Chlorpyrifos‐induced DNA damage in rat liver and brain

  title={Chlorpyrifos‐induced DNA damage in rat liver and brain},
  author={Anugya Mehta and Radhey S. Verma and Nalini Srivastava},
  journal={Environmental and Molecular Mutagenesis},
Chlorpyrifos (O,O'‐diethyl‐O‐3,5,6‐trichloro‐2‐pyridyl phosphorothionate, CPF) is a broad spectrum organophosphate pesticide used to control a variety of pests. The present study was undertaken to test the in vivo genotoxic potential of CPF in rats, using the single cell gel electrophoresis (or comet) assay. The rats were administered 50 mg and 100 mg CPF/kg body weight daily for 1, 2, and 3 days as well as 1.12 mg and 2.24 mg CPF/kg body weight for 90 days. The level of DNA damage was… 

Evaluation of genotoxic potential of commonly used organophosphate pesticides in peripheral blood lymphocytes of rats

Exposure of rat lymphocytes with CPF, MPT, and MLT caused significantly marked increase in DNA damage and DPC formation in time-dependent manner, and MPT caused the highest damage.

Evaluation of DNA damage and cytotoxicity induced by three commonly used organophosphate pesticides individually and in mixture, in rat tissues

Investigation of CPF, MPT, and MLT when given singly or in combination found that MPT caused highest level of DNA damage and brain was maximally affected by these OP compounds, confirming that these pesticides do not potentiate the toxicity of each other.

Evaluation of genotoxicity of monocrotophos and quinalphos in rats and protective effects of melatonin

The co treatment of melatonin has the ability to reduce the genotoxic potential of MCP and QNP under the experimental conditions applied in the present study.

Cytogenetic and Genotoxic Effects of Penconazole and Chlorpyrifos Pesticides in Bone Marrow of Rats

PEN and CPF induced genotoxic and cytogenetic effects in bone marrow showed significant hematological changes, significant increase in DNA damage index and increased the number of nuclei with I, II, III and IV degrees of damage.

In vitro studies on organophosphate pesticides induced oxidative DNA damage in rat lymphocytes.

  • A. OjhaN. Srivastava
  • Biology
    Mutation research. Genetic toxicology and environmental mutagenesis
  • 2014

Role of Ocimum sanctum as a Genoprotective Agent on Chlorpyrifos-Induced Genotoxicity

Results showed that lymphocytes treated with the pesticide exhibited increased DNA damage but the increase was statistically insignificant while in rats pretreated with OE, a significant increase in MI was observed and there was a significant decrease in the frequency of aberrant cells as compared to the rats treated with chlorpyrifos alone.



Effect of chlorpyrifos on thiobarbituric acid reactive substances, scavenging enzymes and glutathione in rat tissues.

Exposure of chlorpyrifos, a widely used pesticide in rats caused significant inhibition of acetylcholinesterase (AChE) activity in different tissues viz., liver, kidney and spleen, and data provide evidence for induction of oxidative stress on CPF exposure.

DNA damage and apoptosis induction by the pesticide Mancozeb in rat cells: involvement of the oxidative mechanism.

Comparative studies on lipid peroxidation and DNA-single strand breaks induced by lindane, DDT, chlordane and endrin in rats.

Lack of carcinogenicity of chlorpyrifos insecticide in a high-dose, 2-year dietary toxicity study in Fischer 344 rats.

CPF was not carcinogenic at dose levels up to 10 mg/kg/day, and the plasma and RBC ChE activities were inhibited in rats given 1.0 mg/ kg/day and this group had similar numbers and types of neoplasms as control rats.

Evaluation of the genotoxic and embryotoxic potential of chlorpyrifos and its metabolites in vivo and in vitro.

Genotoxicity and embryotoxicity of chlorpyrifos and two metabolites and studies of bovine blastocysts obtained from superovulated cows crossed with Dursban 44 treated bulls did not reveal evidence of chromosome aberrations or developmental anomalies associated with pesticide application, but reproductive performance of breeders may be subnormal as a result of severe poisoning.