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ABSTRAKLatar Belakang: Kelahiran prematur masih menjadi salah satu penyebab
utama kematian pada neonatus. Diseluruh dunia kematian akibat kelahiran
prematur menempati posisi kedua pada anak usia dibawah lima tahun. Kelahiran
prematur dapat disebabkan oleh komplikasi dari ibu, janin dan plasenta.
Insufisiensi plasenta merupakan komplikasi kehamilan dimana plasenta tidak
dapat membawa oksigen dan nutrisi yang diperlukan untuk pertumbuhan janin
dalam uterus, sehingga menyebabkan berkurangnya suplai oksigen yang
diperlukan janin dan terjadi keadaan hipoksia dalam uterus. Cygb yang terdapat
dalam plasenta yang berfungsi dalam metabolisme oksigen akan berusaha
menkompensasi keadaan ini agar suplai oksigen kembali normal. Hipoksia yang
terus 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 kemampuan
untuk meningkatkan pembentukan antioksidan sebagai respons dari hiperoksia
atau oksidan lain. ROS yang terbentuk akan ditanggulangi oleh antioksidan yang
ada sel baik yang enzimatik maupun nonenzimatik.
Metode: Plasenta bayi prematur dibagi dalam dua kelompok berdasarkan status
oksigennya menjadi hipoksia dan non hipoksia. Kemudian dilakukan pengukuran
ekspresi mRNA dan protein Cygb, serta aktivitas antioksidan MnSOD, CAT, dan
Gpx.
Hasil: Terjadi peningkatan protein Cygb, akan tetapi terjadi penurunan ekspresi
mRNA Cygb. Terjadi penurunan aktivitas spesifik MnSOD, sedangkan CAT dan
GPx tidak berbeda bermakan. Analisis statistik menunjukan hubungan bermakna
antara aktivitas spesifik MnSOD dengan aktivitas spesifik GPx dan terdapat
hubungan yang bermakana antara mRNA Cygb dengan aktivitas spesifik MnSOD
pada neonatus prematur hipoksia dan tidak hipoksia
Kesimpulan: Terjadi peningkatan protein Cygb dan penurunan mRNA Cygb
untuk mempertahankan homeostasis janin dalam keadaan hipoksia. Antioksidan
pada bayi prematur lebih rendah, akan tetapi hal ini akan dibantu oleh Cygb dalam
mengeliminasi ROS yang ada dalam tubuh, terlihat dari penurunan aktivitas
spesifik MnSOD pada plasenta prematur hipoksia, sedangkan aktivitas spesifik
katalase dan GPx relatif sama.
ABSTRACTBackground: Preterm birth is still one of the main causes of mortality in
neonates. Nowadays, preterm birth is the second most common cause of death in
children younger than five years. Preterm birth can be caused by complications of
the mother, fetus and placenta. Placenta insufficiency is complication of
pregnancy, where the placenta can not carry oxygen and nutrients for fetus growth
in uterus, that lead to decrease oxygen supplies for the fetus and hypoxia in
uterus. Cygb in placenta, that have function in oxygen metabolism will try to
compensate this situation, so the oxygen suplies will back to normal. The hypoxia
will increase reactive oxygen species (ROS). In preterm neonates the increase of
ROS is cause by: First, there is no antioxidant supplies. Second, the lack of
antioxidant respon to hyperoxsia or other oxidan ROS will be eliminate by
antioxidant system with in the cell.
Methods: Placenta from preterm neonates divided in teo groups, hypoxia and non
hypoxia. 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 the
expression of mRNA Cygb decrease in placenta neonates hypoxia. There is
decrease of MnSOD specific activity in placental neonates hypoxia, but not in
CAT and GPx. Statistical analysis show correlation between MnSOD specific
activity with GPx specific activity, and correlation between mRNA Cygb with
MnSOD specific activity.
Conclusion: There is an increase of Cygb protein and decrease of Cygb mRNA in
placental neonates hypoxia, to maintain the neonates homeostasis in hypoxia
environment. Antioxidant is lower in preterm, Cygb with the capability to
eliminate free radical will help antioxidant to reduce the ROS. It was seen at the
decrease of MnSOD specific activity, and the katalase and GPx specific activity is
relatively the same in plasenta hipoksia and non hipoksia, Background: Preterm birth is still one of the main causes of mortality in
neonates. Nowadays, preterm birth is the second most common cause of death in
children younger than five years. Preterm birth can be caused by complications of
the mother, fetus and placenta. Placenta insufficiency is complication of
pregnancy, where the placenta can not carry oxygen and nutrients for fetus growth
in uterus, that lead to decrease oxygen supplies for the fetus and hypoxia in
uterus. Cygb in placenta, that have function in oxygen metabolism will try to
compensate this situation, so the oxygen suplies will back to normal. The hypoxia
will increase reactive oxygen species (ROS). In preterm neonates the increase of
ROS is cause by: First, there is no antioxidant supplies. Second, the lack of
antioxidant respon to hyperoxsia or other oxidan ROS will be eliminate by
antioxidant system with in the cell.
Methods: Placenta from preterm neonates divided in teo groups, hypoxia and non
hypoxia. 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 the
expression of mRNA Cygb decrease in placenta neonates hypoxia. There is
decrease of MnSOD specific activity in placental neonates hypoxia, but not in
CAT and GPx. Statistical analysis show correlation between MnSOD specific
activity with GPx specific activity, and correlation between mRNA Cygb with
MnSOD specific activity.
Conclusion: There is an increase of Cygb protein and decrease of Cygb mRNA in
placental neonates hypoxia, to maintain the neonates homeostasis in hypoxia
environment. Antioxidant is lower in preterm, Cygb with the capability to
eliminate free radical will help antioxidant to reduce the ROS. It was seen at the
decrease of MnSOD specific activity, and the katalase and GPx specific activity is
relatively the same in plasenta hipoksia and non hipoksia]
T-David Limanan.pdf :: Unduh