Journal of Carcinogenesis & Mutagenesis

Abstract

Genetic Damage and Cell Killing Induction by Five Head Lice Treatments on HaCaT Human Skin Cells

Abdullah M Alnuqaydan and Barbara J Sanderson

Background: Chemical head lice treatments used by parents to treat head lice infestation in their children due to their rapid and reliable removal of head lice. However, those treatments can be absorbed through the skin. Children are more sensitive to absorbing chemicals than adults. We hypothesized that synthetic chemical-based head lice treatments cause cytotoxic and genotoxic damage to human skin cells in vitro. Objective: To determine the cytotoxic and genotoxic damage of synthetic chemical-based head lice treatments on HaCaT human skin cells in vitro. Methodology: Cytotoxicity measured by the methyl tetrazolium cytotoxicity (MTT) assay and the crystal violet assay. Also, the mechanism of cell killing was identified by the apoptosis detection, via Flow cytometry assay. The cytokinesis block micronucleus (CBMN) assay detected the frequency of binucleated cells (BN) with micronucleus (MNi), to indicate genetic damage induced by head lice treatments. Results: Tea Tree Oil (TTO), Pure Lavender oil and Pyrethrum did induce significant cytotoxicity. Also, they enhanced both early apoptosis and late apoptosis/necrosis. However, two head lice treatments, Permethrin (Lice Breaker) and Maldison (Malathion) (KP24) did not induce cytotoxicity. Early apoptosis and necrosis were observed in Permethrin treatment and late apoptosis and early necrosis were measured in Maldison (Malathion) (KP24). Moreover, Permethrin (Lice Breaker) and Maldison (Malathion) (KP24) induced micronuclei (MNi) at a frequency significantly higher (range=15-25 MNi/1000 binucleated cells, n=3) than the background frequency (media alone control; MNi range= 6 MNi /1000 binucleated cells, n=3). Conclusion: This study indicates that exposure to chemical based head lice treatments enhanced cell death by both early apoptosis and late apoptosis/necrosis also induced chromosomal damage in human skin cells.