Paraquat modulates immunological function in bone marrow-derived macrophages.

Abstract

The herbicide paraquat (PQ) is known to affect the immune system. Many reports have indicated that PQ impacts on the viability and functions of the immune cells, however, the underlying mechanism in detail is still unknown. The aim of this study was to evaluate the effects of PQ on the free radical production, oxidative stress, cell death and pro-inflammatory gene expression of murine bone marrow-derived macrophages (BMDMs) from C57BL/6NJcl mice in vitro. BMDMs were incubated with PQ at 0, 200 and 400 µM concentrations for 24 h. Intracellular reactive oxygen species (ROS) production, apoptosis, cell viability, nitric oxide, inducible nitric oxide synthase (iNOS), and IL-6 expression levels were measured. The results revealed that PQ treatments led to a decrease in the cell viability and induced apoptotic cell death in a dose-dependent manner. Additionally, PQ also induced the generation of ROS. The mRNA level of the pro-inflammatory mediator genes iNOS and IL-6 were also elevated, while the level of lipid peroxide (malondialdehyde) production remained unaltered. Interestingly, the PQ treatment led to a decrease in the nitric oxide production. These results indicate that the increased cellular ROS production, due to the PQ treatment, induces apoptosis and the herbicide triggers production of iNOS and IL-6 in BMDMs.