• Biomedical Science Letters
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• v.9 no.2
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• pp.93-98
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• 2003

To investigate the cyclohexane and xylene mixture treatment on the liver damage, the rats were treated by the mixture of cyclohexane and xylene (CH＋X) and then, liver damage was demonstrated by liver function findings based on liver weight/body weight, serum level of alanine aminotransferase (ALT), xanthine oxidase (XO) and then compared with cyclohexane treated group (CH group) and xylene-treated group (X). The CH＋X group showed merely severer liver damge than CH or X group. On the other hand, CH＋X group showed lower activity of hepatic cytochrome P-450 dependent aniline hydroxylase (CYPdAH) than CH or X group, but no statical differences were demonstrated among three experimental groups. Especially the hepatic GSH content was merely declined than CH or X group and the activity of hepatic GST was higher in CH＋X group than CH or X group. In conclusion, cyclohexane and xylene mixture treated animals showed merely severer liver damage than cyclohexane or xylene treated group and such a fact may be caused by inhibition of cyclohexane or xylene metabolism and oxygen free radical.

• Proceedings of the Korean Environmental Health Society Conference
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• 2003.06a
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• pp.157-157
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• 2003

To evaluate an effect of pathological liver damage on the cyclohexane metabolism, rats were pretreated with 50% $CCl_4$ dissolved in olive oil (0.1$\mell$/100g body weight) 10 or 17 times intraperitoneally at intervals of every other day. On the basis of liver function and histological findings, the animals pretreated with $CCl_4$ 10 times were identified as acutely liver damaged ones and the animals pretreated with $CCl_4$ 17 times were identified as severly liver damaged ones, with fibrosis, biliary abnormality and mild injury both in the kidneys and the lungs. To these liver damaged animals, cyclohexane (a single dose of 1.56g/kg body weight, i.p.) was administrated at 48 hours after the last injection of $CCl_4$. The rats were sacrificed at 4 or 8 hours after injection of cyclohexane. The cyclohexane metabolites; cyclohexanol (CH-ol), cyclohexane-1, 2-diol (CH-1, 2-diol), cyclohexane-l, 4-diol (CH-1, 4-diol), and their glucuronyl conjugates and cyclohexanone (CH-one) were detected in the urine of cyclohexane treated rats. After cyclohexane treatment, the serum levels of CH-ol and CH-one were remarkably increased at 4 hours and then decreased at 8 hours in normal group. Whereas in liver damaged rats, these cyclohexane metabolites were higher at 8 hours than at 4 hours. The excretion rate of cyclohexane metabolites from serum into urine was more decreased in liver damaged animals than normal group, with the levels of excretion rate being lower in $CCl_4$ 17 times injected animals than 10 times injected ones. However, it was interesting that the urinary concentration of cyclohexane metabolites was generally more increased in liver damaged animals than normal ones, and the increasing rate was higher in $CCl_4$ 17 times injected rats than 10 times injected ones. And liver damaged rats, especially $CCl_4$ 17 times treated ones, had an enhanced ability of glucuronyl conjugation to cyclohexanol analogues compared with normal group. Futhermore, CH-1, 2 and 1, 4-diol were all conjugated with glucuronic acid in $CCl_4$ 17 times injected animals. In conclusion, the metabolic rate of cyclohexane was unexpectably accelerated and it may be caused by physiological adaptation of adjacent intact hepatocyte in damaged liver.

• Biomedical Science Letters
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• v.12 no.4
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• pp.361-370
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• 2006

To evaluate an effect of pathological liver damage on the conjugation of cyclohexane metabolites, rats were pretreated with 50% $CCl_4$ dissolved in olive oil (0.1 ml/100 g body weight) 10 or 17 times intraperitoneally at intervals of every other day. On the basis of liver function, the animals pretreated with $CCl_4$ 10 times were identified as acutely liver damaged ones and the animals pretreated with $CCl_4$ 17 times were identified as severly liver damaged ones. To these liver damaged animals, cyclohexane (a single dose of 1.56 g/kg body weight, i.p.) was administered at 48 hr after the last injection of $CCl_4$. The rats were sacrificed at 4 or 8 hr after injection of cyclohexane. The cyclohexane metabolites, cyclohexanol (CH-ol), cyclohexane-1,2-diol (CH-1,2-diol), cyclohexane-1,4-diol (CH-1,4-diol), and their glucuronyl conjugates and cyclohexanone were detected in the urine of cyclohexane treated rats. The urinary concentration of cyclohexane metabolites was generally more increased in liver damaged animals than normal ones, and the increasing rate was higher in $CCl_4$ 17 times injected rats than 10 times injected ones. And liver damaged.ats, especially $CCl_4$ 17 times treated ones, had an enhanced ability of glucuronyl conjugation to CH-ol analogues compared with normal group. Futhermore, CH-1,2 and 1,4-diol were all conjugated with glucuronic acid in $CCl_4$ 17 times injected animals. On the other hand, the increasing rate of activities of hepatic cytochrome P450 dependent aniline hydroxylase, alcohol dehydrogenase and urine diphosphate glucuronyl transferase was higher in 17 times $CCl_4$-treated rats compared with normal and $CCl_4$ 10 times injected animals. Taken all together, it is assumed that an increased urinary excretion amount of cyclohexane metabolites in liver damaged rats might be caused by an increase in the activities of cyclohexane metabolizing enzymes. And enhanced conjugating ability of CH-ol in liver damaged animals and novel finding of conjugating form of CH-1,2 and 1,4-diol might be caused by increase in the activity of hepatic diphosphouridine glucuronyltransferase.

• Biomedical Science Letters
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• v.12 no.3
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• pp.241-247
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• 2006

To evaluate an effect of pathological liver damage on the cyclohexane (CH) metabolism, rats were pretreated with 50% carbon tetrachloride $(CCl_4)$ dissolved in olive oil (0.1ml/100g body weight) 10 or 17 times intraperitoneally at intervals of every other day. To these liver damaged animals, CH (a single dose of 1.56g/kg body weight, i.p.) was administered at 48hr after the last injection of $CCl_4$. The CH metabolites; cyclohexanol (CH-ol), cyclohexane-l,2-diol (CH-l,2-diol) and cyclohexane-l,4-diol (CH-l,4-diol) and cyclohexanone (CH-one) were detected in the urine of CH treated rats. After CH treatment, the serum levels of CH-ol and CH-one were remarkably increased at 4 hr and then decreased at 8hr in normal group. Whereas in liver damaged rats, these CH metabolites were higher at 8hr than at 4hr. The excretion rate of CH metabolites trom serum into urine was more decreased in liver damaged animals than normal group, with the levels of excretion rate being lower in $CCl_4$ 17 times injected animals than 10 times injected ones. It was interesting that the urinary concentration of CH metabolites was generally more increased in liver damaged animals than normal ones, and the increasing rate was higher in $CCl_4$ 17 times injected rats than 10 times injected ones. Taken all together, it is assumed that reduced urinary excretion rate of CH metabolites in liver damaged rats might be resulted from deteriorated hepatic and renal blood flow, and an increased urinary excretion amount of CH metabolites in liver damaged rats might be caused by reduced expiration amount of the metabolites due to lung damage.

• Applied Microscopy
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• v.35 no.2
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• pp.81-87
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• 2005

To evaluate the effects of ingestion of alcoholic drinks on the toxicities of industrial compounds, cyclohexane (CH) was intraperitoneally administrated to rats (1.56 g/kg body weght), which had been ingested 15% ethanol for up to 6 weeks, 4 times by once a day and every other day. Following the last treatment of ethanol or CH, blood and lung tissues were collected during 24 hours prior to sacrifice of animals. Comparing with the control group, the lung weight per body weight (%) and the protein content in bronchoalveolar lavage fluid were increased in the ethanol-pretreated group, and the glucose-6-phosphatase activity in lung tissues was decreased in the CH-treated group. In a morphological observations, pulmonary embolus were found in the CH-treated group, whereas a partial pulmonary atelectasis and a much increase in pulmonary embolus were shown in the CH-treated group after pretreated with ethanol for 6 weeks. In conclusion, these results indicate that ethanol pretreatment could enhance CH metabolism and that CH treatment with ethanol pretreatment could induce lung injury due to the increased CH metabolism.

• Applied Microscopy
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• v.36 no.4
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• pp.291-297
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• 2006

To evaluate the effects of ingestion of alcoholic drinks on the toxicities of industrial compounds, cyclohexane (CH) was intraperitoneally administrated to rats (1.56g/kg body weight), which had been ingested 15% ethanol for up to 6 weeks,4 times by once a day and every other day. Following the last treatment of ethanol or CH, blood and liver tissues were collected after 4 hours prior to sacrifice of animals. By the injection of CH, liver weight (% of body weight) and xanthine oxidase activity in serum were increased, and glucose-6-phasphatase (G6P) activity in liver was decreased compared to them of control group. The activities of CH metabolizing enzymes, such as cytochrome P450 dependent aniline hydroxylase (CYPdAH) and alcohol dehydrogenase (ADH), were significantly increased by injection of CH, and those activities were the highest in CH-injected group after pretreated with alcohol. Ultrastructurally. both of alcohol treatment and CH injection induced transforming into the smooth-endoplasmic reticulum from rough-endoplasmic reticulum, the those rate was the highest in case of CH-injection after pretreated with alcohol. From these results, it is suggested that alcohol intake on a level without alcoholic degeneration of hepatocytes could enhance the CH metabolism of liver.