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"Hipoksia sistemik kronik dapat menyebabkan kekurangan oksigen pada otak sehingga metabolisme sel menjadi metabolisme anaerob. Konsekuensi metabolisme anaerob ini adalah kekurangan energi dalam bentuk ATP mengingat otak adalah organ yang sangat aktif. Akibat penurunan energi ini terjadi stimulasi yang berlebihan terhadap kanal Ca2+ sehingga terjadi influks Ca2+ yang berlebihan ke dalam sel memicu berbagai macam efek antara lain peningkatan penglepasan neurotransmiter ACh. Hipoksia sendiri memicu pembentukan radikal bebas dengan hasil akhir MDA. Pada kerusakan otak akibat hipoksia GFAP yang merupakan protein spesifik pada astrosit dapat mengalami peningkatan sintesis. Penelitian ini merupakan penelitian ekperimental dengan desain rancang acak lengkap menggunakan hewan coba tikus Spraque Dawley yang diinduksi dengan hipoksia sistemik kronik. Sampel penelitian ini menggunakan jaringan otak bagian korteks dan plasma tikus sebanyak 5 ekor pada tiap kelompok terdiri atas 1 kelompok kontrol dan 4 kelompok perlakuan yang terdiri atas tikus yang diinduksi hipoksia 1 hari, 3 hari, 5 hari dan 7 hari. Parameter yang diperiksa adalah konsentrasi MDA otak dan plasma, aktivitas spesifik enzim AChE jaringan otak serta kadar GFAP jaringan otak. Hipoksia sistemik kronik tidak menimbulkan peningkatan konsentrasi MDA otak sementara dalam plasma terjadi peningkatan yang tidak bermakna konsentrasi MDA plasma. Induksi hipoksia sistemik meningkatkan aktivitas spesifik enzim AChE pada jaringan otak dan meningkatkan kadar GFAP jaringan otak secara bermakna. Sedangkan pada plasma tidak terjadi peningkatan kadar GFAP. Pada induksi hipoksia sistemik ini belum terjadi kerusakan oksidatif. Peningkatan aktivitas spesifik AChE dan kadar GFAP merupakan mekanisme adaptasi otak untuk mencegah terjadinya kerusakan karena hipoksia.

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Chronic systemic hypoxia induced hypoxia in the brain region thus brain cells produce energy by anaerobic metabolism. Anaerobic metabolism cause depletion in ATP synthesis. ATP depletion stimulates alterations on calcium ion in the sitoplasma of neuronal cells through the overstimulation of glutamate receptor. Alterations in intracellular calcium ions stimulates ACh release in neuronal cells. Hypoxia increased free radicals level in the cell, thus increased MDA as the final product of lipid peroxidation by free radicals. Due to respond the brain damage, astrocyte produces more spesific sitosceletal protein called GFAP.

The aim of the study was to analyze the effects of chronic systemic hypoxia in brain damage by measuring the MDA level in brain tissue compared to plasma, spesific activity of AChE in the brain tissue and GFAP level in the brain tissue compared to plasma. Twenty-five male Spraque Dawley rats were subjected to systemic hypoxia by placing them in the hypoxic chamber supplied 8-10% of O2 for 0, 1, 3, 5, and 7 days, respectively. Cortex and hipocampus of brain tissue and blood plasma were used as the sample. MDA levels were measured using Will?s methode. AChE spesific activity was measured using RANDOX Butyrylcholinesterase Colorimetric Methode. GFAP was analyzed using Rat GFAP ELISA kit by CUSABIO.

This study demonstrates that MDA level didn't increase during induced hypoxic systemic in the brain tissue, meanwhile there's no significance increased of MDA levels in plasma. There's significance increased of AChE spesific activity during induced hypoxic systemic in the brain tissue. This study also demonstrates significance increased in brain tissue's GFAP level but not in the plasma during induced systemic hypoxia. We conclude that there?s no oxydative damage in the brain tissue during this induced systemic hypoxia. The increased in AChE spesific activity and GFAP levels showed an adaptive mechanism to protect the brain tissue from hypoxic insult."

"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."

"ABSTRAKHipoksia hipobarik intermiten HHI dengan menggunakan protokol profil penerbangan modifikasi Mulyawan pada ruang hipobarik dapat digunakan sebagai model hipoksia yang bersifat melindungi melalui ekspresi HIF-1? dan protein yang diregulasinya yang bermanfaat dalam mengatasi radikal bebas yang terbentuk selama induksi tersebut. Pada penelitian ini dinilai ekspresi protein sitoglobin Cygb dan neuroglobin Ngb serta aktivitas spesifik asetilkolin esterase AChE sebagai dampak dari induksi HHI pada tikus dewasa. Digunakan 25 tikus Sprague-Dawley dewasa yang terbagi atas dua kelompok kontrol yakni normoksia dan hipoksia hipobarik akut HHA , serta 3 kelompok yang terpapar HHI kelompok pertama terpapar pada hari ke-1 dan ke-8 IHH1x , kelompok ke-2 terpapar pada hari ke-1, -8 dan -15, sedangkan kelompok ke-3 terpapar pada hari ke-1, -8, -15 dan -22 . Sitoglobin dan Ngb menurun pada induksi akut dan meningkat secara signifikan seiring dengan peningkatan frekuensi paparan HHI. Aktivitas spesifik AChE meningkat secara signifikan sejak paparan pertama HHA namun kemudian menurun pada induksi terakhir IHH3x . Dari hasil penelitian ini disimpulkan bahwa pada HHI3x terjadi respons adaptasi yang bersifat melindungi jaringan otak tikus percobaan terhadap perlakuan.

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ABSTRACTProposed as a protective model of hypoxia via HIF 1 expression, intermittent hypobaric hypoxia IHH in the rat, using Mulyawan rsquo s modified flight profile in a hypobaric chamber, is known to be useful in overcoming the free radicals formed during the induction. Using the same method, this study 39 s aims are to investigate cytoglobin Cygb and neuroglobin Ngb protein expressions and specific activity of acetylcholine esterase as the impacts of the IHH induction in adult rats. We used 25 adult Sprague Dawley male, divided into 2 control groups normoxia and acute hypobaric hypoxia AHH , and 3 IHH exposed groups the first group was exposed on day 1 and 8 IHH 1x the second group on day 1, 8 and 15 IHH 2x and the third group on day 1, 8, 15 and 22 IHH 3x . Cytoglobin and Ngb were decreased in the acute induction and increased significantly along with the increasing frequency of the IHH induction. The specific activity was increased significantly since the first AHH induction of hypobaric hypoxia but then decreased in the last induction IHH3x . From these findings, it is concluded that IHH, especially IHH3x, seems to be a protective adaptive response in the rat rsquo s brain tissue. "

"Tujuan umum: Mengetahui profil keamanan dan efek getah J. curcas terhadap jaringan gigi dan periapeks dalam persiapan untuk memanfaatkan pemakaian bahan alami getah J. curcas pada radang pulpa. Tujuan khusus (1) Mengetahui kandungan golongan senyawa getah J. curcas. (2) Mengetahui sitotoksisitas getah J. curcas. (3) Mengetahui toksisitas akut pemberian secara oral dosis tunggal getah J. curcas pada hewan percobaan. (4) Mengetahui aktivitas hemolisis getah J. curcas pada darah manusia secara in vitro. (5) Mengetahui sifat mutagenisitas getah J. curcas. (6) Mengetahui efek getah J. curcas terhadap pembebasan interleukin-1β oleh sel makrofag. (7) Mengetahui efek getah J. curcas terhadap pembebasan kolagenase pada set fibroblast. (8) Mengetahui efek histopatologik getah J. curcas terhadap pulpa dan jaringan periapeks gigi pada hewan percobaan. (9) Mengetahui efek getah J. curcas terhadap kekerasan macro jaringan keras gigi manusia secara in vitro. (10) Mengetahui efek getah J. curcas terhadap jaringan keras gigi manusia dalam hal kelarutan unsur kalsium dan fosfat secara in vitro. Metode penelitian: Disain penelitian eksperimental dan eksplorasi. Penelitian dibagi atas (1) skrining fitokimia, (2) tahap 1 dan (3) tahap 2 evaluasi biologik getah J. curcas. Untuk standardisasi getah J. curcas diambil dari satu petak tanaman dalam satu musim, kemudian diukur pH, volume basah, diliofilisasi, diukur berat kering, dan disimpan pada -20°C sebagai sampel. (1). Skrining fitokimia getah J. curcas. Analisis kualitatif golongan senyawa diidentifikasi dari ekstrak eter, etil asetat, dan air. (2). Uji toksisitas 1. Uji sitotoksisitas. (1) Metoga agar overlay. Getah J. curcas dan kontrol diserap oleh cakram selulosa, kemudian diletakkan di atas permukaan agar yang menutupi selapis sel Fib L929 yang telah diwarna neutral red. Evaluasi berdasar luas zona dekolorisasi dan zona lisis yang terbentuk setelah 24 jam. (2) Assay MTT. Getah J. curcas dalam medium diberikan pada kultur set Fib L929 cell line dan sel primer fibroblast gingiva manusia yang tumbuh dalam mikroplat 96-sumur. Setelah 1-4 hari, dilakukan assay MTT. Evaluasi berdasar perbandingan nilai OD kontrol dan perlakuan. 2. Uji toksisitas akut. Mencit diberi getah J. curcas secara intragastrik sebanyak 1 kali. Dihitung LD5O berdasar jumlah mencit yang mati. Dibandingkan antara kelompok perlakuan dan kontrol dalam hal tanda toksisitas, berat badan selama 2 minggu, pemeriksaan makroskopik dan mikroskopik organ tubuh. 3. Uji hemolisis. Darah dicampur dengan berbagai konsentrasi getah J. curcas. Evaluasi berdasar pembebasan hemoglobin, dibandingkan OD kelompok perlakuan dengan kontrol positif air, dan kontrol negatif salin. 4. Uji mutagenisitas. Getah J. curcas dikultur dengan bakteri S. typhi dan E. coil mutan. Evaluasi berdasar penghitungan koloni reversi bakteri, dibandingkan kelompok perlakuan, kontrol positif dan kontrol negatif. (3) Efek getah J. curcas terhadap makrofag dan fibroblast 1. Efek getah J. curcas terhadap pembebasan IL-1β. Lima dosis getah J. curcas dimasukkan ke dalam kultur makrofag peritoneum mencit BALB/c, secara bersamaan, sebelum, atau sesudah pemberian LPS. Setelah 1 dan 2 hari, IL-1β dalam supernatan diukur secara ELISA dengan Quantikine IL-1β for mouse kit. 2. Efek getah J. curcas terhadap pembebasan kolagenase oleh fibroblast. Empat dosis getah J. curcas dan IL-1β dimasukkan dalam kultur sel primer fibroblast gingiva manusia. Setelah 1-4 hari kolagenase dalam supematan diukur dengan assay kolagenase. Hasil degradasi kolagen dipisahkan dengan SDS-PAGE. Pita 3/4 αA diukur dengan program komputer Adobe Photo. (4) Efek histopatologik getah J. curcas pada jaringan pulpa dan periapeks. Getah J. curcas dimasukkan ke dalam kavitas gigi monyet. Setelah 3 hari, gigi diproses untuk pembuatan sediaan histologik. Evaluasi berdasar perbandingan pemeriksaan keadaan mikroskopik jaringan pulpa dan peripeks dalam hal inflamasi dan nekrosis, antara kelompok kontrol dan perlakuan. (5) Efek getah J. curcas terhadap jaringan keras gigi. 1. Efek getah J. curcas terhadap kekerasan mikro dentin dan email. Mahkota gigi premolar dibelah 4 longitudinal, lalu ditanam di dalam akrilik dengan 1 permukan tidak tertutup akrilik. Setelah direndam dalam 3 konsentrasi getah J. curcas, permukaan dentin dan email diberi indentasi oleh intan Knoop. Evaluasi berdasar perbandingan KHN kelompok kontrol dan perlakuan. 2. Efek getah J. curcas terhadap kelarutan kalsium dan fosfat. Mahkota gigi premolar utuh dibelah 4 secara longitudinal, lalu direndam dalam 3 konsentrasi getah J. curcas. Setelah 1-3 hari, kalsium dan fosfat yang larut dalam rendaman diukur berturut-turut dengan alat atomic absorption spectrophotometer (AAS) dan spektrofotometer (metoda asam askorbat). Hasil penelitian pH getah J. curcas rata-rata 3,49 ± 0,09 dan perbandingan berat kering/volume basah 15,12 ± 0,31%. (1) Skrining fitokimia: getah J. curcas mengandung golongan senyawa sterol, aglikon flavon, tanin, senyawa pereduksi, glikosida steroid, poliose, dan saponin. (2) Uji toksisitas 1.(1) Sitotoksisitas getah J. curcas pada metoda agar overlay ditemukan zona dekolorisasi indeks 2 dari 5 indeks zona. Tak ada lisis sel, bentuk sel masih jelas. (2) Assay MTT: pads getah J. curcas kadar 0,25% terhadap Fib L929 dan kadar 0,12% terhadap fibroblast gingiva, sel nekrosis. 2.(1) LD50 > 5 g/kg BB, sehingga getah J. curcas dapat diklasifikasi dalam toksik ringan. (2) Tidak ada perbedaan berat badan. (3) Tidak ada perbedaan makroskopik dan mikroskopik organ tubuh yang diperiksa. (4) Terjadi inaktivitas pada hari 1 pada kelompok perlakuan, selanjutnya tidak ada perbedaan. 3. Aktivitas hemolisis getah J. curcas 15% adalah 6,5% dibanding air. Tidak ada hemolisis pada konsentrasi getah J. curcas yang lebih rendah. 4. Tidak ada aktivitas mutagenisitas getah J. curcas. (3) Efek getah J. curcas terhadap makrofag dan fibroblast 1. (1) LPS meningkatkan pembebasan 1L-1β oleh makrofag. (2) Pemberian getah J. curcas menghambat pembebasan 1L-1β oleh makrofag. 2. (1) Makin lama waktu kultur, produksi kolagenase makin banyak. (2) Getah J. curcas menurunkan pembebasan kolagenase oleh fibroblast. (4) Efek histopatologik getah J. curcas terhadap jaringan pulpa dan periapeks (1) Inflamasi dan nekrosis terj adi pads daerah yang terbatas dekat dengan daerah yang kontak dengan getah J. curcas. Di bawahnya terdapat jaringan pulpa normal. (2) Tingkat inflamasi pulpa kelompok perlakuan tidak lebih parah dari kelompok kontrol. (3) Tidak ada radang periapeks pads kelompok kontrol dan perlakuan. (5) Efek getah J. curcas terhadap jaringan keras gigi. 1. Efek getah J. curcas terhadap kekerasan mikro dentin dan email. (1) Kekerasan mikro dentin tidak berbeda bermakna pada 1 dan 2 hari perendaman getah J. curcas antara kelompok kontrol dan perlakuan. Namur lebih kecil setelah 3 hari pada konsentrasi getah 15%. (2) Kekerasan mikro email tidak berbeda antara kelompok kontrol dan perlakuan pada 1 dan 3 hari, Namun lebih kecil setelah 2 hari pada konsentrasi getah J. curcas 15%. 2. Kadar kalsium dan fosfat yang larut meningkat sesuai dengan kenaikan konsentrasi getah J. curcas. Namun lama perendaman tidak berpengaruh secara bermakna terhadap kelarutan kalsium. Kesimpulan (1) Getah J. curcas mengandung sterol, aglikon flavon, tanin, senyawa pereduksi, glikosida steroid, poliose, dan saponin. (2) Tahap 1 evaluasi biologik: getah J. curcas relatif aman pada hewan percobaan berdasar LD50>5 g/kg BB sehingga termasuk dalam klasifkasi toksik ringan; hemolisis 6,5% dibanding air; tidak mutagen; dan sitotoksik dengan nekrosis koagulasi. (3) Uji tahap 2: getah J. curcas cukup efektif dalam menanggulangi pulpalgia, berdasar nekrosis pulpa terbatas, tidak ada kelainan periapeks; kekerasan mikro email dan dentin tidak turun pada 1 hari; menghambat pembebasan IL-1β dan kolagenase. Namun getah melarutkan kalsium dan fosfat. Kesimpulan penelitian: penelitian dapat dilanjutkan ke tahap uji klinik atau tahap 3.

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Biological Study on the Effects of Jatropha Curcas (Euphorbiaceae) Latex on Dental and Periapical TissuesObjective: The objective of this study was to evaluate the safety level and the effects of J. curcas latex on dental and periapical tissues. The aims in details were (1) to identify the main classes of chemical constituent in J. curcas latex; (2) to evaluate the cytotoxicity of J. curcas latex; (3) to determine the acute toxicity of J. curcas latex after single oral administration on mice; (4) to assess hemolytic activity of J. curcas latex; (5) to evaluate mutagenic activity of J. curcas latex; (6) to evaluate the effect on J. curcas latex of IL-1 il release from macrophages; (7) to evaluate the effect of J. curcas latex on collagenase release from fibroblasts; (8) to assess the histopathological effects of J. curcas latex on monkey dental pulp and periapical tissues; (9) to determine the effects of J. curcas latex to dentin and enamel micro-hardness; (10) to assess the effects of J. curcas latex on dissolving calcium and phosphate. Methods: Research design was experimental and explorative. To standardize the sample, J. curcas latex was collected from Balittro, Bogor in 1997, then the pH and wet volume were measured, the latex was lyophilized, dry weight was measured, and latex was stored at-20°C as sample. Biological evaluation was grouped into (1) phytochemical sreening, (2) toxicity test, (3) effects of J.curcas latex on cell, (4) effects of J.curcas latex on dental pulp and periapical tissues, and (5) effects of J.curcas latex on dental hard tissues, (1). Phytochemical screening: the main classes of chemical constituents of J. curcas latex were analyzed qualitatively from ether, ethyl acetate, and water extracts. (2). Toxicity test 1. Cytotoxicity test. (1) Agar overlay technique. J. curcas latex was imbibed in cellulose discs and put on the surface of agar overlaying a neutral red stained Fib L929 cell monolayer. Evaluation was judged on zone index and lysis index after 24 hours incubation. (2) MT assay. J. curcas latex was added to human gingival fibroblasts and Fib L929 cell culture in 96-well micro-plates. After 1-4 days of incubation, MTT assay was performed. Evaluation was based on comparing the OD values of control and test groups. 2. Acute toxicity. A single dose of J. curcas latex was given to male and female mice, intragastrically. LD50 was determined based on mortality rate. Assessment was also performed on 2 weeks observations of body weight, macroscopic and microscopic examinations of several organs. 3. Hemolysis test. Blood was mixed with several concentrations of J. curcas latex. The result was the extent of hemolysis expressed based on the absorbance of the test samples, negative and positive controls. 4. Mutagenicity test. L curcas latex was added to the S. ryphi and E. coil mutans culture. Assessment was based on bacterial revertant colonies, compare to positive and negative controls. (3) Effects of J.curcas latex on macrophages and fibroblasts 1. Effects of .T. curcas latex on the release of IL-1 β from macrophages. Five doses of J. curcas latex from 75-1200 μg/ml were added into the culture of BALB/c mice peritoneal macrophages, along with, after, or before addition of LPS. Following 1-3 days of incubation, IL-1P presence in supernatant was measured by ELISA using Quantikine ]L-1P for mouse kit. 2. Effects of J. curcas latex on the release of collagenase. Four doses of J. curcas latex from 37.5-300 µg/ml were added to human gingival fibroblasts cell culture. After 1-4 days of incubation, collagenase in the supernatant was assayed with collagen. The degradation products were then separated by SDS-PAGE and the density of 3/4 αA bands was measured semi quantitatively by Adobe Photo computer program. (4) Effects of J.curcas latex on dental pulp and periapical tissues. The latex of J. curcas was brought in contact with dental pulp and sealed. Assessment was based on the presence of inflammation and necrosis in dental pulp and periapical tissues, histopathologically. (5) Effects of J.curcas latex on dental hard tissues 1. Effects of J. curcas latex on dentin and enamel micro-hardness. Intact premolar crowns were cut longitudinally into 4 fragments, followed by embedding of each fragment in acrylats leaving 1 free surface. The fragments were then soaked in 3 concentrations of J. curcas latex from 3.7-15% for 1-3 days. The dentin and enamel micro-hardness were assessed by Knoop hardness measurement. 2. Effects of J. curcas latex on dissolved calcium and phosphate. Intact premolar crowns were cut longitudinally into 4 fragments, followed by soaking the fragments in 3 concentration of J. curcas latex from 3.7-15% for 1-3 days. The dissolved calcium and phosphate were measured according to atomic absorption spectrophotometer and spectrophotometer (ascorbic acid method), respectively. Results: The mean ± SD of J. curcas latex pH was 3.49 ± 0.09. The dry weight/wet volume was 15.12 ± 0.31%. (1). Phytochemical screening: sterols, flavone aglycones, tannins, reducing compounds, sterol glycosides, poliose, and saponins were identified in J. curcas latex. (2) Toxicity test 1. (1) Agar overlay technique. 2-5 mm decoloration zones were observed, indicating that J. curcas latex was cytotoxic. No lysis of cells was observed within the decolorized zone. (2) MTT assay. At 2.5 mg/ml J. curcas latex no living Fib L929 cells were observed, while the same result was shown at 1.2 mg/ml J. curcas latex on human gingival fibroblasts. 2. LD50 was more than 5 g/kg BW, hence dry J. curcas latex may be classified into mildly toxic substance. No significant body weight difference was observed. Macroscopic and microscopic examination on several organs showed no differences between test and control groups. 3. 6,5% hemolytic activity of 15% J. curcas latex compared to water was observed, while no hemolisis was observed with lower concentrations of latex. 4. No mutagenic ativity was observed with J. curcas latex. (3) Effects of J.curcas latex on macrophages and fibroblasts 1. (1) LPS increased the release of IL-1β. (2) J. curcas latex inhibited the release of IL-lβ from macrophages. 2. (1) The longer the duration of incubation, the more collagenase was released. (2) J. curcas latex decreased collagenase release by human gingival fibroblast. (4) Effects of I. curcas latex on dental pulp and periapical tissues. Inflammation and necrosis were observed in a limited area, which was in direct contat with J. curcas latex, underneath was normal pulp. Inflammation in the pulp of test group was not greater than in the control group. No inflammation or necrosis in periapical tissues was observed in all groups. (5) Effects of J. curcas latex on dental hard tissues 1. (1) The micro-hardness of dentin was not lowered after 1 and 2 days treatment, but lower after 3 days at 15% J. curcas latex. (2) The enamel microhardness was not decreased after 1 and 3 days immersion in J. curcas latex, but decreased after 2 days at 15% J. curcas latex. 2. The calcium and phosphate release were increased in accordance to the concentration of J. curcas latex. The duration of treatment did not influence the release of calcium, while it influenced the release of phosphate. Conclusions (1) J. curcas latex contains sterols, flavone aglycones, tannins, reducing compounds, sterol glycosides, poliose, and saponins. (2) Level 1 biological evaluation: J. curcas latex is relatively safe in animals based on LD50>5 g/kg BW, 6,5% hemolysis compared to water, not mutagenic, but cytotoxic with coagulative necrosis. (3) Level 2 biological evaluation: J. curcas latex seems to be effective in relieving pulpal pain. It caused coagulative necrosis in pulp, which was in direct contact with J. curcas latex while the tissue underneath was normal. It did not cause inflammation of periapical tissues, and did not lower the dentin and enamel micro-hardness after 1 day of exposure, but it lowered the microhardness after 3 days. It inhibited IL-1β and collagenase release. It dissolved dental calcium and phosphate."