Nekrosis hati akibat karbon tetraklorida (CC1&) diperkeras oleh berbagai macam obat/zat kimia yang dimetabolisme di hati dan berperan sebagai 'inducer' sitokrom P-450 seperti misalnya fenobarbital dan DDT. Steroid depo-medroksiprogesteron asetat (DMPA) yang banyak dipakai sebagai obat pencegah kehamilan juga dimetabolisme di dalam hati, Penelitian ini untuk melihat pengaruh DMPA terhadap luas nekrosis hati akibat CC14. Digunakan 60 mencit betina C3H, tidak sedang bunting, umur 10-12 minggu yang sebagian diberi CC14, sebagian lagi diberi DMPA 10 atau 100x3 mg/kg BB 7 atau 14 hari sebelum pemberian CC14, dan sebagian lagi untuk kelola. Dua puluh empat jam setelah pemberian CC14 mencit dimatikan, dibuat sediaan mikroskopik hati dari lobus kiri dengan pulasan hematoksilin-eosin. Luas nekrosis sentral hati diukur dalam persentase pada setiap sediaau mikroskopik. Hasil dan Kesimpulan: Didapatkan nekrosis sentrolobulus hati pada seluruh mencit kelompok CCIA dan kelompok DMPA + CC1h. Dibandingkan dengan kelompok yang mendapat CC1 , terlihat sedikit kenaikan luas nekrosis sentrolobulus pada kelompok mencit yang mendapat DMPA + CC1 (terutama pada kelompok yang mendapat DMPA 100x3 mgfkg BB, 7 hari sebelum pemberian CCIA. Namun demikian tidak terdapat perbedaan bermakna antara kelompok-kelompok tersebut (tes Kruskal-Wallis dan Mann Whitney, u 52). Hal ini mungkin disebabkan karena rendahnya haik kadar medroksiprogesterqn asetat (MPA) di dalam darah maupun 'metabolism rate' MPA di dalam mikrosom sel hati, sehingga tidak cukup kuat berperan sebagai 'inducer' sitokrom P-450 yang akan menimbulkan perbedaan bermakna luas nekrosis sentrolobulus hati. Tentunya hal ini perlu penegasan dengan memeriksa sitokrom P-450 di dalam sel hati di bawah pengaruh DMPA.

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Necrosis of the liver due to carbon tetrachloride (CCI4) are increased by various drugs / chemicals which are metabolized in the liver and acted as cytochrome P-450 inducer such as phenobarbital and DDT. Steroid depo-medroxyprogesterone acetate (DMPA) which is used as a birth control drug, is also metabolized in the liver. The objective of this study is to know the influence of DMPA on the width of centrolobular necrosis in the liver caused by CCl. Sixty non-pregnant female C3H mice, 10-12 weeks old, were divided into groups given CCl4, DMPA 10 or 100x3 mg/kg body weight 7 or 15 days prior to CCl& treatment and solvent as control group. Mice were killed 24 hours after CC1& administration and specimens were taken for microscopic slides from the left lobe of the liver and stained by haematoxylin-eosin. The width of the centrolobular necrosis was measured in percentage for each microscopic slide.

Findings and Conclusions: Centrolobular necrosis was found in all mice in the CClh and DMPA + CCl4 groups. Compared with the CCl4 group, there was a slight increase in the width of centrolobular necrosis in the DMPA + CCIA groups (especially those groups receiving DMPA 100x3 mg/kg, 7 days prior to CCl4 administration). But neither group of mice showed any significant difference in the ratio of the width of centrolobular necrosis (Kruskal-Wallis and Mann-Whitney test, a 52). This might be caused by the low level of medroxyprogesteron acetate (MPA) in the blood and by a very slow metabolism rate of MPA by the liver microsome, so it is not strong enough to act as Cytochrome P-650 inducer to give significant difference in the width of the centrolobular necrosis. Further confirmation is necessary to determine the amount of cytochrome P-A50 in the liver under the influence of DMPA.