Perbandingan Efek Ranitidin, Dexametason dan Kombinasinya terhadap Kadar Asam Format Darah dan Pelepasan Sitokrom C Retina pada Model Tikus Intoksikasi Metanol Akut
DOI:
https://doi.org/10.21776/ub.jkb.2011.026.03.8Abstract
Keracunan metanol dapat menyebabkan toksisitas visual. Asam format merupakan metabolit yang bertanggung jawab terhadap terjadinya asidosis metabolik dan toksisitas visual yang menyebabkan kerusakan mitokondria dengan petanda penting pelepasan sitokrom C. Penelitian ini dilakukan untuk mengetahui pengaruh ranitidin dan perbedaannya dengan dexametason serta kombinasinya terhadap kadar asam format darah dan pelepasan sitokrom C retina tikus coba yang diinduksi metanol akut melalui penelitian eksperimental dengan desain post only with control. Hewan coba tikus Stratus Novergicus strain  Wistar  dibagi  dalam  lima  kelompok  dengan  7  kali  pengulangan  yaitu  kontrol negatif  dan positif ,  dan tiga kelompok  perlakuan  dengan  pemberian  ranitidin,  dexametason  dan  kombinasinya  secara  intraperitoneal.  Dilakukan pengukuran  kadar  asam  format  dengan  metode  kolorimetrik  pada  sampel  serum  darah  dan  pelepasan  sitokrom  C,  analisa data  menggunakan  One Way  ANOVA  dengan  post  hoc  test.  Hasil menunjukkan  rerata  kadar  asam  lebih  tinggi  format  pada tikus  dengan  intoksikasi  methanol  (10.441,8  ng/mL)  dibandingkan  pada  kondisi  normal  (3.612,6  ng/mL).  Pemberian ranitidin menghasilkan kadar asam format yang paling rendah (2.341,6 ng/mL) dibandingkan pemberian dexametason (5.919,2  ng/mL)  atau  kombinasi  keduanya  (2.913,2  ng/mL).Downloads
References
Jacobsen D, Sebastian CS, Baron SK, Carriere EW, and Mc Martin KE. Effect of 4-Methylpirazole, Methanol/Ethylen Glycol Antidote, in Health Human. The Journal of Emergency Medicine. 1990; 8(4): 455-461.
Lieber CS. Alcohol: Its Metabolism and Interaction with Nutrients. Annual Review of Nutrition. 2000; 20: 395-430.
Yasmine dan Prayitnaningsih S. The Visual Outcome of ToxicOptic Neuropathy Caused by Alcohol Intoxication Treated with Megadose Intravenous Steroid. Indonesian Ophthalmology Association Annual Meeting. Makasar, 2009.
Barceloux D, Bond GR, Krenzelok EP, et al. American Academy of Clinical T oxicology Practice Guidelines on the Treatment of Methanol Poisoning. Journal of Toxicology-Clinical Toxicology. 2002; 40(4): 415–446.
Tezel G and Yang X. Caspase Independent Component of Retina Ganglion Cell Death,In Vitro. Investigative Opthalmology & Visual Science. 2004; 45(11): 4049-4059.
El-Bakary AA, El-Dakrory SA, Attalla SM, Hasanein NA, and Malek HA. Ranitidin as an Alcohol Dehydrogenase Inhibitor in Acute Metanol Toxicity in Rats. Human & Experimental Toxicology. 2010; 29(2): 93-101.
Zrenner E and Hart W. Drug Induced and Toxic Disorder in Neuro Ophthalmology. In: SchielferU(Ed). Clinical Neuro-Ophthalmology. New York: Springer Berlin Heidelberg; 2007; p. 223-232.
Hovda KE and Jacobsen D. Fomepizole May Ameliorate the Need of Hemodialysis in Metanol Poisioning. Human & Experimental Toxicology. 2008; 27(7): 539-546
Garcia-Ruiz G, Collel A, Morales A, Kaplowitz N, and Fernandez-Checa JC. Role of Oxidative Stress Generated from the Mitochondrial Electron Transport Chain and Mitochondrial Glutathione Status in Loss of Mitochondrial Function and Activation of Transcriptional Factor Nf-{Kappa} B: Studies with Isolated Mitochondria and Rat Hepatocytes. Molecular Pharmacology. 1995; 48(5): 825-834.
Seme MT, Summerfelt P, Neitz J, Eells JT, and Henry MM. Differential Recovery of Retinal Function After Mitochondrial Inhibition by Methanol Intoxication. Investigative Ophthalmology & Visual Science. 2001; 42(3): 834-841.
Seme MT, Summerfelt P, Henry MM, Neitz J, and Eells JT. Formate Induced Inhibition of Photoreceptor Function in Methanol Intoxication. Journal of Pharmacology and Experimental Therapeutics. 1999; 289(1): 361-370.
Bang JS, Yang HS, Rho SS, and Chang YH. A Case of Toxic Amblyopia Caused by Methanol Intoxication. Journal of the Korean Ophthalmological Society. 2007; 48(12): 1731-1738.
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