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Pendimethalin induces oxidative stress, DNA damage, and mitochondrial dysfunction to trigger apoptosis in human lymphocytes and rat bone-marrow cells

Authors
  • Ansari, Sabiha M.1
  • Saquib, Quaiser2
  • Attia, Sabry M.3
  • Abdel-Salam, Eslam M.1
  • Alwathnani, Hend A.1
  • Faisal, Mohammad1
  • Alatar, Abdulrahman A.1
  • Al-Khedhairy, Abdulaziz A.2
  • Musarrat, Javed4, 5
  • 1 King Saud University, Department of Botany and Microbiology, College of Science, Riyadh, 11451, Saudi Arabia , Riyadh (Saudi Arabia)
  • 2 King Saud University, Zoology Department, College of Science, Riyadh, 11451, Saudi Arabia , Riyadh (Saudi Arabia)
  • 3 King Saud University, Department of Pharmacology and Toxicology, College of Pharmacy, Riyadh, 11451, Saudi Arabia , Riyadh (Saudi Arabia)
  • 4 Baba Ghulam Shah Badshah University, School of Biosciences and Biodiversity, Rajouri, Jammu And Kashmir, India , Rajouri (India)
  • 5 Aligarh Muslim University, Department of Agricultural Microbiology, Faculty of Agricultural Sciences, Aligarh, UP, 202002, India , Aligarh (India)
Type
Published Article
Journal
Histochemistry and Cell Biology
Publisher
Springer Berlin Heidelberg
Publication Date
Nov 18, 2017
Volume
149
Issue
2
Pages
127–141
Identifiers
DOI: 10.1007/s00418-017-1622-0
Source
Springer Nature
Keywords
License
Yellow

Abstract

Pendimethalin (PM) is a dinitroaniline herbicide extensively applied against the annual grasses and broad-leaved weeds. There is no report available on PM-induced low-dose genotoxicity in human primary cells and in vivo test models. Such data gap has prompted us to evaluate the genotoxic potential of PM in human lymphocytes and rats. PM selectively binds in the minor groove of DNA by forming covalent bonds with G and C nitrogenous bases, as well as with the ribose sugar. PM induces micronucleus formation (MN) in human lymphocytes, indicating its clastogenic potential. Comet assay data showed 35.6-fold greater DNA damage in PM (200 μM)-treated human lymphocytes. Rat bone-marrow cells, at the highest dose of 50 mg/kg b w/day of PM also exhibited 10.5-fold greater DNA damage. PM at 200 μM and 50 mg/kg b w/day induces 193.4 and 229% higher reactive oxygen species generation in human lymphocytes and rat bone-marrow cells. PM-treated human lymphocytes and rat bone-marrow cells both showed dysfunction of mitochondrial membrane potential (ΔΨm). PM exposure results in the appearance of 72.2 and 35.2% sub-G1 apoptotic peaks in human lymphocytes and rat bone-marrow cells when treated with 200 μM and 50 mg/kg b w/day of PM. Rats exposed to PM also showed imbalance in antioxidant enzymes and histological pathology. Overall, our data demonstrated the genotoxic and apoptotic potentials of PM in human and animal test models.

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