The hematological effects of methyl parathion in rats

Çelik İ., Suzek H.

JOURNAL OF HAZARDOUS MATERIALS, vol.153, no.3, pp.1117-1121, 2008 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 153 Issue: 3
  • Publication Date: 2008
  • Doi Number: 10.1016/j.jhazmat.2007.09.067
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.1117-1121
  • Van Yüzüncü Yıl University Affiliated: Yes


The effects of methyl parathion (MP) at sublethal concentration on hematological constituent [red blood corpuscles (RBC), white blood corpuscles (WBC), mean cell volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), platelet (PLT) counts, hemoglobin (Hb) and hematocrite (HCT) levels] and serum damage marker enzymes [aspartate aminotransferase (AST), alanin aminotransferase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH)l of rats were investigated under laboratory conditions. 5 and 10 ppm dosages of NIP were administered orally to six female rats ad libitum during the tests for 4 weeks consecutively. MP treatments caused different effects on the hematological constituents and the serum marker enzymes of the treatment groups as compared to the controls. According to the results, MP treatments increased significantly the levels of serum marker enzyme activities except for ALT with both dosages and LDH with 5 ppm dosage. Also, the hematological constituents were affected by MP. For example, WBC significantly increased in rats treated with both dosages of MP whereas the other hematologic constituents did not change at 5 and 10 ppm of MP treatments. The observations presented led us to conclude that the administration of subacute NIP elevates tissue damage serum marker enzymes, and increases the number of WBC in rats. These data, along with the determined changes suggest that MP produce substantial systemic organ toxicity in rats during the period of a 28-day subacute exposure. (C) 2007 Elsevier B.V. All rights reserved.