Kesimpulan Jurnal

ANTICONVULSIVE EFFECTS OF SUPEROXIDE DISMUTASE AND CATALASE

Pada setengah dari kelinci percobaan, dengan pemberian Niwana (dengan dosis 1 mg/kg) dan katalase (150.000 UI/kg) secara intraperitoneal 30 menit sebelum pemberian penthylentetrazol (pemicu kejang, dengan dosis 100 mg/kg i.v.), ternyata dapat mencegah kejang. Sedangkan setengahnya lagi mengalami sekali kejang dalam durasi singkat setelah pemberian penthylentetrazol.

Penemuan klinis, penemuan berdasarkan percobaan ini, dan penemuan berdasarkan literatur mengindikasikan : adanya peningkatan lemak peroksida (lipid peroxidation) pada fokus epileptogenik di otak, peningkatan produk-produk lemak peroksida di dalam cairan serebrospinal dan pada plasma darah perifer dari pasien epilepsi – mengindikasikan adanya peran pathogenesis penting dari defisiensi antioksidan dan/atau stress oksidatif pada kasus epilepsi idiopatik. Dan hal tersebut mungkin juga dipengaruhi adanya penurunan aktivitas gluthatione peroksidase dan/atau penurunan fungsi haptoglobin, transferrin dan seruloplasmin. Para peneliti ini berpikir bahwa kombinasi dari obat antiepilepsi dan agen – agen antioksidan untuk terapi epilepsi idiopatik dapat memberikan hasil yang lebih efektif. Namun hal ini masih memerlukan penelitian lebih lanjut.

ANTICONVULSIVE EFFECTS OF SUPEROXIDE DISMUTASE AND CATALASE

Penyakit Alzheimer’s merupakan penyakit neurodegeneratif yang ditandai dengan adanya penumpukan amyloid-ß ekstraselular, dan juga ditandai dengan adanya penurunan fungsi ingatan dan kognitif, yang diduga terjadi akibat peningkatan produksi amyloid-ß. Peran neurotoksik amyloid-ß sudah sejak lama diketahui.

Beberapa penelitian lainnya telah mengimplikasikan stress oksidatif sebagai etiologi dari penyakit Alzheimer’s. Stres oksidatif terjadi terutama sebagai akibat dari produksi berlebihan radikal bebas oksigen (reactive oxygen species) oleh mitokondria, dan radikal bebas oksigen ini terutama didetoksifikasi oleh enzim antioksidan mitokondria yaitu Superoxide Dismutase (SOD-2).

Data – data yang dimiliki para peneliti ini juga sama dengan yang ditunjukkan oleh beberapa penelitian lain bahwa ada keterlibatan radikal bebas oksigen mitokondira pada penyakit Alzheimer’s. Penelitian-penelitian tersebut secara khusus menghubungkan defisiensi SOD-2 dengan peningkatan patologi penyakit Alzheimer’s dan penurunan radikal bebas oksigen mitokondria dengan perbaikan fungsi kognitif.

Penemuan para peniliti ini, bersama dengan hasil penelitian sebelumnya, secara kuat menduga bahwa radikal bebas oksigen di mitokondria mempengaruhi proses pembentukan amyloid-ß, yaitu dengan jalan mengubah amyloid-ß fibrilar menjadi plak.

Keterlibatan stress oksidatif dalam perjalanan penyakit Alzheimer’s telah sejak lama diketahui dan diselidiki. Hal tersebut mempengaruhi adanya penelitian tentang penggunaan terapi antioksidan untuk penyakit Alzheimer’s selama beberapa tahun belakangan.

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