Protective role of caffeic acid phenethyl ester against to chlorpyrifos-ethyl acute poisoning

DEVECİ H. A., KARAPEHLİVAN M., KAYA İ., KÜKÜRT A., Alpay M.

ANKARA UNIVERSITESI VETERINER FAKULTESI DERGISI, cilt.62, sa.4, ss.255-260, 2015 (SCI-Expanded, Scopus, TRDizin) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 62 Sayı: 4
  • Basım Tarihi: 2015
  • Doi Numarası: 10.1501/vetfak_0000002689
  • Dergi Adı: ANKARA UNIVERSITESI VETERINER FAKULTESI DERGISI
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.255-260
  • Anahtar Kelimeler: Caffeic acid phenetyl ester, chlorpyrifos-ethyl, oxidative stress, paraoxonase, total antioxidant, SERUM PARAOXONASE, ORGANOPHOSPHORUS INSECTICIDE, ANTIOXIDANT ENZYMES, DNA-DAMAGE, TOXICITY, RATS, PESTICIDES, GENERATION, STRESS, LIVER
  • Ankara Üniversitesi Adresli: Evet

Özet

The present study aimed to investigate the caffeic acid phenetyl ester (CAPE) effect on levels of paraoxonase (PON1) activity, oxidative stress index (OSI), total antioxidant (TAS) and total oxidant (TOS) levels in acute poisoning of chlorpyrifos-ethyl (CPF). All experiments conducted on 32 male Mus musculus sp. mice divided into 4 equal groups each 25-30 g as following. Group I were treated with saline (% 0.9 NaCl) by intraperitoneal injection (i.p.). Group II with 101 mg/kg CPF plus saline subcutaneously; group III with 10 mu mol/kg CAPE intraperitonally; group IV with 101 mg/kg CPF plus 10 mu mol/kg CAPE were applied. After serum samples obtained, PON1 activity, OSI, TAS and TOS levels were measured. In this study, PON1 189.21 +/- 22.31 U/L; TAS 1.03 +/- 0.13 mmol Trolox eqivalen/L; TOS 7.10 +/- 0.69 mu mol H2O2 equiv./L and OSI 0.69 +/- 0.09 arbitrary unit levels were found during CFP applications. As conclusion, OSI and TOS levels were increased while serum PON1 activity and TAS levels decreased under CPF intoxication compared to group I. Additionally, CAPE was demonstrated the protective effect by reducing CPF-induced oxidative stress.