255% on week 3, 5 and 8 respectively. Compared to the control, diameter of proximal convoluted tubules in kidney was increased 37% and 43% or week 5 and 8 in treated group. Whereas, height of epithelial cells in the proximal tubules was reduced at all time points. These results suggest that microstructure of liver and kidney was changed by treatment of estrogen receptor agonist PPT in the male mice.

• Korean Journal of Veterinary Research
• /
• v.18 no.2
• /
• pp.87-95
• /
• 1978

Election microscopic investigation were conducted on the mature mouse (B.W. about 25g) liver which was treated with Ginseng water extract during three, six and nine days respectivelly after carbon tetracholride injection into abdominal cavity. The results obtained were as follows: The liver cells of control group treated with carbon tetrachloride alone were restored slowly. The liver cells of experimental group treated with Ginseng water extract after carbon tetrachloride injection, however, were shown the appearance of well-developed ${\gamma}-ER$ and Golgi complex, marked aggregation of glycogen particles, and a number of large lipid droplets which are attached markedly with glycogen particles as compared to the control group. As these findings, it could be suggested that Ginseng gives an activation to restore the damaged liver cells.

• Clinical Nutrition Research
• /
• v.12 no.2
• /
• pp.154-167
• /
• 2023

Hepatic encephalopathy (HE) associated with liver failure is accompanied by hyperammonemia, severe inflammation, depression, anxiety, and memory deficits as well as liver injury. Recent studies have focused on the liver-brain-inflammation axis to identify a therapeutic solution for patients with HE. Lipocalin-2 is an inflammation-related glycoprotein that is secreted by various organs and is involved in cellular mechanisms including iron homeostasis, glucose metabolism, cell death, neurite outgrowth, and neurogenesis. In this study, we investigated that the roles of lipocalin-2 both in the brain cortex of mice with HE and in Neuro-2a (N2A) cells. We detected elevated levels of lipocalin-2 both in the plasma and liver in a bile duct ligation mouse model of HE. We confirmed changes in cytokine expression, such as interleukin-1β, cyclooxygenase 2 expression, and iron metabolism related to gene expression through AKT-mediated signaling both in the brain cortex of mice with HE and N2A cells. Our data showed negative effects of hepatic lipocalin-2 on cell survival, iron homeostasis, and neurite outgrowth in N2A cells. Thus, we suggest that regulation of lipocalin-2 in the brain in HE may be a critical therapeutic approach to alleviate neuropathological problems focused on the liver-brain axis.

• Nuclear Medicine and Molecular Imaging
• /
• v.43 no.5
• /
• pp.468-477
• /
• 2009

Purpose: Hydrodynamic-based procedure is a simple and effective gene delivery method to lead a high gene expression in liver tissue. Non-invasive imaging reporter gene system has been used widely with herpes simplex virus type 1 thymidine kinase (HSV1-tk) and its various substrates. In the present study, we investigated to image the expression of HSV1-tk gene with 5-(2-iodovinyD-2'-deoxyuridine (IVDU) in mouse liver by the hydrodynamicbased procedure. Materials and Methods: HSV1-tk or enhanced green fluorescence protein (EGFP) encoded plasmid DNA was transferred into the mouse liver by hydrodynaminc injection. At 24 h post-injection, RT-PCR, biodistribution, fluorescence imaging, nuclear imaging and digital wholebody autoradiography (DWBA) were performed to confirm transferred gene expression. Results: In RT-PCR assay using mRNA from the mouse liver, specific bands of HSV1-tk and EGFP gene were observed in HSV1-tk and EGFP expressing plasmid injected mouse, respectively. Higher uptake of radiolabeled IVDU was exhibited in liver of HSV1-tk gene transferred mouse by biodistribution study. In fluorescence imaging, the liver showed specific fluorescence signal in EGFP gene transferred mouse. Gamma-camera image and DWBA results showed that radiolabeled IVDU was accumulated in the liver of HSV1-tk gene transferred mouse. Conclusion: In this study, hydrodynamic-based procedure was effective in liver-specific gene delivery and it could be quantified with molecular imaging methods. Therefore, co-expression of HSV1-tk reporter gene and target gene by hydrodynamic-based procedure is expected to be a useful method for the evaluation of the target gene expression level with radiolabeled IVDU.

• Applied Biological Chemistry
• /
• v.38 no.2
• /
• pp.168-173
• /
• 1995

To investigate the effects of endosulfan on cytochrome P-450 enzymes in mouse(Balb c.), endosulfan was given by an intraperitoneal dose of 7.5 mg/kg. The treatment of endosulfan increased the cytochrome P-450 content by 3.3 to 4.2 fold, cytochrome $b_5$ content by 2.3 to 3.8 fold, NADPH cytochrome P-450 reductase activity by 5.3 to 6.4 fold and total haem content by 3.1 to 3.6 fold of mouse liver after 48 hrs of intraperitoneal injection. Endosulfan cytochrome P-450 absorption spectrum exhibited miximum at 387 nm and 389 nm and broad near 407 nm in the liver microsome. Reduced P-450-CO spectrum of the liver microsome exposed by the treatment of endosulfan showed maximum at 449 nm and 450 nm compared to that of the control having maximum at 451 nm, which indicated endosulfan induced cytochrome P-450 new isozymes. Aldrin epoxidase activities in the mouse liver and kidney were increased by 2.8 and 2.1 fold by the treatment of endosulfan. Also 7-ethoxyresorufin dealkylase activities in the mouse liver and kidney were elevated by 1.7 and 1.8 fold by treatment of endosulfan.

• Journal of Environmental Health Sciences
• /
• v.48 no.2
• /
• pp.106-115
• /
• 2022

Background: Current research suggests that humans are exposed to microplastics through consumption of foods and beverages, the airway route, and a variety of other means. Objectives: We evaluated oxidative stress and inflammation from polyethylene microplastics (PE-MPs) in the neonatal liver through intragastric administration or intratracheal instillation in pregnant mice. Methods: PE-MPs were administered from gestational day 9 to postnatal day 7. The intragastric administration group (0.01 mg/mouse/day or 0.1 mg/mouse/day) and intratracheal instillation group (6 ㎍/mouse/day or 60 ㎍/mouse/day) of PE-MPs were administered. After sacrifice, the oxidative stress and inflammation of the neonatal livers were measured. Results: As a result of the oxidative stress caused by PE-MPs in the neonatal livers, glutathione peroxidase decreased in a concentration-dependent manner in the intragastric administration group compared to the control group and intratracheal instillation decreased in high concentration PE-MPs. The catalase level increased at high concentrations of intragastric administration and intratracheal instillation. To confirm the level of inflammation caused by PE-MPs, monocyte chemoattractant protein-1 and tumor necrosis factoralpha were increased compared to the control group except for intratracheal intilation-high concentration PEMPs. The C-reactive protein level was decreased by intragastric administration compared to the control group and intratracheal instillation was increased compared to the control group. Conclusions: Despite the difficulty in comparing the toxic intensity between intragastric administration and intratracheal instillation of PE-MPs, our study revealed that oxidative stress and inflammation were induced in the neonatal liver. However, it is necessary to evaluate the toxic effects of microplastics on various organs as well. Overall, the present study indicates that the evaluation of toxic effects of long-term microplastic exposure, potential of microplastic toxicity on next-generation offspring and toxicity mechanism in human should be considered for further investigations.