• Journal of Environmental Health Sciences
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• v.27 no.2
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• pp.10-16
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• 2001

To evaluate an effect of circadian variation on the xylene metabolizing enzyme activities, 50% m-xylene in olive oil(0.25 $m\ell$/100g body weight) was intraperitoneally administered to the rats every other day for 6 days both in the night; 24:00 and the day; 12:00. Then animals were sacrigiced at 8hr after last injection of m-xylene. Hepatic microsomal cytochrome p450 contents were more increased both in control and xylene treated rats of night phase than those of day phase. But the activity of hepatic alcohol dehydrogenase(ADH) in control of night phase showed the similar value with that in those of day phase and xylene treated rats of day phase showed an increasing tendency of hepatic ADH activity as those of night phase showing similar activity. Furthermore, control rats of night phase than those of day phase. And by xylene treatment, enzyme activities of rats of day phase were higher tendency in rats of control but those of night phase were somewhat inhibited. Besides, xylene-treated animals of night phase showed increasing tendency of urinary methylhippuric acid concentration compared with those of day phase. On the other hand, liver weight per body weight(%), hepatic lipid peroxide content and serum xanthine oxidase activity were higher in night phase. And the activities of hepatic oxygen free radical metabolizing enzymes such as xanthine oxidase, gluthathione S-transferase, and xylene-treated rats of night phase than those of day phase. In conclusion, it can be hypothesized on the basis of the results that the accumulation rate of m-xylene intermediate metabolite, i.e. m-methylbenzaldehyde in liver tissus may be higher in night phase than in day phase and it may be responsible for higher liver toxicity in bight phase than in day phase.

• Journal of Environmental Health Sciences
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• v.12 no.1
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• pp.25-38
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• 1986

This paper was intented to charily the cause of an increase of serum guanase activity in rats following injection of $CCI_4$. The cause of increasing serum guanase was focused on the change of guanase activities in both serum and liver, and additionally, these results were compared with the previously known alanine aminotransferase (ALT). Concomitantly the microscopic investigation on the histologic changes, and the determination of lipid peroxides of liver were combined in this experiment for a correlation to observe that the activity of guanase would be effected by the various degree of hepatic injury induced by $CCI_4$. The serum levels of guanase were increased about 2 fold in the fatty change stage (3-12 days), 5.2 fold representing the peak value in necrosis stage (21days), 4.5 fold in early cirrhosis stage (48 days), and 2 fold in severe cirrhosis stage (92 days). These changes of serum guanase activity showed similar patterns to those of ALT activity and lipid peroxides in liver cell. The changes of liver guanase activities showed an increase, whereas ALT activities in liver were markedly decreased. It is likely that the increase of serum guanase activity is based on the excess leaking of guanase into blood by the result of accelerated enzyme synthesis in liver cell of $CCI_4$ intoxicated rats. In addition, the possibility could not be ruled out, however, that the increase of serum guanase activity would be caused by the alteration of membrane permeability.

• Clinical and Experimental Pediatrics
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• v.59 no.4
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• pp.196-201
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• 2016

Chronic granulomatous disease (CGD) is a rare inherited disorder caused by defective nicotinamide adenine dinucleotide phosphate oxidase enzyme and characterized by recurrent bacterial and fungal infections. Although liver abscess is a common manifestation of CGD, its management in CGD patients is not well-defined. In addition, the generalized guidelines for treating liver abscesses do not necessarily apply to CGD patients. Corticosteroids are commonly used to control granulomatous complications, such as inflammatory gastrointestinal and genitourinary lesions, in patients with CGD, Corticosteroids have also been used in combination with antimicrobials to treat refractory infections in patients with CGD. Because corticosteroids are capable of suppressing symptomatic inflammation, all potential infections must be adequately controlled prior to corticosteroid initiation. We report 3 typical CGD cases with liver abscesses refractory to conventional treatments that were successfully treated with the concomitant use of corticosteroid and antimicrobials. It remains unclear whether corticosteroid therapy is required for liver abscesses in CGD refractory to conventional treatments. However, based on our observations, use of corticosteroids in combination with optimal antimicrobials should be considered for refractory liver abscesses in CGD.

• Journal of the Korean Society of Food Science and Nutrition
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• v.28 no.2
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• pp.471-476
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• 1999

The effects of total dietary restriction(100% restriction of energy intake) on thiobarbituric acid reactive substance(TBARS) contents and intracellular antioxidant enzymes activities in the liver and kidney of young male Sprague Dawley rats were studied. The TBARS contents were reduced in both liver and kidney, up to 77% and 79% of the control rats, fed ad libitum, respectively at 7 days after dietary restriction . Superoxide dismutase(SOD) activities in the liver and kidney of rats were increased significantly by total dietary restriction. However, the activity of catalase in kidney was decreased 27% at 6 days after dietary restriction, but this enzyme activity did not change in liver. The changes of glutathione peroxidae(GSHPx) and catalase activities in the liver and kidney of rats with dietary restriction were not significant. These result suggested that dietary restriction reduce the free radical induced by tissue damage, as determined by TBARS content, in both the liver and kidney but the changes of activities of antioxidant enzymes may not be a contributory factor in reducing oxidative damage to tissue.

• Toxicological Research
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• v.19 no.2
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• pp.105-114
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• 2003

TO evaluate an effect of cyclohexane treatment on the degree of liver damage, rats were induced liver damage with 10 or 17 times $CCl_4$ injection (0.1 m1/100 g body wt., 50% $CCl_4$ dis-solved in olive oil) at intervals of every other day. Cyclohexane (1.56 g/kg body wt., i.p.) was administrated to the animals at 48 hours after the last pretreatment of $CCl_4$ . Rats were sacrificed at 4 hours after injection of cyclohexane. On the basis of histopathological findings, liver weight/body weight (LW/ BW, %), activities of serum alanine aminotransferase (ALT), xanthine oxidase (XO) and akaline phosphatase (ALP), and contents of liver protein and manlondialdehyde (MDA), $CCl_4$ -pretreatment induced liver damage. And $CCl_4$ 17 times treated group showed more severe liver damage than $CCl_4$ 10 times treated group. Administration of one dose of cyclohexane to $CCl_4$ 10 times treated animals resulted in the enhanced liver damage; liver necrosis with proliferation of fibroblast and bile duct abnormality, and increase in hepatic MDA content and the activities of serum ALP and ALT, But the enhanced liver damage was not found in $CCl_4$ 17 times treated animals. Serum cyclohexanone concentrations at 4 or 8 hours after injection of cyclohexane were higher in all liver damaged groups than normal group and were somewhat higher In $CCl_4$ 17 times treated animals than $CCl_4$ 10 times treated ones. Among the oxygen free radical metabolizing enzymes, hepatic cytochrome P45O dependent aniline hydroxylase (CYPdAH) activity in cyclohexane metabolizing enzyme system was meaningfully increased by the injection of cyclohexane to the liver damaged rats, with increased Vmax and high affinity to aniline. LW/BW (%) and activities of serum XO and ALT were more significantly increased in liver damaged groups than normal group by administration of cyclohexanone. In conclusion, it is assumed that an enhancement of liver damage by injection of one dose of cyclohexane to liver damaged animals might be caused by oxygen free radicals and cyclohexanone.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.196-196
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• 2001

Stereoselective metabolism and inhibitory potential of lansoprazole enantiomers were evaluated from the incubational studies of human liver microsomes and eDNA-expressed CYP isoforms in vitro. The formation of lansoprazole sulfone from both enantiomers appeared to be catalyzed by single and low affinity enzyme. Lansoprazole 5-hydroxylation, however, appeared to be mediated by two kinetically distinct CYP enzymes.(omitted)

• Journal of Microbiology
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• v.37 no.1
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• pp.41-44
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• 1999

Human mitochondrial aldehyde dehydrogenase 2 (ALDH2) is mainly responsible for oxidation of acetaldehyde generated during alcohol oxidation in vivo. A full-length cDNA of human liver ALDH2 was successfully expressed using a vaccinia virus-T7 RNA polymerase system. The expressed ALDH2 had an enzymatic activity as high as the native human liver ALDH2 enzyme.

• YAKHAK HOEJI
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• v.33 no.1
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• pp.54-63
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• 1989

Examination of the subacute toxicity of captafol showed that. 1) In the captafol administered group, the body weight was significantly decreased but the amounts of AST, ALT, LDH, BUN, TG in serum were remarkably elevated in comparision to those of the control group. 2) In captafol treated animals, the amount of cytochrome P-450 and the activity of NADPH-cytochrome c reductase in liver and in kidney were decreased, but TAB value in serum and in liver and total ATPase activity in liver and in kideny were found to be remakably elevated. 3) When captafol administered with ethanol to the group, the group showed elevated serum levels of AST, ALT and BUN but the amount of cytochrome P-450 and the activity of NADPH-cytochrome c reductase in liver and in kidney were decreased as the group which was treated with captafol only.

• The Korean Journal of Physiology
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• v.13 no.1_2
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• pp.23-28
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• 1979

The following results were drawn from the experiment conducted to see the effect of ginseng alcohol extract on the mitochondrial oxidation of the rat liver. 1) Mitochondrial oxygen consumption increased in the low concentration and decreased in the high concentration of ginseng alcohol extract. 2) When the mitochondria was destroyed mechanically or was swollen by low concentration of $AgNO_3$, mitochondrial oxygen consumption was inhibited in all concentration of ginseng alcohol extract. 3) Oxygen consumption of intact mitochondria increased in the low concentration but decreased in the high concentration of sodium deoxycholate. 4) Ginseng alcohol extract inhibited cytochrome oxidase activities of liver mitochondria. These results suggest that low concentration of ginseng alcohol extract activates the oxygen consumption of liver mitochondria by increasing the permeability of the mitochondrial membrane and high concentration of the extract inhibit the oxygen consumption by inhibiting the enzyme activity related to respiration.

• Korean Journal of Pharmacognosy
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• v.24 no.1
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• pp.63-68
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• 1993

Meliae toosendan Fructus is the fruit of Melia toosendan $S_{IEB}$. et $Z_{UCC}$. (Meliaceae), which is written in oriental terminology as clearing heat and drying dampness, and also explained using liver, stomach and small intestine for channels entered. Among the five fractions prepared from methanol whole extractive of the herb, the chloroform fraction which suggests the presence of triterpenoid, flavonoid and alkaloid stimulated the activities of drug metabolizing enzymes and bile secretion and lowered the serum transaminase activities of liver damaged by carbon tetrachloride.