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Abstrak :
Pencegahan penyakit tular vektor nyamuk kini dipersulit dengan munculnya resistensi vektor terhadap insektisida. Insektisida organofosfat (OP)-malation merupakan salah satu insektisida yang masih digunakan di Indonesia, oleh karena itu pengawasan status resistensi vektor terhadap insektisida tersebut perlu dilakukan. Dua mekanisme utama yang mendasari resistensi vektor terhadap malation adalah peningkatan enzim metabolik esterase dan insensitif enzim asetilkolinesterase (AChE). Penelitian sebelumnya di Indonesia telah melaporkan keterlibatan enzim esterase pada resistensi vektor terhadap malation, namun peran insensitif AChE belum diketahui jelas. Penelitian ini merupakan penelitian deskriptif menggunakan nyamuk Aedes aegypti dari Jawa Tengah. Penelitian dilakukan pada bulan April-Oktober 2013 di Lembaga Eijkman. Aedes aegypti sensitif dan resistan malation hasil bioassay dianalisis secara molekuler untuk mengetahui aktivitas enzim AChE yang tersisa setelah dihambat oleh malation. Selain itu, tiga mutasi titik (G119S, F290V, dan F455W) pada gen Ace1 juga dideteksi untuk melihat pengaruh ada tidaknya ketiga mutasi tersebut terhadap aktivitas enzim AChE setelah dihambat oleh malation. Aktivitas enzim AChE ditentukan berdasarkan metode Ellman, sedangkan deteksi mutasi G119S dengan metode PCR-RFLP, dan mutasi F290V-F455W dengan metode PCR-Sequencing. Tidak ada perbedaan "aktivitas sisa" enzim AChE yang bermakna dan tidak ditemukan mutasi G119S, F290V, dan F455W pada Ae. aegypti resistan. Hasil ini menandakan bahwa mekanisme insensitif AChE tidak mendasari resistensi Ae. aegypti terhadap malation di Jawa Tengah. Walaupun demikian, terdapat peningkatan "aktivitas sisa" AChE yang tidak bermakna pada Ae. aegypti resistan dibanding Ae. aegypti sensitif. Hasil ini menandakan bahwa kemungkinan terdapat peran enzim lain yang dapat memetabolisme malation lebih cepat atau terjadi peningkatan produksi AChE pada nyamuk resistan sehingga AChE tetap dapat menghidrolisis substratnya (asetilkolin). Mekanisme insensitif AChE belum terlibat penuh dalam mendasari resistensi Ae. aegypti terhadap malation di Jawa Tengah, namun kemungkinan mekanisme ini terlibat dapat diteliti lebih lanjut dengan menganalisis peningkatan produksi enzim AChE yang juga dapat memengaruhi aktivitas AChE selain mutasi gen Ace1.

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The prevention of mosquito-borne diseases becomes difficult to overcome since the vectors have developed resistance to insecticides. The molecular basis of resistance to insecticides therefore need to be explored to determine the resistance status earlier. In Indonesia, organophosphate (OP)-malathion insecticide has been widely used to control vector population and therefore the resistance status to this insecticide should be under control. Two main mechanisms have known to be associated with resistance to malathion, previous studies in Indonesia reported that esterase responsible in resistance to malathion, however the insensitive AChE-based mechanism remain to be determined. Descriptive study was conducted at Eijkman Institute during April to October 2013 using Aedes aegypti from Central Java. Malathion sensitive and resistant Ae. aegypti from bioassay were subjected to molecular analysis to compare the remaining activitiy of AChE between those mosquitoes after inhibited by malathion. The presence of three point mutations (G119S, F290V, and F455W) in the Ace1 gene associated with resistance to malathion were also detected to see the effect of the absence or presence of those mutations to AChE activity. The results showed that AChE remaining activities in the resistant Ae. aegypti have no significantly different compare to those in the sensitive Ae. aegypti. No associated mutations found in the Ace1 gene (G119S, F290V, or F455W) as well. These results indicated that insensitive AChE-based mechanism is not involved in Ae. aegypti resistance to malathion in Central Java. However, we noticed that the remaining activities of AChE are increased insignificantly in resistant Ae. aegypti, suggesting the possibilities of metabolic enzyme which can degrade insecticide faster or could be due to overproduction of AChE enzyme which may increase the hydrolizing process of acetylcholine (ACh). Insensitive AChE-based mechanism is still not fully involved in Ae. aegypti resistance to malathion in Central Java, however the potency of its involvement should be further analyzed by considering the overproduction of AChE enzyme itself which could contribute in AChE activity enhancement other than Ace1 gene mutation.

Abstrak :
Ae. aegypti merupakan nyamuk yang dapat menularkan berbagai patogen penyakit seperti virus, bakteri dan parasit sehingga disebut sebagai vektor. Berbagai penyakit manusia yang diperantarai oleh nyamuk Ae. aegypti antara lain adalah demam berdarah DBD , Chikungunya, Yellow Fever dan Zika. Terjadinya resistensi pada berbagai insektisida, termasuk piretroid merupakan masalah yang sekarang dihadapi di berbagai negara. Pada penelitian ini dilakukan uji bioassay WHO pada Ae. aegypti Palembang dan Jakarta dengan menggunakan insektisida piretroid permetrin 0,25 . Fragmen gen VGSC yang berkaitan dengan resistensi piretroid L982, S989, I1011, L1014, V1016 dan F1534 dari strain resistan dan sensitif diamplifikasi dan dianalisis. Uji kerentanan menunjukkan adanya resistensi pada Ae. aegypti Palembang dan Jakarta. Dari hasil analisis fragmen gen VGSC diketahui terdapat mutasi S989P dan/atau V1016G pada Ae. aegypti Palembang resistan dan S989P dan/atau V1016G pada Ae. aegypti Jakarta resistan. ...... Ae. aegypti mosquito is a vector that could transmit various pathogens, such as viruses, bacteria, and parasites. Several human diseases transmitted by Ae. aegypti mosquito are dengue fever DHF , Chikungunya, Yellow Fever and Zika. The occurance of resistance to various insecticides, including pyrethroid, is a current problem faced by various countries. In this research, a WHO bioassay test on Palembang and Jakarta Ae. aegypti was conducted using 0.25 permethrin pyretroid insecticide. VGSC gene fragments associated with pyrethroid resistance L982, S989, I1011, L1014, V1016 and F1534 of resistant and sensitive strains were amplified and analyzed. The test showed the presence of resistance in Palembang and Jakarta Ae. aegypti. From the results of VGSC gene fragment analyses, it was known that there were mutations S989P and or V1016G on resistant Palembang Ae. aegypti and S989P and or V1016G on resistant Jakarta Ae. aegypti.