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"Hipertensi merupakan salah satu kondisi medis yang cukup serius karena dapat meningkatkan risiko penyakit jantung, otak, ginjal dan penyakit lainnya. Wilayah di DKI Jakarta dengan prevalensi hipertensi tertinggi berdasarkan diagnosis dokter yaitu Kota Jakarta Pusat sebesar 12,16%. Partikulat meter organik dan komponen partikulat meter dapat memicu proinflammatory effects pada paru-paru karena kemampuannya mengakibatkan stress oksidatif. Penelitian ini bertujuan untuk menyusun model pengaruh pajanan PM2,5 di udara ambien terhadap kejadian hipertensi melalui stress oksidatif dan sitokin inflamasi pada penduduk di Jakarta Pusat. Penelitian dilakukan pada penduduk dewasa (18-65 tahun) di Kota Jakarta Pusat dengan disain studi hybrid cross sectional ecology. Pengumpulan data secara cluster random sampling dengan analisis data dilakukan melalui pemodelan regresi logistik multilevel dan cox regresi proporsional hazard.Hasil analisis menunjukkan terdapat asosiasi antara PM2,5 di udara ambien dengan biomarker stress oksidatif (IOR PM2,5: 2,185173-2,185176) dan dengan biomarker sitokin inflamasi (IOR PM2,5: 1,21-1,91). Pemodelan multivariat dengan cox regresi proporsional hazard menunjukkan bahwa variabel umur dan indeks massa tubuh merupakan confounder hubungan antara stress oksidatif dengan hipertensi dan antara sitokin inflamasi dengan hipertensi dengan nilai Rasio Prevalens adjusted (95% CI) masing-masing sebesar 1,19 (0,69-2,03) dan 0,99 (0,58-1,72). Dapat disimpulkan bahwa variabel konsentrasi PM2,5 di udara ambien memiliki peran terhadap terjadinya hipertensi, stress oksidatif dan sitokin inflamasi pada penduduk di Jakarta Pusat.

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Hypertension is a serious medical condition that can increase the risk of heart, brain, kidney and other diseases. The area in DKI Jakarta with the highest prevalence of hypertension based on doctor diagnosis is Central Jakarta city about 12.16%. Organic particulate matters and particulate matter components can trigger proinflammatory efects in the lung due to their ability to cause oxidative stress. This study aims to develop a model of the Influence of PM2,5 Exposure in Ambient Air on Hypertension Occurrence through Oxidative Stress and Inflammatory Cytokines among residents in Central Jakarta. The study was conducted among adult residents (age 18-65 years) in Central Jakarta with hybrid cross sectional study design. Data collected using cluster random sampling with data analysis carried out through multilevel logistic regression modeling and cox proportional hazard regression.

Results show there is an association between PM2.5 in ambient air with oxidative stress biomarkers (IOR PM2.5: 2.185173-2.185176) and with inflammatory cytokine biomarkers (IOR PM2.5: 1.21-1.91). Multivariate modeling with Cox regression proportional hazard shows that age and body mass index are confounders of the relationship between oxidative stress with hypertension and between inflammatory cytokines with hypertension with an adjusted prevalence ratio (95% CI) value of 1.19 (0.69-2.03) and 0.99 (0.58-1.72). It can conclude that concentration of PM2.5 in ambient air has a role on hypertension, oxidative stress and inflammatory cytokine among residents in Central Jakarta."

"[ABSTRAKDoksorubisin merupakan salah satu antikanker golongan antrasiklin yang efektif,untuk keganasan di darah. Akan tetapi, seperti antikanker konvensional padaumumnya, penggunaan doksorubisin dapat menyebabkan berbagai efek samping padaorgan lain, misalnya pada testis sehingga penggunaannya di klinis menjadi terbatas.Hal ini disebabkan karena mekanisme antikanker doksorubisin dapat jugamenimbulkan toksisitas pada testis. Peningkatan stress oksidatif adalah salah satumekanisme dapat menyebabkan kerusakan pada organ tersebut. Mangiferin sebagaizat antioksidan alami, terkandung dalam Mangifera Indica L. diperkirakan dapatdigunakan untuk mengurangi toksisitas testis. Namun sampai saat ini, belum adapenelitian yang mengeksplor efek proteksi mangiferin terhadap kerusakan oksidatiftestis yang diinduksi doksorubisin.Penelitian ini menggunakan tikus jantan Sprague Dawley, yang dibagi menjadi empatkelompok. Masing-masing kelompok terdiri dari enam ekor tikus. Tikus padakelompok kontrol negatif diberikan doksorubisin secara intraperitoneal (dosis total 15mg/kgBB) dan kelompok normal diberikan NaCl 0,9%. Mangiferin (dosis 30 dan 60mg/kg BB) diberikan oral selama tujuh minggu. Setelah, tujuh minggu tikusdimatikan dan testis dikumpulkan untuk analisis parameter stress oksidatif biokimiakadar MDA (malonedyaldehide), aktivitas SOD (Superoxide Dysmutase), perubahanhistologi dan apoptosis kaspase-9 dan kaspase-12. Hasil penelitian menunjukkanbahwa pemberian doksorubisin selama dua minggu dapat meningkatkan kadar MDA,menyebabkan kerusakan sel spermatogenik, sel Sertoli dan penciutan diametertubulus seminiferus testis, peningkatan ekspresi kaspase-9 di sisi luminal yangdiberikan doksorubisin. Pemberian mangiferin dosis 30 dan 60 mg/kg BB selamatujuh minggu dapat mengurangi kerusakan sel spermatogenik dan sel Sertoli tubulusseminiferus testis, penurunan kadar MDA dan penurunan ekspresi kaspase-9 padakelompok perlakuan diberikan doksorubisin dan mangiferin. Perbaikan parameterparameterini mengindikasikan bahwa mangiferin mempunyai efek proteksi terhadapkerusakan sel spematogenik dan sel sertoli tubulus seminiferus testis tikus yangdiberikan doksorubisin.

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ABSTRACTDoxorubicin, one of the anthracycline anticancer class, is effective especially in bloodmalignancy. However, as in the general use of the conventional anticancer-drugs.Doxorubicin can cause various side effects in other organs, such as the testes so thatits use in clinical become limited. This is because of the anticancer mechanism cancause cytotoxicity on testes. The increased oxidative stress is the main mechanismthat can be the causal. Mangiferin as a natural antioxidant substance, contained inMangifera Indica L., is expected to reduce the toxicity. The Antioxidants areexpected to reduce the toxicity of the testes. But until now, no studies have exploredthe effects of mangiferin protection against oxidative damage induced testiculardoxorubicin.This study used male Sprague Dawley rats, which were divided into four groups.Each group consisted of six mice. Rats in the negative control group was givenintraperitoneal doxorubicin (total dose 15 mg/kg) and the normal group was givennormal saline 0.9%. Mangiferin (doses of 30 and 60 mg/kg) was administered orallyfor seven weeks to the treatment gtoups (both DOX and MAG were given). Afterseven weeks-off, testes of mice were collected for analysis of biochemical parametersi.e. oxidative stress levels of MDA and SOD activity, histology and apoptosis of thecaspase-9 and of the caspase-12. The results showed that administration ofdoxorubicin for two-weeks can cause damage to Sertoli, spermatogenic cells andshrinking of diameter of testicular seminiferous tubules, increasing the levels ofMDA, increasing in the expression of caspase-9 on the luminal side in the treatmentgroup was given doxorubicin. This possibility of the doxorubicin dose given is tootoxic to the testes in this study. Mangiferin dose administration of 30 and 60 mg / kgfor seven-weeks can reduce the damage of Sertoli and spermatogenic cells of thetesticular seminiferous tubules, decrease levels of MDA, reduce Sertoli,spermatogenic cell and diameter of the testicular seminiferous tubulus damage,decrease caspase-9 expression only on luminal side of the seminiferus tubulus in thegroups given both of doxorubicin and mangiferin. these parameters indicate thatmangiferin, which has antioxidant?s activity, provides protective effects againstoxidative damage in spematogenic and Sertoli cell testicular seminiferous tubules ofmice given doxorubicin, Doxorubicin, one of the anthracycline anticancer class, is effective especially in bloodmalignancy. However, as in the general use of the conventional anticancer-drugs.Doxorubicin can cause various side effects in other organs, such as the testes so thatits use in clinical become limited. This is because of the anticancer mechanism cancause cytotoxicity on testes. The increased oxidative stress is the main mechanismthat can be the causal. Mangiferin as a natural antioxidant substance, contained inMangifera Indica L., is expected to reduce the toxicity. The Antioxidants areexpected to reduce the toxicity of the testes. But until now, no studies have exploredthe effects of mangiferin protection against oxidative damage induced testiculardoxorubicin.This study used male Sprague Dawley rats, which were divided into four groups.Each group consisted of six mice. Rats in the negative control group was givenintraperitoneal doxorubicin (total dose 15 mg/kg) and the normal group was givennormal saline 0.9%. Mangiferin (doses of 30 and 60 mg/kg) was administered orallyfor seven weeks to the treatment gtoups (both DOX and MAG were given). Afterseven weeks-off, testes of mice were collected for analysis of biochemical parametersi.e. oxidative stress levels of MDA and SOD activity, histology and apoptosis of thecaspase-9 and of the caspase-12. The results showed that administration ofdoxorubicin for two-weeks can cause damage to Sertoli, spermatogenic cells andshrinking of diameter of testicular seminiferous tubules, increasing the levels ofMDA, increasing in the expression of caspase-9 on the luminal side in the treatmentgroup was given doxorubicin. This possibility of the doxorubicin dose given is tootoxic to the testes in this study. Mangiferin dose administration of 30 and 60 mg / kgfor seven-weeks can reduce the damage of Sertoli and spermatogenic cells of thetesticular seminiferous tubules, decrease levels of MDA, reduce Sertoli,spermatogenic cell and diameter of the testicular seminiferous tubulus damage,decrease caspase-9 expression only on luminal side of the seminiferus tubulus in thegroups given both of doxorubicin and mangiferin. these parameters indicate thatmangiferin, which has antioxidant’s activity, provides protective effects againstoxidative damage in spematogenic and Sertoli cell testicular seminiferous tubules ofmice given doxorubicin]"

"Latar belakang: Hipoksia hipobarik seringkali terjadi pada orang yang terbiasa berada di tempat berketinggian rendah dan tiba-tiba berpindah ke tempat yang tinggi, seperti penerbang pesawat militer dan pendaki gunung. Kondisi hipoksia menginduksi stress oksidatif. Salah satu molekul yang dapat terdampak oleh stress oksidatif adalah protein, menyebabkan peningkatan kadar karbonil melalui proses karbonilasi protein. Otot rangka adalah jaringan yang sangat rentan mengalami stress oksidatif pada kondisi hipoksia, terutama yang melibatkan karbonilasi protein, mengingat kandungan protein dan kebutuhan oksigen yang tinggi pada jaringan tersebut. Peneliti tertarik untuk meneliti pengaruh induksi hipoksia hipobarik intermiten terhadap kadar karbonil pada hewan coba tikus.Metode: Sebuah penelitian eksperimental in vivo dilakukan dengan mengkondisikan empat kelompok tikus pada keadaan hipoksia hipobarik di dalam hypobaric chamber sebanyak satu kali (I), dua kali (II), tiga kali (III), dan empat kali (IV). Satu kelompok berperan sebagai kontrol. Musculus gastrocnemius semua tikus diambil untuk diukur kadar karbonilnya. Karbonil dimodifikasi oleh 2,4-dinitrofenilhidrazin (DNPH) sebelum diukur kadarnya dengan spektrofotometri. One-Way ANOVA digunakan untuk analisis data.Hasil: Rata-rata kadar karbonil pada kelompok kontrol, I, II, III, dan IV secara berturut-turut adalah 2.801±0.1198, 3.909±0.3172, 5.577±0.3132, 3.823±0.3038, dan 3.731±0.2703 nmol/ml. Rata-rata kadar karbonil masing-masing kelompok I, II, III, dan IV berbeda signifikan (p < 0,05) dengan kelompok kontrol (kelompok yang tidak memperoleh paparan hipoksia hipobarik intermiten).Kesimpulan: Terdapat perbedaan kadar karbonil yang signifikan antara musculus gastrocnemius tikus Sprague-Dawley yang diberi perlakuan hipoksia hipobarik intermiten dan yang tidak diberi perlakuan hipoksia hipobarik intermiten.

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Introduction: Hypobaric hypoxia often occurs in people who are used to low altitudes and suddenly move to high places, such as military airplane pilots and mountain climbers. Hypoxic conditions induce oxidative stress. Oxidative stress can affect proteins, causing increased carbonyl levels through protein carbonylation. Skeletal muscle is susceptible to oxidative stress under hypoxic conditions, especially those involving protein carbonylation, given the high protein content and oxygen demand. We are interested in examining the effect of intermittent hypobaric hypoxia induction on carbonyl levels in rats.

Method: An in vivo experimental study was carried out by conditioning four groups of rats in a hypobaric hypoxic state in a hypobaric chamber once (I), twice (II), three times (III), and four times (IV). One group acted as control. Carbonyl content of gastrocnemius muscle of all rats was measured. The carbonyl is modified by 2,4-dinitrophenylhydrazine (DNPH) before its concentration is measured by spectrophotometry. One-Way ANOVA was used for data analysis.

Result: The average carbonyl content in the control group, I, II, III, and IV were 2.801±0.1198, 3.909±0.3172, 5.577±0.3132, 3.823±0.3038, and 3.731±0.2703 nmol/ml, respectively. The average carbonyl levels of each group I, II, III, and IV were significantly different (p < 0.05) with the control group (the group that did not receive intermittent hypobaric hypoxia exposure).

Conclusion: There was a significant difference in carbonyl levels between the gastrocnemius muscle of Sprague-Dawley rats treated with intermittent hypobaric hypoxia and those not treated with intermittent hypobaric hypoxia."

"Kanker secara umum disebabkan oleh bahan-bahan kimia yang berbahaya akibat paparan lingkungan. Paparan gas buang kendaraan bermotor dan asap rokok merupakan polutan yang cukup potensial menyebabkan kanker. Paparan gas buang kendaraan bermotor banyak dialami pekerja lalu lintas sehingga resiko kanker pada polisi lalu lintas cukup tinggi. Gaya hidup sebagian polisi lalu lintas yang merokok juga menjadi penyebab salah satu potensi resiko kanker yang tinggi. Resiko kanker ini disebabkan adanya mekanisme stress oksidatif. Stress oksidatif merupakan salah satu penyebab pemicu pembentukan radikal bebas yang dapat menyebabkan terjadinya kanker. Sebelum pembentukan sel kanker terjadi, sel memiliki sistem pertahanan terhadap pembentukan sel kanker. Sistem pertahanan sel ini berupa perbaikan susunan basa DNA. Sistem perbaikan yang sering terjadi pada basa guanin terjadi dengan menglepaskan DNA-adduct, 8-hidroksi-2’-deoksiguanosin, umumnya digunakan sebagai biomarker resiko terhadap kanker. Metode pengukuran 8-hidroksi-2’-deoksiguanosin dapat dilakukan dengan HPLC-UVvis. Dari sampel urin sebanyak 17 orang, pengukuran dilakukan dengan membandingkan konsentrasi 8-hidroksi-2’-deoksiguanosin pada polisi lalu lintas yang merokok sebanyak 8 orang dengan polisi lalu lintas yang tidak merokok sebanyak 9 orang. Rerata konsentrasi 8-hidroksi-2’-deoksiguanosin pada polisi lalu lintas yang merokok sebesar 0,619 mg/g kreatinin dan pada polisi lalu lintas yang tidak merokok sebesar 0,268 mg/g kreatinin. Hasil analisis mengindikasikan bahwa polisi lalu lintas yang merokok memiliki resiko terhadap penyakit kanker lebih tinggi dibandingkan dengan polisi lalu lintas yang tidak merokok.

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Cancer is generally caused by chemicals hazardous because of environmental exposure. Exposure of motor vehicle exhaust gas and cigarette smoke is a pollutant that is potentially causing cancer. Exposure of motor vehicle exhaust gas received traffic workers and raised the risk of cancer for them. Lifestyle of smoking by traffic police is one another of the potential cancer risk. The risk caused by mechanism oxidative stress. Oxidative stress is one of the reason to make free radicals and can cause the cancer. Before the formation of cancer cells, the cell has a defense system against formation of cancer cell. This cell defense system can repair DNA base. System improvements cell can release guanine-adducts, 8-hydroxy-2'-deoxyguanosine, is generally as a biomarker of cancer risk. Methods of measuring 8-hydroxy-2'-deoxyguanosine can be done by HPLC-UVvis. The measurement of the urine samples from 17 persons, measurements were done by comparing between the concentration of 8-hydroxy-2'-deoxyguanosine of smoking’ traffic police (8 persons) and the not smoking’ traffic police (9 persons). The mean concentration of 8-hydroxy-2'-deoxyguanosine on smoking’ traffic police at 0.619 mg per g creatinine and the not smoking’ traffic police at 0.268 mg per g creatinine. The analysis result indicates that the smoking’ traffic police have an increased risk of cancer is higher than the not smoking’ traffic police."

"Pendahuluan: Peningkatan karbondioksida pada atmosfer berdampak pada perubahan iklim. Peningkatan karbondioksida dapat mempengaruhi tubuh manusia terutama pada sistem imun manusia, yang diketahui dapat menurunkan produksi sel T. Pada penelitian ini menggunakan subjek berupa sel Peripheral Blood Mononuclear Cell (PBMC) yang menjadi representatif dari sistem imun manusia. Berbagai respon mungkin akan ditunjukkan jika PBMC dipaparkan karbon dioksida dengan konsentrasi lebih tinggi dari normal, tetapi pada penelitian ini hanya spesifik melihat pada kadar hidrogen peroksida melalui pengukuran kadar DCFH-DA. Metode: PBMC yang sudah diisolasi dari subjek dipaparkan karbon dioksida 5% sebagai kontrol dan 15% sebagai uji. Waktu pemaparan dilakukan selama 24 jam dan 48 jam. Pada waktu akhir waktu inkubasi untuk masing-masing kelompok akan dilakukan pengukuran kadar DCFH-DA dengan fluorometri. Hasil yang didapat berupa absorbansi/sel yang akan dianalisis lebih lanjut melalui SPSS versi 24. Hasil: Didapatkan jumlah hidrogen peroksida lebih tinggi dibandingkan dengan kontrol secara signifikan (p<0.05) saat diinkubasi selama 24 jam tetapi tidak signifikan pada waktu inkubasi 48 jam. Perbandingan konsentrasi hidrogen peroksida antara 24 dan 48 jam menunjukkan penurunan secara signifikan konsentrasi saat diinkubasi 48 jam jika dibanding 24 jam. Kesimpulan: Paparan karbon dioksida selama 24 jam dapat meningkatkan produksi hidrogen peroksida dibandingkan kontrol, namun hal ini tidak terjadi pada PBMC yang dipaparkan karbondioksida selama 48 jam.

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Introduction: Increased carbon dioxide in the atmosphere has an impact on climate change. Increased carbon dioxide can affect the human body, especially in the human immune system, which is known to reduce the production of T cells. So as to represent the human immune system, this study uses the subject of Peripheral Blood Mononuclear Cell (PBMC) cells. Various responses might be demonstrated if PBMCs were exposed to carbon dioxide concentrations higher than normal, but in this study only specifically looked at hydrogen peroxide levels by measuring DCFH-DA levels. Method: PBMC which had been isolated from the subject were exposed to 5% carbon dioxide as a control and 15% as a test. Exposure time is 24 hours and 48 hours. At the end of the incubation time for each group, measurement of DCFH-DA with fluorometry will be carried out. The results obtained in the form of absorbance / cells will be further analyzed through SPSS version 24 Result : There was a significant increase in the amount of hydrogen peroxide compared to the control (p <0.05) when incubated for 24 hours but not significantly at 48 hours incubation time. Comparison of hydrogen peroxide concentrations between 24 and 48 hours shows a significant decrease in concentration when incubated 48 hours when compared to 24 hours (p<0.05). Conclusion: Exposure to carbon dioxide for 24 hours can increase hydrogen peroxide production compared to control, but there is no significant change in hydrogen peroxide production was observed in 48 hours of carbon dioxide exposure."

"Latar Belakang: Hiperglikemia kronik pada diabetes akan menyebabkan peningkatan produksi reactive oxygen species ROS yang berkontribusi terhadap progresifitas nefropati. Kurkumin telah terbukti memiliki khasiat renoprotektif pada nefropati diabetik melalui efek antioksidan. Tetapi, kurkumin memiliki kekurangan yaitu, bioavailabilitas rendah, metabolisme lintas pertama yang ekstensif, dan kelarutan yang buruk. Penelitian ini bermaksud untuk mengetahui efek kurkumin dalam bentuk nanopartikel nanokurkumin terhadap tikus diabetes yang diinduksi Streptozotocine-Nikotinamide terhadap progresifitas nefropati melalui hambatan stress oksidatif. Metode: Tikus jantan Sprague Dawley diinduksi diabetes melalui pemberian Nikotinamide 100 mg/kg , dilanjutkan dengan Streptozotocine 55 mg/kg , dosis tunggal, intraperitoneal. Kemudian, tikus dibagi menjadi 4 kelompok; normal, DM tanpa treatment, DM treatment kurkumin 100 mg/kg, dan DM treatment nanokurkumin 100 mg/kg, selama 30 hari. Fungsi fisiologis dinilai berdasarkan BB, GDP, dan rasio berat ginjal. Fungsi ginjal dinilai berdasarkan klirens kreatinin, BUN, dan proteinuria. Kerusakan histologis dinilai dari scoring pewarnaan HE. Stress oksidatif diukur dari kadar malondialdehyde MDA dan kadar superoxide dismutase SOD. Hasil: Meski tidak signifikan, pemberian nanokurkumin menunjukkan efek yang lebih baik daripada pemberian kurkumin berdasarkan parameter SOD, GDP, berat badan, rasio berat ginjal, klirens kreatinin, protein urin, dan gambaran histopatologi. Pemberian nanokurkumin secara signifikan menurunkan kadar BUN. Kesimpulan: Setelah 30 hari pemberian nanokurkumin 100 mg/kg BB maupun kurkumin dengan dosis sama tidak dapat menurunkan stress oksidatif, namun dapat mencegah progresifitas nefropati diabetikum.

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Background: Chronic hyperglycaemia in diabetes leads to the overproduction of reactive oxygen species ROS that these contribute to the development of diabetic nephropathy. Curcumin, has been recently discovered to have renoprotective effects on diabetic nephropathy DN through its antioxidant properties. However, low peroral bioavailability, extensive first pass metabolism, and low solubility is a major limiting factor for the success of clinical utilization of curcumin. The present study was undertaken to examine the effect of curcumin formed in nanoparticles nanocurcumin treatment in Streptozotocine Nicotinamide induced diabetic rat on the progressivity of nephropathy through its stress oxidative inhibition.

Method: Diabetes was induced by Nicotinamide 100 mg kg followed by Streptozotocine 55 mg kg, single dose, intraperitoneal, in male Sprague Dawley rats. Then rats divided into four groups, namely normal, diabetic, diabetic treated with curcumin 100 mg kg, and diabetic treated with nanocurcumin 100 mg kg for 30 days. Physiological function was assessed by body weight, FBG, and kidney weight ratio. Renal function was assessed by creatinine clearance, BUN, and proteinuria. Diabetic renal damage was determined by Hematoxyclin Eosin HE staining. Oxidative stress was measured by renal malonaldehyde MDA level, and superoxide dismutase SOD level.

Result: Although did not significant, nanocurcumin showed better effect than curcumin based on SOD, FBG, body weight, kidney weght ratio, creatinine clearance, proteinuria, and renal histopathological changes. Nanocurcumin showed significant decreases in BUN level.

Conclusion: After 30 days of treatment, both nanocurcumin and curcumin 100 mg kg did not decreases oxidative stress but showed inhibition in progressivity of nephropathy."

"Pendahuluan: Peningkatan karbondioksida pada atmosfer berdampak pada perubahan iklim. Peningkatan karbondioksida dapat mempengaruhi tubuh manusia terutama pada sistem imun manusia, yang diketahui dapat menurunkan produksi sel T. Pada penelitian ini menggunakan subjek berupa sel Peripheral Blood Mononuclear Cell (PBMC) yang menjadi representatif dari sistem imun manusia. Berbagai respon mungkin akan ditunjukkan jika PBMC dipaparkan karbon dioksida dengan konsentrasi lebih tinggi dari normal, tetapi pada penelitian ini hanya spesifik melihat pada kadar hidrogen peroksida melalui pengukuran kadar DCFH-DA. Metode: PBMC yang sudah diisolasi dari subjek dipaparkan karbon dioksida 5% sebagai kontrol dan 15% sebagai uji. Waktu pemaparan dilakukan selama 24 jam dan 48 jam. Pada waktu akhir waktu inkubasi untuk masing-masing kelompok akan dilakukan pengukuran kadar DCFH-DA dengan fluorometri. Hasil yang didapat berupa absorbansi/sel yang akan dianalisis lebih lanjut melalui SPSS versi 24. Hasil: Didapatkan jumlah hidrogen peroksida lebih tinggi dibandingkan dengan kontrol secara signifikan (p<0.05) saat diinkubasi selama 24 jam tetapi tidak signifikan pada waktu inkubasi 48 jam. Perbandingan konsentrasi hidrogen peroksida antara 24 dan 48 jam menunjukkan penurunan secara signifikan konsentrasi saat diinkubasi 48 jam jika dibanding 24 jam. Kesimpulan: Paparan karbon dioksida selama 24 jam dapat meningkatkan produksi hidrogen peroksida dibandingkan kontrol, namun hal ini tidak terjadi pada PBMC yang dipaparkan karbondioksida selama 48 jam.

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Introduction: Increased carbon dioxide in the atmosphere has an impact on climate change. Increased carbon dioxide can affect the human body, especially in the human immune system, which is known to reduce the production of T cells. So as to represent the human immune system, this study uses the subject of Peripheral Blood Mononuclear Cell (PBMC) cells. Various responses might be demonstrated if PBMCs were exposed to carbon dioxide concentrations higher than normal, but in this study only specifically looked at hydrogen peroxide levels by measuring DCFH-DA levels.

Method: PBMC which had been isolated from the subject were exposed to 5% carbon dioxide as a control and 15% as a test. Exposure time is 24 hours and 48 hours. At the end of the incubation time for each group, measurement of DCFH-DA with fluorometry will be carried out. The results obtained in the form of absorbance / cells will be further analyzed through SPSS version 24.

Result : There was a significant increase in the amount of hydrogen peroxide compared to the control (p <0.05) when incubated for 24 hours but not significantly at 48 hours incubation time. Comparison of hydrogen peroxide concentrations between 24 and 48 hours shows a significant decrease in concentration when incubated 48 hours when compared to 24 hours (p<0.05).

Conclusion: Exposure to carbon dioxide for 24 hours can increase hydrogen peroxide production compared to control, but there is no significant change in hydrogen peroxide production was observed in 48 hours of carbon dioxide."

"Bekatul umumnya digunakan sebagai pakan ternak atau dibuang. Padahal, bekatul dapat diekstraksi menjadi minyak bekatul yang mengandung antioksidan untuk melindungi diri dari radikal bebas yang menyebabkan stress oksidatif. Penelitian ini merupakan penelitian eksperimental menggunakan sampel tersimpan 24 tikus wistar terbagi dalam enam kelompok, yaitu kelompok kontrol, kelompok diberikan CCl4 0,55g/kgBB kemudian dibedah 2 hari setelahnya, kelompok diberikan minyak bekatul 0,5mL/hari selama 52 hari kemudian diberikan CCl4 0,55g/kgBB kemudian dibedah 2 hari setelahnya, kelompok diberikan minyak bekatul 1,5 mL/hari selama 52 hari kemudian diberikan CCl4 0,55g/kgBB kemudian dibedah 2 hari setelahnya, kelompok diberikan CCl4 0,55g/kgBB kemudian 2 hari setelahnya diberi minyak bekatul 0,5mL/hari selama 59 hari kemudian dibedah esoknya, kelompok diberikan CCl4 0,55g/kgBB kemudian 2 hari setelahnya diberi minyak bekatul 1,5mL/hari selama 59 hari kemudian dibedah esoknya. Selanjutnya mengukur absorbansi lalu menghitung MDA plasma dengan membandingkan absorbansinya dengan standar MDA. Kelompok CCl4 0,55 g/kgBB memiliki MDA lebih tinggi dibandingkan kelompok kontrol secara signifikan. MDA kelompok minyak bekatul 0,5 ml dan 1,5 ml kemudian diinduksi CCl4 0,55 g/kgBB lebih rendah dibandingkan kelompok CCl4 meskipun tidak signifikan. MDA kelompok CCl4 kemudian diberikan minyak bekatul lebih rendah dibandingkan kelompok CCl4 meskipun tidak signifikan. Minyak bekatul 0,5 ml maupun 1,5 ml menurunkan MDA plasma dibandingkan kelompok CCl4 dalam preventif maupun kuratif meskipun tidak signifikan. MDA kelompok preventif lebih rendah dibandingkan kuratif meskipun tidak signifikan. Dosis 1,5 ml menurunkan MDA plebih besar dibandingkan 0,5 ml meskipun tidak signifikan.

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Rice bran used as animal feed or discarded. But, rice bran can be extracted into oil contains antioxidants to protect body from free radicals that cause oxidative stress. It is an experimental study using stored samples of 24 wistar rats divided into six groups: control group, group given CCl4 0.55g/kgBW then dissected 2 days later, group given rice bran oil 0.5mL/day for 52 days then given CCl4 0.55g/kgBW then operated 2 days later, group given rice bran oil 1.5 mL/day for 52 days then given CCl4 0,55g/kgBW then operated 2 days later, group given CCl4 0,55g/kgBW then 2 days later given rice bran oil 0.5mL/day for 59 days then operated next day, group given CCl4 0.55g/kgBB then 2 days later given rice bran oil 1.5mL/day for 59 days then operated tomorrow. Measuring absorbance and calculate plasma MDA by comparing absorbance with MDA standard. 0.55g/kgBW CCl4 group have significantly higher MDA than control group. MDA of 0.5ml and 1.5ml rice bran oil group then induced by CCl4 0.55 g/kgBW is lower than CCl4 group although not significant. MDA of CCl4 group then given rice bran oil is lower than CCl4 group although not significant. Rice bran oil 0.5ml and 1.5ml decreased plasma MDA compared to CCl4 group in both preventive and curative, although not significant. MDA of preventive group is lower than curative group, although not significant. 1.5ml dose decrease MDA more than 0.5ml, although not significant."

"Malondialdehyde (MDA) telah banyak dilaporkan sebagai biomarker, produk genotoksik endogen yang terbentuk dari hasil lipid peroksidasi dan stress oksidatif dapat mengikat dan memodifikasi protein, phospholipid maupun DNA membentuk adduct yang stabil. Peningkatan stress oksidatif memicu dalam pembentukan adduct telah dikaitkan dengan berbagai pola penyakit seperti kanker, penyakit kardiovaskular dan neurodegeneratif. Studi ini salah satunya bertujuan untuk mengetahui efek sinergis pembentukan DNA Adduct (8-hydroxy-2-deoxyguanosine (8-OHdG) secara in vitromakibat reaksi dari malondialdehyde (MDA) dan/atau paparan Cr (VI) dengan bantuan H2O2 melalui reaksi Fenton terhadap DNA murni 2’-deoxyguanosine (dG) pada variasi suhu 37oC dan 60oC, pH 7,4 dan 8,4 serta lama inkubasi 3 dan 16 jam. Sedangkan studi in vivo dilakukan dengan treatment pada kelompok tikus (Rattus norvegicus) galur Wistar dengan paparan MDA (10 mg/kgBB), dan kelompok tikus dengan paparan campuran MDA (10mg/kgBB) dan Cr(VI) (0,4mg/kgBB) selama 28 hari. Sampel urin dikumpulkan setiap minggu. Pembentukan 8-OHdG secara in vitro dianalisis dengan HPLC, sedangkan pembentukan 8-OHdG pada sampel urin tikus dianalisis dengan menggunakan LC-MS/MS dengan kromatografi fasa terbalik. Dari hasil penelitian ini diperoleh nilai validasi instrumen UHPLC dengan nilai regresi linier (R) 0,9973 dengan LOD adalah 11,03 μg/L dan nilai LOQ adalah 36,77 μg/L. Pada perlakuan secara in vitro paparan senyawa MDA pada kondisi suhu inkubasi 60oC selama 3 jam, pH 7,4 dihasilkan konsentrasi 8-OHdG paling tinggi yaitu 404,09 μg/L. Pada penelitian secara in vitro juga diperoleh data bahwa terdapat efek sinergis peningkatan konsentrasi 8-OHdG yang dihasilkan dari reaksi in vitro 2’deoksiguanosin dengan MDA + Cr (VI) sebagai senyawa radikal bebas yang memicu terjadinya kerusakan DNA. Pada pengamatan secara in vivo terhadap tikus percobaan yang dipaparkan senyawa xenobiotik (MDA dan Cr (VI) juga ditemukan gejala klinis penurunan berat badan sebelum dan sesudah paparan. Hasil analisis sampel urin perlakuan in vivo dengan instrument LCMS/MS terlihat adanya efek sinergis pada paparan MDA + Cr (VI).

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Malondialdehyde (MDA) has been widely reported as a biomarker, an endogenous genotoxic product that is formed from the results of lipid peroxidation and oxidative stress that can bind and modify proteins, phospholipids and DNA to form stable adducts. Increased oxidative stress triggers in adduct formation have been linked to various disease patterns such as cancer, cardiovascular and neurodegenerative diseases. One of the purposes of this study is to determine the synergistic effect of the formation of DNA Adduct (8-hydroxy-2-deoxyguanosine (8-OHdG) in vitro due to the reaction of malondialdehyde (MDA) and /or exposure to Cr (VI) with the presence of H2O2 through the Fenton reaction to DNA. 2'-deoxyguanosine (dG) at various temperatures of 37oC, 60oC, pH 7.4 and 8.4 and incubation time of 3 and 16 hours. In vivo study has been carried out on exposed groups of rat (10 mg/kgBW) MDA, and Cr (VI) (0.4mg/kgBW) for 28 days. Urine samples were collected every week. 8-OHdG formation in vitro was analyzed by HPLC, while the formation of 8-OHdG in rat urine samples was analyzed using LC-MS/MS with reverse phase chromatography. The results of this study obtained the validation value of the UHPLC instrument with a linear regression value (R) 0.9973, LOD was 11.03 μg/L and the LOQ value is 36.77 μg/L. In in vitro treatment, exposure to MDA compounds at an incubation temperature of 60oC for 3 hours, pH 7.4 resulted in the highest 8-OHdG concentration of 404.09 μg/L. In in vitro studies, data also showed that there was a synergistic effect of increasing the concentration of 8-OHdG resulting from the in vitro reaction of 2'deoxiguanosine with MDA + Cr (VI) as free radical compounds that trigger DNA damage. In vivo observations of rat exposed to xenobiotic compounds (MDA and Cr (VI) also found clinical symptoms of weight loss before and after exposure. The results of the analysis of urine samples treated in vivo with the LCMS/MS instrument showed a synergistic effect on MDA + Cr (VI) exposure."

"IntroductionThe emerging of chronic kidney disease (CKD) as one of the dominant causes for death and suffering over the past two decades has been concerning. Additionally, increase oxidative stress in urban area and its association with other chronic diseases raising a notion of increase in chronic disease in area with low socio-economic status, namely, urban kampung. Due to that, this research was carried out to find the association between plasma MDA and factors related to decrease renal function in adult urban kampung population.MethodThis is cross-sectional research that used secondary data from participant with age ranging from 30-60 years and living in four area in Jakarta-Tangerang. Participants’ MDA level was measured as an indicator for oxidative stress. Kidney markers including eGFR, urea, and creatinine were also measured.ResultsFrom 153 participants, high level of oxidative stress was not found and all within normal capacity (0.1−2.9 µmol/L). Overall kidney function using eGFR showed 58.8% normal condition and function and 41.2% with decreased kidney function. Only 1.3% had increased creatinine levels (>1.3 mg/dL), while 51% of participants had increased urea level (>20 mg/dL).ConclusionNo association between high plasma MDA and decreased kidney marker was found in adult participant of urban kampung area in Jakarta-Tangerang.

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Latar Belakang

Meningkatnya angka penyakit ginjal kronik sebagai salah satu penyebab kematian dan penderitaan pasien sangat menghawatirkan. Peningkatan stress oksidatif di wilayah urban dan hubungannya dengan banyak penyakit kronis menyebabkan dugaan peningkatan penyakit kronik di wilayah dengan sosio-ekonomik yang rendah seperti di kampung urban. Oleh karena itu penelitian ini dilaksanakan untuk mencari tahu adanya hubungan asosiatif antara hasil plasma MDA sebagai indikator stress oksidatif dengan penurunan fungsi ginjal.

Metode

Metode penelitian merupakan penelitian potong lintang (cross-sectional) dengan data sekunder yang berasal dari partisipan berumur 30-60 tahun di 4 wilayah kampung kota Jakarta-Tangerang. Partisipan dinilai menggunakan Plasma MDA sebagai indikator stress oksidatif dan penanda fungsi ginjal yaitu eGFR, urea, dan creatinin.

Hasil

Dari 153 partisipan, tidak ditemukan tingkat oksidatif tinggi dan semua berada pada batas normal (0.1−2.5 µmol/L). Hasil kondisi ginjal partisipan menggunakan eGFR terdiri dari 58.8% kondisi ginjal normal dan 41.2% mengalami penurunan funsi ginjal. Hanya 1.3% mengalami kenaikan nilai creatinine (>1.3 mg/dL) dan lebih dari 51% partisipan mengalami kenaikan nilai ureum (>20 mg/dL).

Kesimpulan

Hubungan Asosiatif antara tinggi plasma MDA dan penanda penurunan fungsi ginjal tidak ditemukan pada partisipan dewasa yang tinggal di daerah kampung urban"