Dergiler / İstanbul Kuzey Klinikleri / 2020 / Cilt: 7 - Sayı: 6

Comparison of effects of high and low doseparacetamol treatment and toxicity on brain and liver in rats

Sayfa
541–550
Yayın Tarihi
2022-10-18
DOI
—
🏛️Bu makalenin bibliyografik verileri ve tam metin bağlantısı DergiPark üzerinden sağlanmıştır.
DergiPark Kaydı ↗
✨

Yapay Zeka Hızlı Bakış & Çıkarımlar

AI Insight
⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

The caspase 3 level in the liver was statistically significantly higher in the low dose group compared to the other groups (p

📌 3 Maddede Bu Makale

🎯
Amaç & Hipotez:OBJECTIVE: Paracetamol is thought that it acts by inhibiting the central cyclooxygenase (COX) enzyme; its mechanism of action is still not fully explained.
📊
Temel Bulgular & Veri:At doses of 20–500 mg/kg, paracetamol was administered intraperitoneally once a day for one and three days.
💡
Sonuç & Katkı:The caspase 3 level in the liver was statistically significantly higher in the low dose group compared to the other groups (p
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Alan Parametreleri

Abstract

OBJECTIVE: Paracetamol is thought that it acts by inhibiting the central cyclooxygenase (COX) enzyme; its mechanism of action is still not fully explained. Although its most important side effect is hepatoxicity, it is thought to cause toxicity on the brain in recent years. The present study aims to investigate the treatment and toxic effects of low and high doses of paracetamol on the liver and brain.METHODS: Wistar-albino rats were used in this study. At doses of 20–500 mg/kg, paracetamol was administered intraperitoneally once a day for one and three days. The brain and liver were used for immunohistochemical evaluation using COX-3, prostaglandin E2 (PGE2) and caspase 3 antibodies and for total antioxidant (TAS), total oxidant (TOS) and oxidative stress index (OSI) measurements. Results were evaluated using the Kruskal Wallis test (SPSS ver.24).RESULTS: The liver COX-3 levels were significantly lower in both groups with higher doses (p0.05). The caspase 3 level in the liver was statistically significantly higher in the low dose group compared to the other groups (p

🔖

Bu Makaleye Atıf Yap

YAŞAR, S., ERTEN, R., ARIHAN, O., ÖKSÜZ, E., OTO, G. (2022). Comparison of effects of high and low doseparacetamol treatment and toxicity on brain and liver in rats. İstanbul Kuzey Klinikleri, Cilt: 7 - Sayı: 6, 541–550. https://ajindex.com/articles/551342

📄 Tam Metin PDF Okuyucu

📄

PDF görüntüleyici hazırlanıyor...

Kaynakça (14)

  1. Bertolini A, Ferrari A, Ottani A, Guerzoni S, Tacchi R, Leone S. Paracetamol: new vistas of an old drug. CNS Drug Rev 2006;12:250–75
  2. Chandrasekharan NV, Dai H, Roos KL, Evanson NK, Tomsik J, Elton TS, et al. COX-3, a cyclooxygenase-1 variant inhibited by acetaminophen and other analgesic/antipyretic drugs: cloning, structure, and expression. Proc Natl Acad Sci U S A 2002;99:13926–31
  3. Kis B, Snipes JA, Busija DW. Acetaminophen and the cyclooxygenase-3 puzzle: sorting out facts, fictions, and uncertainties. J Pharmacol Exp Ther 2005;315:1–7
  4. Li S, Dou W, Tang Y, Goorha S, Ballou LR, Blatteis CM. Acetaminophen: antipyretic or hypothermic in mice? In either case, PGHS-1b (COX-3) is irrelevant. Prostaglandins Other Lipid Mediat 2008;85:89–99
  5. Davis M, Labadarios D, Williams RS. Metabolism of paracetamol after therapeutic and hepatotoxic doses in man. J Int Med Res 1976;4:40–5
  6. Mitchell JR, Jollow DJ, Potter WZ, Gillette JR, Brodie BB. Acetaminophen-induced hepatic necrosis. IV. Protective role of glutathione. J Pharmacol Exp Ther 1973;187:211–7
  7. Burcham PC, Harman AW. Acetaminophen toxicity results in site-specific mitochondrial damage in isolated mouse hepatocytes. J Biol Chem 1991;266:5049–54
  8. Tsokos-Kuhn JO, Hughes H, Smith CV, Mitchell JR. Alkylation of the liver plasma membrane and inhibition of the Ca2+ ATPase by acetaminophen. Biochem Pharmacol 1988;37:2125–31
  9. Isobe-Harima Y, Terai S, Miura I, Segawa M, Murata T, Itamoto K, et al. A new hepatic encephalopathy model to monitor the change of neural amino acids and astrocytes with behaviour disorder. Liver Int 2008;28:117–25
  10. Aggarwal S, Kramer D, Yonas H, Obrist W, Kang Y, Martin M, et al. Cerebral hemodynamic and metabolic changes in fulminant hepatic failure: a retrospective study. Hepatology 1994;19:80–7
  11. Upadhya SC, Tirumalai PS, Boyd MR, Mori T, Ravindranath V. Cytochrome P4502E (CYP2E) in brain: constitutive expression, induction by ethanol and localization by fluorescence in situ hybridization. Arch Biochem Biophys 2000;373:23–34
  12. Courad JP, Besse D, Delchambre C, Hanoun N, Hamon M, Eschalier A, et al. Acetaminophen distribution in the rat central nervous system. Life Sci. 2001;69:1455–64
  13. Micheli L, Fiaschi AI, Cerretani D, Giorgi G. Effect of acetaminophen on glutathione levels in several regions of the rat brain. Curr Ther Res 1993;53:730–6
  14. Naziroğlu M, Uğuz AC, Koçak A, Bal R. Acetaminophen at different doses protects brain microsomal Ca2+-ATPase