• Journal of Veterinary Clinics
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• v.36 no.5
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• pp.278-281
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• 2019

A 12-year-old castrated male Maltese dog was presented with a small-sized mass at the left fifth mammary gland. The dog had concurrent poorly responsive pruritus affecting the feet, pinnae, and trunk, a cystolith, and biliary sludge. Serum chemistry revealed elevated liver enzymes. The mammary gland mass was cytologically diagnosed as an early-stage mammary simple carcinoma and was surgically excised. Nine months after the diagnosis of the mammary carcinoma, hyperadrenocorticism was confirmed by adrenocorticotropic hormone stimulation test. This report describes the clinical signs, diagnostic imaging findings, and prognosis in a castrated male Maltese dog with mammary carcinoma.

• Radiation Oncology Journal
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• v.22 no.4
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• pp.280-287
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• 2004

Purpose: This study was carried out to determine the protective effects of vitamin C on the hepatotoxicily induced by radiation. Materials and Methods : The Spraque Dawley rats were randomly divided into 3 groups; the control group, the radiation exposed group, aud the radiation and vitamin C-treated group. SOD activity, ca-talase, malondialdehyde and liver enzymes were analyzed to assess the antioxidant effects of vitamin C. Results: The increased level of malondialdehyde and the decreased catalase activity that were induced by radiation were improved after vitamin C but there was no statistical significance among three groups. The superoxide dismutase activity of the liver was increased by vitamin C, but there were no statistically significant differences between the vitamin C-treated group and the non vitamin C-treated group. The level of liver enzymes in sera such as glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, lactate dehyrogenase and alkaline phosphatase were remarkably elevated by radiation. The levels of those enzymes were decreased in the vitamin C-treated group and statistical significance was noted for the GPT level ($p<0.01$). On the electromicrographic findings, the hepatic cell destruction was considerably decreased in the vitamin C-treated group. Conclusion: Vitamin C is thought to be an effective antioxidant against the hepatotoxicity induced by radiation.

• Pediatric Infection and Vaccine
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• v.24 no.3
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• pp.141-145
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• 2017

Purpose: Clinical and laboratory features of two Kawasaki disease (KD) groups were evaluated; the patient with pyuria and those without pyuria. Methods: From January 2015 to December 2016, the medical records of 140 (86 males and 54 females) inpatients with KD were retro-spectively analyzed. Results: Forty-eight KD patients (34.3%) presented with pyuria. KD patients with pyuria showed a higher level of C-reactive protein (CRP) and a higher proportion of elevated liver enzymes than those without pyuria. There were no differences in the proportions of unresponsiveness to intravenous immunoglobulin and coronary artery lesions between the two groups. Six KD patients (12.5%) with pyuria underwent a renal imaging study to rule out the possibility of a urinary tract infections. Thirty-two KD patients (66.7%) with pyuria received treatment with antibiotics in addition to the standard treatment for KD. Conclusions: KD patients with pyuria showed a higher level of CRP and elevated levels of liver enzymes than those without pyuria. These findings suggest that KD patients with pyuria have more severe systemic inflammation than those without pyuria.

• The Journal of Internal Korean Medicine
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• v.32 no.4
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• pp.487-496
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• 2011

Objectives : The aim of this study was to investigate the hepatoprotective effect of Soshiho-tang (SSH) in mouse primary liver cells against hydrogen peroxide ($H_2O_2$)-induced oxidative stress. We also elucidated the molecular mechanism of hepatoprotective effect by SSH. Methods : Cell viability, level of ALT, AST and LDH, intracellular ROS level, mRNA expression and activity of antioxidant enzymes were used to evaluate hepatoprotection of SSH against $H_2O_2$. Target gene expressions were analyzed by real-time PCR. Results : Pre-treatment with SSH for 1 hour prevented cytotoxicity against $H_2O_2$. $H_2O_2$-induced ROS level decreased under SSH pre-treatment. mRNA expression of GPx and SOD increased in SSH-treated cells. In addition, HSP72 and HSP40 gene expression were elevated under SSH-treatment. Conclusions : These results indicate that SSH protects mouse primary liver cells from $H_2O_2$-induced oxidative injury. This hepatoprotective activity of SSH is mediated by decreasing intracellular ROS and increasing antioxidant enzyme expression (GPx and SOD) and stress response protein (HSP72 and HSP40).

• Journal of Nutrition and Health
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• v.35 no.9
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• pp.919-925
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• 2002

Iron deficiency is a severe nutritional problem in the world. Coffee intake of the people is increasing every year and it can increase the loss of several essential body minerals including iron. Either iron deficiency or coffee intake may increase the oxidative stress of the body. However, the effect of iron deficiency and/or coffee intake on peroxidation have not been studied much. Therefore, the aim of this study was to investigate the effect of coffee intake on oxidative stress and antioxidative enzyme activities of iron-deficient rats. Forty-eight male rats of Sprague-Dawley strain were divided into two groups by dietary iron levels. Iron deficient group were fed 5 ppm iron diet and iron-sufficient group were fed 50 ppm iron diet. Each iron group were divided into three sub-groups by coffee levels (0%, 1%, 4%) included in the experimental diet. The experimental diets were fed for 4 weeks. The hemoglobin level was significantly low in iron deficient group and the level was exacerbated by high coffee intake. The malondialdehyde concentration of the plasma and liver were not affected by iron or coffee level in this study. However, plasma aspartate aminotransferase and alanine aminotransferase, the indicator of the liver damage, were increased by high coffee intake. The erythrocyte and liver superoxide dismutase (SOD) activities were elevated in iron deficient groups. Coffee intake increased erythrocyte SOD activity in iron sufficient groups. Glutathione peroxidase and catalase activities were not influenced much by either iron or coffee intake. In conclusion, high coffee intake in iron deficiency may not only increase the anemia symptoms, but also may increase the oxidative stress of the body.(Korean J Nutrition 35(9) : 919~925, 2002)

• Nutritional Sciences
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• v.7 no.2
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• pp.76-82
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• 2004

Pine needles are known as a traditional medicine and their ingestion has been shown to be beneficial to human beings. Following induction of the neoplastic process in rats by azoxymethane (AOM), we determined the effects of pine needle supplementation on colon carcinogenesis and on antioxidant systems in the blood and liver. Five week old male Fisher 344 rats were injected with AOM (15 mg/kg) once a week for two weeks. After the second injection, 18 rats were randomly assigned into two groups and were fed a casein-based high-fat diet (120 g fat and 1 g cholesterol/kg diet) with or without pine needle powder (10%w/w). After 6 weeks, rats receiving pine needle powder showed a 40% lower incidence of the number of colonic preneoplastic lesions (aberrant crypts) and a 52% lower incidence of aberrant crypt foci (p<0.01). A significantly elevated level of erythrocyte catalase activity was observed in the pine needle supplemented group (17.4$\pm$1.1 vs. 24.5$\pm$1.5, p<0.01). Pine needle supplementation also increased liver glutathione peroxidase activity (7.5$\pm$0.6 vs. 14.6$\pm$0.6, p<0.01). Other antioxidant parameters such as erythrocyte glutathione peroxidase, liver catalase activity, and plasma total antioxidant potential (TRAP), showed no statistical differences between the two groups. Our data demonstrate that pine needle supplementation improves the antioxidant system and suppresses the formation of colonic preneoplastic lesions in AOM-treated rats. This result provides additional insights into the chemo-preventative properties of pine needles.

• Genomics & Informatics
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• v.8 no.1
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• pp.41-49
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• 2010

Statins are competitive inhibitors of hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase and used most frequently to reduce plasma cholesterol levels and to decrease cardiovascular events. However, statins also have been reported to have undesirable side effects such as myotoxicity and hepatotoxicity associated with their intrinsic efficacy mechanisms. Clinical studies recurrently reported that statin therapy elevated the level of liver enzymes such as ALT and AST in patients suggesting possible liver toxicity due to statins. This observation has been drawn great attention since statins are the most prescribed drugs and statin-therapy was extended to a larger number of high-risk patients. Here we employed rat primary hepatocytes and microarray technique to understand underlying mechanism responsible for statin-induced liver toxicity on cell level. We isolated genes whose expressions were commonly modulated by statin treatments and examined their biological functions. It is of interest that those genes have function related to response to stress in particular immunity and defense in cells. Our study provided the basic information on cellular mechanism of statin-induced cytotoxicity and may serve for finding indicator genes of statin -induced toxicity in rat primary hepatocytes.

• Archives of Pharmacal Research
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• v.18 no.3
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• pp.189-194
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• 1995

The focus of this study was to investigate the influences of enzymatic scavengers of active oxygen metabolites and phospholipase $A_2$ inhibitor on hepatic secretory and microsomal function during hepatic ischemia/reperfusion. Rats were pretreated with free radical scavengers such as superoxide dismutase (SOD), catalase, deferoxamine and phospholipase $A_2$ inhibitor such as quinacrine and then subjected to 60 min. no-flow hepatic ischemia in vivo. After 1, 5 hr of reperfusion, bile was collected, blood was obtained from the abdominal aorta, and liver microsomes were isolated. Serum aminotransferase (ALT) level was increased at 1 hr and peaked at 5 hr. The increase in ALT was significantly attenuated by SOD plus catalase, deferoxamine and quinacrine especially at 5 hr of reperfusion. The wet weight-to-dry weight ratio of the liver was significantly increased by ischemia/reperfusion. SOD and catalase treatment minimized the increase in this ratio. Hepatic lipid peroxidiltion was elevated by ischemia/reperfusion, and this elevation was inhibited by free radical scavengers and quina crine. Bile flow and cholate output, but not bilirubin output, were markedly decreased by ischemia/reperfusion and quinacrine restored the secretion. Cytochrome $P_{450}$ content was decreased by ischemia/reperfusion and restored by free radical scavengers and quinacrine to the level of that of the sham operated group. Aminopyrine N-demethylase activity was decreased and aniline p-hydroxylase was increased by ischemia/reperfusion. The changes in the activities of the two enzymes were prevented by free radical scavengers and quinacrine. Our findings suggest that ischemia/reperfusion diminishes hepatic secretory functions as well as microsomal drug metabolizing systems by increasing lipid peroxidation, and in addition to free radicals, other factors such as phospholipase $A_2$ are involved in pathogenes of hepatic dysfunction after ischemia/reperfusion.

• BLOOD RESEARCH
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• v.53 no.4
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• pp.314-319
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• 2018

Background Iron overload is a risk factor affecting all patients with thalassemia intermedia (TI). We aimed to determine whether there is a relationship of serum ferritin (SF) and alanine aminotransferase (ALT) with liver iron concentration (LIC) determined by R2 magnetic resonance imaging (R2-MRI), to estimate the most relevant degree of iron overload and best time to chelate in patients with TI. Methods In this cross-sectional study, 119 patients with TI (mean age years) were randomly selected and compared with 120 patients who had a diagnosis of thalassemia major (TM). Correlations of LIC, as determined by R2-MRI, with SF and ALT levels, were assessed in all participants. A P-value <0.05 was considered statistically significant. Results SF and LIC levels were lower in patients with TI than in those with TM; only ferritin values were significant. We found a statistically significant relationship between SF and LIC, with cut-off estimates of SF in patients with TI who had splenectomy and those who entered puberty spontaneously (916 and 940 ng/mL, respectively) with LIC >5 mg Fe/g dry weight (P<0.0001). A significant relationship was also found for patients with TI who had elevated ALT level (63.5 U/L), of 3.15 times the upper normal laboratory limit, using a cut-off for LIC ${\geq}5mg\;Fe/g\;dry\;weight$. Conclusion We determined the cut-off values for ALT and SF indicating the best time to start iron chelation therapy in patients with TI, and found significant correlations among iron overload, SF, and ALT.

• The Korean Journal of Pharmacology
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• v.21 no.1
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• pp.1-11
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• 1985

The effects of feeding indole, indole-3-carbinol and benzofuran (all at 5 mmole/kg body wt./day) on various hepatic microsomal and cytosolic enzyme activities involved in xenobiotic metabolism have been compared. Benzofuran was found to elevate the activities of many enzymes both in microsomes (e.g., aniline hydroxylase, 7-ethoxycoumarin O-deethylase, p-nitrophenol UDPGA-transferase and epoxide hydrolase) and in cytosol (e.g., glutathione reductase, glutathione S-transferase, NADH:quinone reductase and UDP-glucose dehydrogenase). The structures of indole and indole-3-carbinol are similar to benzofuran except for the substitution of nitrogen with oxygen atom within the furan ring. Results showed that the activities of UDPGA-transferase and NADH:quinone reductase were not elevated by these indole compounds. While the chemical structure of these two indole compounds are identical except for the presence of the carbinol (methanol) group in indole-3-carbinol, there were marked differences in the types and activities of microsomal enzymes that were enhanced. Among the microsomal enzyme activities determined, indole elevated only the NADPH:cytochrome c reductase, while indole-3-carbinol increased several mixed function oxidase and particularly the epoxide hydrolase activities. Based on the chemical structures of tested compounds and the observed results, possible explanations for the mechanisms involved in elevating epoxide hydrolase activity by benzofuran and indole-3-carbinol are discussed.