• Korean Journal of Food Science and Technology
• /
• v.28 no.5
• /
• pp.801-805
• /
• 1996

This study was performed to investigate the effect of serum enzyme activities in rats after administration of aluminum compound. Seventy five male Sprague-Dawley rats were divided into five groups consisting of control, $250\;ppm\;AlCl_3,\;500\;ppm\;AlCl_3,\;250\;ppm\;Al_2(SO_4)_3$ and $500ppm Al_2(SO_4)_3$ groups and kept on the diet for 2 weeks. The weight gain increased from 0.53 to 3.35% in $AlCl_3$ adiministration groups but decreased from 2.82 to 6.16% in $Al_2(SO_4)_3$, administration groups as compared to control group. As compared to control group, activities of lactate dehydrogenase (LDH) and aspartate amino transaminase (AST) in serum increased 29.43 to 57.68% and 0.68 to 9.97% in $AlCl_3$ adiministration groups, and 74.60 to 29.33% and 21.04 to 24.79% in $Al_2(SO_4)_3$ adiministration groups, respectively. However, alanine amino transminase (ALT) decreased from 12.69 to 25.42% in $AlCl_3$ adiministration groups and from 24.32 to 39.62% in $Al_2(SO_4)_3$ administration groups. Cholinesterase activity increased from 28.98 to 12.73% as compared to control group by administration of $AlCl_3$ and decreased from 3.93 to 14.48% by administration of $Al_2(SO_4)_3$.

• Journal of Life Science
• /
• v.18 no.10
• /
• pp.1342-1347
• /
• 2008

The purpose of present study was to investigate the protective effect of silkworm excrement powder (SEP) on alcohol-induced hepatotoxicity in rats. Semisynthetic diet supplemented with SEP (3%, w/w) given to alcohol-feeding rats for 30 days, then blood and tissues were collected, processed and used for alcohol concentration mensuration, various biochemical estimations and histopathological examination. Chronic alcohol administration resulted in significantly increase in the activities of the clinically important liver marker enzymes, alanine aminotransferase (ALT), aspartate aminotransferase (AST), $\gamma$-glutamyl transpeptidase ($\gamma$-GTP) and lactate dehydrogenase (LDH). Also, a highly significant increase in the blood alcohol level by alcohol treatment was observed. But alcohol-induced elevation of ALT and LDH levels markedly prevented and the level of blood alcohol decreased in SEP treated rats as compared to alcohol-administered control rats. SEP supplementation showed highly decreased the concentrations of total lipid, triglyceride and cholesterol in serum, as compared with alcohol treated control rats. Alcohol treatment induced the marked accumulation of large lipid droplets, hepatocytes necrosis and inflammation in the liver, but SEP administration attenuated to alcohol-induced accumulation of lipid droplets and hepatocyte necrosis. The results indicated that SEP may exert a protective effect against alcoholic hepatotoxicity through decreasing the activity of hepatic marker enzymes.

• Korean Journal of Clinical Laboratory Science
• /
• v.48 no.1
• /
• pp.1-7
• /
• 2016

The aim of this study was to evaluate the cytotoxicity of cadmium chloride ($CdCl_2$), toxicant, and the protective effect of Chelidonium majus (CM) extract on $CdCl_2$-induced cytotoxicity in cultured NIH3T3 fibroblasts. Cell viability, the effect of butylated hydroxytoluene (BHT) against $CdCl_2$, and the antioxidative effects including DPPH-free radical scavenging activity, superoxide anion-radical scavenging activity (SSA), and lactate dehydrogenase (LDH) activity were assessed. $CdCl_2$ caused a significant dose-dependent decrease in cell viability, and $XTT_{50}$ value was determined at 38.7uM of $CdCl_2$. It was determined as highly-toxic by Borenfreund and Puerner' toxic criteria. BHT of antioxidant significantly increased cell viability severely damaged by $CdCl_2$-induced cytotoxicity in these cultures. In the protective effect of CM extract on $CdCl_2$-induced cytotoxicity, CM extract significantly increased cell viability, DPPH-free radical scavenging activity, SSA and inhibitory activity of LDH. From these results, it is suggested that oxidative stress is involved in the cytotoxicity of $CdCl_2$, and CM extract showed protective efficacy on $CdCl_2$-induced cytotoxicity via antioxidative effects. Conclusively, natural resources like CM extract may be a putative antioxidative agent for the detoxification or diminution of toxicity correlated with oxidative stress.

• Toxicological Research
• /
• v.16 no.1
• /
• pp.47-52
• /
• 2000

To evaluate the renal toxicity of the antitumor agent, 1-(N-methyl) piperazinyl-3-phenyl-isoquinoline(CWJ-$\alpha$-5), rats were terated with CWJ-$\alpha$-5 (acute : 100mg/kg, i.p., single and subacute : 10mg/kr, i.p., daily for 7 days). The changes in the body weights, water consumption, kidney weights and urine volume after and during the treatment were observed. The concentrations of urinary creatinine, the activities of N-acetyl-$\beta$-D-glucosaminidase (NAG), alanine aminopeptidase (AAP), $\gamma$-glutamyl transpeptidase ($\gamma$-GT) and lactate dehydrogenase (LDH) in 24 hr urine were also determined. The body weight and water consumption were decreased after the acute and subacute administration. However, the excretion of urine was not changed except the 1 day after the acute treatment. The excretion of creatinine was significantly decreased from 1 day after acute administration and continuously decreased. Also the excretion of creatinine was decreased during subacute administration. However, the protein excretion did not changed in both treatment. Those indicate that CWJ-$\alpha$-5 might decrease the metabolic rate of muscle. The urinary activities of NAG, AAP, $\gamma$-GT, and LDH were significantly affected by the drug treatment. The urinary activities of NAG, AAP and $\gamma$-GT were significantly increased 1 and 3 days after the acute administration and then returned to the control value. However, the urinary activities of LDH were increased 7 days after acute treatment. During subacute treatment, the urinary activities of $\gamma$-GT were not changed. However, the urinary activities of NAG, AAP and LDH were only significantly increased after the third administration. These results indicate that either the high acute dose or the subacute administration with low dose of the compound might induce a temporal damage in the kidney cells.

• Journal of Preventive Medicine and Public Health
• /
• v.33 no.1
• /
• pp.117-124
• /
• 2000

Objectives : It is the objective of this study to compare hepatotoxicity of nickel chloride and cadmium chloride with each other through IPRL(Isolated Perfused Rat Liver) method. Methods : Biochemical indicator of hepatic function such as AST(aspartate aminotransferase), ALT(alanine aminotransferase), LDH(lactate dehydrogenase) and perfusion flow rate were used as the indicator of hepatotoxicity. Oxygen consumption rate were used as vability indicator. $300({\pm}50)g$ - weighted rats were allocated randomly to each group($0{\mu}M,\;50{\mu}M,\;200{\mu}M\;NiCl_2\;and\;CdCl_2$ exposure) by 5, totally 25. After Krebs-Ringer bicarbonate butler solution flowed into the penal vein and passed the liver cell, it flowed out of vena cava. Liver was administered with each $NiCl_2\;and\;CdCl_2$ of each concentration and observed with buffer solution sampling time. Butler which got out of liver was sampled and then biochemical indicator of hepatotoxicity was measured. Results : AST, ALT, and LDH in buffer increased with sampling time much more in $CdCl_2$ exposure group than $NiCl_2$ exposure group in both 50 and $200{\mu}M$ and statistical significance w3s verified with 2-way repeated ANOVA. Viability was decreased more and more in all substances during passed time. Conclusions : It is inferred that $CdCl_2$ has stronger hepatotoxicity than $NiCl_2$. IPRL method would be used widely for acute hepatotoxicity when considerating the benefit of it.

• Journal of Life Science
• /
• v.26 no.12
• /
• pp.1458-1465
• /
• 2016

We investigated the neuroprotective effect of an ethanol extract from Asparagus cochinchinensis (AC) against glutamate-induced toxicity in the HT22 hippocampal cell, which is an ideal in vitro model for oxidative stress. The neuroprotective effects of AC in HT22 cells were evaluated by analyzing cell viability, lactate dehydrogenase (LDH), flow cytometry for cell death types, reactive oxygen species (ROS), mitochondria membrane potential (MMP), and Western blot assays. In the cell death analysis, AC treatment resulted in significantly attenuated glutamate-induced loss of cell viability with a decrease in LDH release. AC treatment also reduced glutamate-induced apoptotic cell death. In the ROS and MMP analysis, AC treatment inhibited the elevation of intracellular ROS induced by glutamate exposure and the disruption of MMP. In oxidative stress-related proteins analysis, AC treatment inhibited the expression of poly ADP ribose polymerase and heme oxygenase-1 by glutamate. These results indicate that AC exerts a significant neuroprotective effect against glutamate-induced hippocampal damage by decreasing ROS production and stabilizing MMP. Thus, AC potentially provides a new strategy for the treatment of oxidative stress-related diseases.

• Tuberculosis and Respiratory Diseases
• /
• v.63 no.1
• /
• pp.24-30
• /
• 2007

Background: Pleural effusion develops in approximately 40% of pneumonia patients. In 5-10% of these cases, it progresses to complicated parapneumonic effusion (CPPE) or empyema that requires drainage. The prognostic factors of CPPE and empyema remain to be clarified. We examined the treatment outcomes of CPPE and empyema and elucidating their prognostic factors. Methods: One hundred and fifteen patients with CPPE or empyema, who were diagnosed and treated in Kyungpook National University Hospital (Daegu, Korea) between September 2001 and December 2005, were retrospectively analyzed. All the data was acquired from their chart review, and regarding treatment results, the time to defervescence and the length of hospital stay were analyzed. Results: The treatment was successful in 101 patients with a success rate of 87.8%. Multivariate analysis showed the level of pleural fluid lactate dehydrogenase (LDH) to be a significant prognostic factor (odds ratio [OR] 7.37; 95% confidence interval [CI], 1.63 to 33.37; p=0.009). Pussy pleural fluid (r=0.236; p=0.01) and the frequency of urokinase use (r=0.257; p=0.01) correlated with the time to defervescence. However, there was no clinical factor that correlated with the length of hospital stay. Conclusion: The pleural fluid LDH level is a useful prognostic factor for monitoring treatment results of CPPE and empyema.

• Journal of agriculture & life science
• /
• v.46 no.5
• /
• pp.47-55
• /
• 2012

Polyclonal antisera against regional (abdominal and subcutaneous) fats were developed to reduce body fat in rats. Isolation and culture of abdominal and subcutaneous adipocytes of rats were performed for analyzing lactate dehydrogenase (LDH) concentration. At the level of 1:1,000 dilution, little antibody reactivity appeared in non-immunized serum whereas both of antisera against abdominal (AAb) and subcutaneous adipocyte plasma membrane proteins (SAb) had relatively strong reactivity till the level of 1:128,000 dilutions. Compared with regional fats, extremely low reactivities of AAb and SAb were detected with PMP of the organs (p<0.001). Both AAb and SAb were most strongly reacted with each adipocyte plasma memebrane proteins and showed statistically (p<0.01) higher cross-reactivities compared with non-immunized serum based on LDH analysis. In conclusion, these results may indicate that the present polyclonal antibodies against regional inedible adipocyte plasma membrane proteins are well developed and have safety in cross-reactivities with body organs.

• Asian Pacific Journal of Cancer Prevention
• /
• v.15 no.4
• /
• pp.1617-1620
• /
• 2014

Background: Evidence shows direct link of HER2 to increased glycolysis and over production of lactate dehydrogenase (LDH). HER2 overexpression, high LDH and low glucose pleural levels are associated with poor prognosis in lung cancer. Here, their relationships were investigated. Materials and Methods: HER2 positivity was studied using immunohistochemistry in non-small cell lung cancer. Glucose and LDH levels were measured using commercial colorimetric kits. Results: Of 42 patients (29 adenocarcinoma and 13 squamous cell carcinoma), 28 (66.7%) were HER2-negative, 14 (33.3%) were HER2- positive, including 9 (21.4%) weakly stained (1+) and 5 (11.9%) moderately stained (2+) samples. The relationship between HER2 and glucose and LDH levels were tested in 20 newly diagnosed lung cancer patients who had simultaneous pleural and serum samples. Pleural and serum LDH levels were increased, and pleural glucose levels were decreased with the scale of HER2 positivity, and that the difference in glucose levels between HER2-negative group and HER2-positive patients scored at 2+ reached statistical significance (p=0.02). This latter group all had pleural glucose levels below 40 mg/dl. Conclusions: For the first time, we showed a significant association between low pleural glucose level and overexpression of HER2 in lung cancer. Further investigations are warranted to disclose the association of HER2 with low pleural glucose levels in other populations, with a larger sample size, in malignant pleural effusions caused by other types of cancer, and finally to assess employment as a screening tool for finding HER2-positive cases of lung cancer.

• Korean Journal of Pharmacognosy
• /
• v.23 no.4
• /
• pp.259-263
• /
• 1992

The neuroprotective effect of betaine, one of the components of Lycii Fructus, on glutamate-induced neurotoxicity in primary cultured chicken brain cells were examined. Betaine was found to attenuate glutamate-induced neurotoxicity at the concentration of $5{\sim}10{\;}mM$ in both morphological and chemical aspects. The pretreatment of chicken brain cells with $5{\sim}10{\;}mM$betaine for 2hr at the 12 th day of culture before the 40min-exposure to $500\;{\mu}M$ glutamate significantly increased the survival rate of nerve cells in chicken brain. Betaine could also raise the decreased LDH-level in chicken brain cells which were induced neurotoxicity with $100\;{\mu}M$ glutamate. LDH value was decreased to 63% of control level in chicken brain cells at the time of 48 hr after the exposure to glutamate. However, the pretreatment of chicken brain cells with 5 mM betaine for 2 hr before the exposure to glutamate prevent the decrease of LDH in cells showing 90% of control level. Nevertheless, the remarkable neuroprotective effect of betaine on the glutamate-induced neurotoxicity in cultured chicken brain cells could not be observed when betaine was simultaneously administrated with glutamate.