[ABSTRAK
Latar Belakang: Kelahiran prematur masih menjadi salah satu penyebabutama kematian pada neonatus. Diseluruh dunia kematian akibat kelahiranprematur menempati posisi kedua pada anak usia dibawah lima tahun. Kelahiranprematur dapat disebabkan oleh komplikasi dari ibu, janin dan plasenta.Insufisiensi plasenta merupakan komplikasi kehamilan dimana plasenta tidakdapat membawa oksigen dan nutrisi yang diperlukan untuk pertumbuhan janindalam uterus, sehingga menyebabkan berkurangnya suplai oksigen yangdiperlukan janin dan terjadi keadaan hipoksia dalam uterus. Cygb yang terdapatdalam plasenta yang berfungsi dalam metabolisme oksigen akan berusahamenkompensasi keadaan ini agar suplai oksigen kembali normal. Hipoksia yangterus menerus ini dapat menyebabkan meningkatnya reactive oxygen species(ROS). Pada neonatus prematur terjadi peningkatan ROS dapat melalui dua jalur,yaitu : pertama, tidak tersedianya antioksidan. Kedua, berkurangnya kemampuanuntuk meningkatkan pembentukan antioksidan sebagai respons dari hiperoksiaatau oksidan lain. ROS yang terbentuk akan ditanggulangi oleh antioksidan yangada sel baik yang enzimatik maupun nonenzimatik.Metode: Plasenta bayi prematur dibagi dalam dua kelompok berdasarkan statusoksigennya menjadi hipoksia dan non hipoksia. Kemudian dilakukan pengukuranekspresi mRNA dan protein Cygb, serta aktivitas antioksidan MnSOD, CAT, danGpx.Hasil: Terjadi peningkatan protein Cygb, akan tetapi terjadi penurunan ekspresimRNA Cygb. Terjadi penurunan aktivitas spesifik MnSOD, sedangkan CAT danGPx tidak berbeda bermakan. Analisis statistik menunjukan hubungan bermaknaantara aktivitas spesifik MnSOD dengan aktivitas spesifik GPx dan terdapathubungan yang bermakana antara mRNA Cygb dengan aktivitas spesifik MnSODpada neonatus prematur hipoksia dan tidak hipoksiaKesimpulan: Terjadi peningkatan protein Cygb dan penurunan mRNA Cygbuntuk mempertahankan homeostasis janin dalam keadaan hipoksia. Antioksidanpada bayi prematur lebih rendah, akan tetapi hal ini akan dibantu oleh Cygb dalammengeliminasi ROS yang ada dalam tubuh, terlihat dari penurunan aktivitasspesifik MnSOD pada plasenta prematur hipoksia, sedangkan aktivitas spesifikkatalase dan GPx relatif sama.
ABSTRACT
Background: Preterm birth is still one of the main causes of mortality inneonates. Nowadays, preterm birth is the second most common cause of death inchildren younger than five years. Preterm birth can be caused by complications ofthe mother, fetus and placenta. Placenta insufficiency is complication ofpregnancy, where the placenta can not carry oxygen and nutrients for fetus growthin uterus, that lead to decrease oxygen supplies for the fetus and hypoxia inuterus. Cygb in placenta, that have function in oxygen metabolism will try tocompensate this situation, so the oxygen suplies will back to normal. The hypoxiawill increase reactive oxygen species (ROS). In preterm neonates the increase ofROS is cause by: First, there is no antioxidant supplies. Second, the lack ofantioxidant respon to hyperoxsia or other oxidan ROS will be eliminate byantioxidant system with in the cell.Methods: Placenta from preterm neonates divided in teo groups, hypoxia and nonhypoxia. And the sample is measure for mRNA Cygb expression, Cygb proteins,and antioxidant activity for MnSOD, CAT and GPx.Results: The Cygb protein increase in placenta neonates hypoxia, but theexpression of mRNA Cygb decrease in placenta neonates hypoxia. There isdecrease of MnSOD specific activity in placental neonates hypoxia, but not inCAT and GPx. Statistical analysis show correlation between MnSOD specificactivity with GPx specific activity, and correlation between mRNA Cygb withMnSOD specific activity.Conclusion: There is an increase of Cygb protein and decrease of Cygb mRNA inplacental neonates hypoxia, to maintain the neonates homeostasis in hypoxiaenvironment. Antioxidant is lower in preterm, Cygb with the capability toeliminate free radical will help antioxidant to reduce the ROS. It was seen at thedecrease of MnSOD specific activity, and the katalase and GPx specific activity isrelatively the same in plasenta hipoksia and non hipoksia, Background: Preterm birth is still one of the main causes of mortality inneonates. Nowadays, preterm birth is the second most common cause of death inchildren younger than five years. Preterm birth can be caused by complications ofthe mother, fetus and placenta. Placenta insufficiency is complication ofpregnancy, where the placenta can not carry oxygen and nutrients for fetus growthin uterus, that lead to decrease oxygen supplies for the fetus and hypoxia inuterus. Cygb in placenta, that have function in oxygen metabolism will try tocompensate this situation, so the oxygen suplies will back to normal. The hypoxiawill increase reactive oxygen species (ROS). In preterm neonates the increase ofROS is cause by: First, there is no antioxidant supplies. Second, the lack ofantioxidant respon to hyperoxsia or other oxidan ROS will be eliminate byantioxidant system with in the cell.Methods: Placenta from preterm neonates divided in teo groups, hypoxia and nonhypoxia. And the sample is measure for mRNA Cygb expression, Cygb proteins,and antioxidant activity for MnSOD, CAT and GPx.Results: The Cygb protein increase in placenta neonates hypoxia, but theexpression of mRNA Cygb decrease in placenta neonates hypoxia. There isdecrease of MnSOD specific activity in placental neonates hypoxia, but not inCAT and GPx. Statistical analysis show correlation between MnSOD specificactivity with GPx specific activity, and correlation between mRNA Cygb withMnSOD specific activity.Conclusion: There is an increase of Cygb protein and decrease of Cygb mRNA inplacental neonates hypoxia, to maintain the neonates homeostasis in hypoxiaenvironment. Antioxidant is lower in preterm, Cygb with the capability toeliminate free radical will help antioxidant to reduce the ROS. It was seen at thedecrease of MnSOD specific activity, and the katalase and GPx specific activity isrelatively the same in plasenta hipoksia and non hipoksia] |
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