Journals / Kafkas Üniversitesi Veteriner Fakültesi Dergisi / 2011 / Cilt: 17 - Sayı: 6

Akut toksisite sıçan modelinde diazinonun neden olduğu akciğer, karaciğer ve böbrek hasarı üzerine kafeik asit fenetil ester, elajik asit, Sulforafan ve Kurkumin’in etkileri

Effects of caffeic acid phenethyl ester, ellagic acid, sulforaphane and curcumin on diazinon induced damage to the lungs, liver and kidneys in an acute toxicity rat model

Pages
927–933
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

These findings led us to believe that CAPE, EA, SFN and CUR may be used as protective medicines in acute DI intoxication.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:The aim of this study was to investigate the possible protective effects of caffeic acid phenethyl ester (CAPE), ellagic acid (EA), sulforaphane (SFN) and curcumin (CUR) against the toxic effects of diazinon (DI).
📊
Key Findings & Data:Sixty Sprague Dawley rats were randomly divided into 10 groups.
💡
Conclusion & Impact:These findings led us to believe that CAPE, EA, SFN and CUR may be used as protective medicines in acute DI intoxication.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:toksikoloji · asetilkolinesteraz · amilaz

Abstract

The aim of this study was to investigate the possible protective effects of caffeic acid phenethyl ester (CAPE), ellagic acid (EA), sulforaphane (SFN) and curcumin (CUR) against the toxic effects of diazinon (DI). Sixty Sprague Dawley rats were randomly divided into 10 groups. Five groups were allocated as control groups comprising unmedicated control, CAPE, EA, SFN and CUR control groups. The remaining five groups were the study groups comprising DI, DI + CAPE, DI + EA, DI + SFN, and DI + CUR groups. The animals were sacrified 24 h after drug administrations. DI caused a decrease in acetyl cholinesterase (AChE) activity (P<0.05) and increases in &#947;-glutamyltransferase (GGT) and amylase activities. It also damaged the kidney, liver, and lung tissues. The negative effects of DI on these enzymes were confirmed histopathologically. Also, CAPE, EA, SFN and CUR reduced amylase and GGT activities and caused an increase in the AChE activities that were increased due to the toxic effects of DI. Thus, it was determined bio- chemically and histopathologically that these medication reduced the degenerative toxic effects created by DI in the lung, liver and kidney tissues. These findings led us to believe that CAPE, EA, SFN and CUR may be used as protective medicines in acute DI intoxication.

Özet

Bu çalışmanın amacı kafeik asit fenetil ester (CAPE), elajik asit (EA), Sulforafan (SFN) ve Kurkumin (CUR)’in, diazinon (DI)’un toksik etkilerine karşı muhtemel koruyucu etkilerini araştırmaktır. Çalışmada 60 adet Sprague Dawley sıçan eşit şekilde ve rastgele 10 gruba ayrıldı. Kontrol grupları; kontrol, CAPE, EA, SFN ve CUR grupları olarak 5 gruba ayrıldı. Geri kalan 5 grup ise çalışma grupları olarak; DI, DI + CAPE, DI + EA, DI + SFN ve DI + CUR gruplarına ayrıldı. Hayvanlar ilaç uygulamalarından 24 saat sonra sakrifiye edildi. DI, asetil kolin esteraz (AChE) aktivitelerine azaltıcı (P<0.05) ve γ-glutamiltransferaz (GGT) ile amilaz aktivitelerine artırıcı şekilde etkiye neden oldu. Bu enzimler üzerine DI’un negatif etkileri, dokular üzerine histopatolojik olarak da doğrulandı. Ayrıca CAPE, EA, SFN ve CUR, DI’un toksik etkilerine karşı γ-glutamiltransferaz (GGT) ile amilaz aktivitelerine azaltıcı ve asetil kolin esteraz (AChE) aktivitelerine ise artıcı şekilde etkiye neden oldu. Bu şekilde, biyokimyasal ve histopatolojik olarak ilaçların, DI’un neden olduğu dejeneratif ve toksik etkileri azalttığı belirlendi. Bu bulgular, akut DI toksikasyonunda CAPE, EA, SFN ve CUR’in koruyucu amaçla kullanılabileceği fikrini bize verdi.

🔖

Cite This Article

ALP, H., AYTEKİN, İ., ESEN, H., BAŞARALI, K., KUL, S. (2011). Akut toksisite sıçan modelinde diazinonun neden olduğu akciğer, karaciğer ve böbrek hasarı üzerine kafeik asit fenetil ester, elajik asit, Sulforafan ve Kurkumin’in etkileri. Kafkas Üniversitesi Veteriner Fakültesi Dergisi, Cilt: 17 - Sayı: 6, 927–933. https://ajindex.com/articles/273208

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (13)

  1. World Health Organization (WHO): Guidelines for poison control,
  2. Bagchi D, Bagchi M, Hassoun EA, Stohs SJ: In vitro and in vivo generation of reactive oxygen species, DNA damage and lactate dehydrogenase leakage by selected pesticides. Toxicology, 104, 129-140, 1995
  3. Colovic M, Krstic D, Petrovic S, Leskovac A, Joksic G, Savic J, Frankoc M, Trebsec P, Vasic V: Toxic effects of diazinon and its photodegradation products. Toxicology Letters, 193, 9-18, 2010
  4. Cox C: Diazinon. J Pestic Reform, 12, 30-35, 1992
  5. Ilhan A, Koltuksuz U, Ozen S, Uz E, Ciralik H, Akyol O: The effects of caffeic acid phenethyl ester (CAPE) on spinal cord ischemia/reperfusion injury in rabbits. Eur J Cardio Thorac Surg, 16, 458-463, 1999
  6. Hepsen IF, Bayramlar H, Gultek A, Ozen S, Tilgen F, Evereklioglu C: Caffeic acid phenethyl ester to inhibit posterior capsule opacification in rabbits. J Cataract Refract Surg, 23, 1572-1576, 1997
  7. Orhan H, Marol S, Hepsen IF, Sahin G: Effects of some probable antioxidants on selenite-induced cataract formation and oxidative stress-related parameters in rats. Toxicology, 139, 219-232, 1999
  8. Uz E, Sogut S, Sahin S, Var A, Ozyurt H, Gulec M, Akyol O: The protective role of caffeic acid phenethyl ester (CAPE) on testicular tissue after testicular torsion and detorsion. World J Urol, 20, 264-270, 2002
  9. Gurel A, Armutcu F, Hosnuter M, Unalacak M, Kargı E, Altınyazar C: Caffeic acid phenethyl ester improves oxidative organ damage in rat model of thermal trauma. Physiol Res, 53, 675-682, 2004
  10. Zhu H, Jia Z, Strobl JS, Ehrich M, Misra HP, Li Y: Potent induction of total cellular and mitochondrial antioxidants and phase 2 enzymes by cruciferous sulforaphane in rat aortic smooth muscle cells: Cytoprotection against oxidative and electrophilic stres. Cardiovasc Toxicol, 8, 115-125, 2008
  11. Zhao J, Kobori N, Aronowski J, Dasha PK: Sulforaphane reduces infarct volume following focal cerebral ischemia in rodents. Neuroscience Letters, 393, 108-112, 2006
  12. Hu R, Hebbar V, Kim BR, Chen C, Winnik B, Buckley B, Soteropoulos P, Tolias P, Hart RP, Kong ANT: In Vivo pharmacokinetics and regulation of gene expression profiles by ısothiocyanate sulforaphane in the rat. J Pharmacol Exp Ther, 310, 263-271, 2009
  13. Hanlon N, Coldham N, Gielbert A, Kuhnert N, Sauer MJ, King LJ: Absolute bioavailability and dose-dependent pharmacokinetic behavi