Author
Meola, Shirlee | |
BARHOUM, R - TEXAS A&M UNIVERSITY | |
MEOLA, ROGER - TEXAS A&M UNIVERSITY | |
SCHNEIDER, I - WALTER REED ARMY INST RES | |
MILES, J - TEXAS A&M UNIVERSITY | |
BURGHARDT, R - TEXAS A&M UNIVERSITY |
Submitted to: Society of Toxicology
Publication Type: Abstract Only Publication Acceptance Date: 3/15/1996 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Endpoints of cellular injury caused by exposure of insect epithelial cell lines derived from Anopheles gambiae and Aedes albopictus mosquito larvae and a clonal rat hepatocyte cell line (Clone 9) to the synthetic pyrethroid insecticide, permethrin, were evaluated by laser cytometry. Permethrin acts primarily on nerve cells by modulating voltage activated sodium channels and little is known about other endpoints affected in nonexcitabl cells. Kinetic analyses of intracellular glutathione (GSH) and intracellular Ca**2+ content ([Ca**2+]i), reactive oxygen species (ROS) production, mitochondrial (MMP) and plasma membrane potentials (PMP), intracellular pH, and gap junctional intercellular communication (GJIC) were performed. A. gambiae and A. albopictus cells exhibited IC50 values of 15 ng/ml and 300 ng/ml respectively after 72 hr exposure to the toxin. The Clone 9 cells did not show any growth inhibition when treated with permethrin even at the highest concentration used (100 ug/ml). A. gambiae cells treated at the IC50 concentration for 1 hr at room temperature exhibited changes only in MMP indicating sustained depolarization. However, A. albopictus cells treated at the IC50 and Clone 9 cells (1 ug/ml) for 1 hr exhibited similar changes in ROS, MMP, and GSH levels. These studies identify cellular targets of injury in nonexcitable cells caused by permethrin exposure although insect cells are much more sensitive than mammalian cells. |