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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2003.6
- 수록면
- 105 - 114 (10page)
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To evaluate an effect of cyclohexane treatment on the degree of liver damage, rats were induced liver damage with 10 or 17 times CCl4 injection (0.1 ml/100 g body wt., 50% CCl₄dissolved 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 CCl4. 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 malondialdehyde (MDA), CCl₄-pretreatment induced liver damage. And CCl₄17 times treated group showed more severe liver damage than CCl₄10 times treated group. Administration of one dose of cyclohexane to CCl₄10 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 CCl₄17 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 CCl₄17 times treated animals than CCl₄10 times treated ones. Among the oxygen free radical metabolizing enzymes, hepatic cytochrome P450 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.
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 malondialdehyde (MDA), CCl₄-pretreatment induced liver damage. And CCl₄17 times treated group showed more severe liver damage than CCl₄10 times treated group. Administration of one dose of cyclohexane to CCl₄10 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 CCl₄17 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 CCl₄17 times treated animals than CCl₄10 times treated ones. Among the oxygen free radical metabolizing enzymes, hepatic cytochrome P450 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.
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