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Pesticides are chemical substances used to kill unwanted fungi, weeds and insects. In many countries, there is currently concern regarding the adverse effects of pesticides on health. It has been reported that pesticides may cause cancer, respiratory diseases, organ diseases, system failures, nervous system disorders and asthma, which are closely connected with immune disorders. Therefore, this study reviewed the immunotoxicity of pesticides that are currently used or prohibited from being used, especially their effects on leukocytes such as T cells, B cells, NK cells and macrophages. These immune cells play crucial roles in innate and adaptive immune systems to protect hosts. Pesticides are known to have possible toxicological modes of action to induce oxidative stress, mitochondrial dysfunction, and endoplasmic reticulum (ER) stress in living organisms. According to previous studies, pesticides such as atrazine (ATR), organophophorus (OP) compounds, carbamates, and pyrethroids were shown to inhibit the survival and growth of leukocytes by inducing apoptosis or cell cycle arrest and interfering with the specific immunological functions of each type of immune cells. These results suggest the immunotoxicity of pesticides toward specific immune cells. To substantiate the overall immunocompromised effects of pesticides, there is a need to collect and thoroughly analyze additional information regarding other immunological toxicities. Pesticides are known to have possible toxicological modes of action, which interfere with specific immunological functions of each type of immune cells. In this review, immunotoxicity of pesticides toward specific immune cells was described. Schematic representation of pathways through which immunotoxic effects of various pesticides may lead to immune cell disorders and death. Unlabelled Image • Pesticides are known to have possible toxicological modes of action. • Pesticides interfere with specific immunological functions of each type of immune cells. • In this review, immunotoxicity of pesticides toward specific immune cells was described. [ABSTRACT FROM AUTHOR]

Fludioxonil is fungicide used in agriculture, which is present in fruits and vegetables. In this study, the effects of fludioxonil on human immune cell viability, apoptosis, cell cycle arrest, and mitochondrial membrane potential were examined in human immune cells, such as Jurkat T cells and Ramos B cells. To examine the cell viability, Jurkat T cells and Ramos B cells were treated with fludioxonil (10−9–10−5 M) for 24 h and 48 h. Water soluble tetrazolium salt assay showed that fludioxonil decreased Jurkat T cell and Ramos B cell viability. Jurkat T cell viability decreased at 24 and 48 h, but Ramos B cell viability decreased only at 48 h. JC-1 dye revealed decreased mitochondrial membrane potential in fludioxonil-treated Jurkat T cells and Ramos B cells. To evaluate apoptosis, annexin-V conjugated FITC, AF488, and propidium iodide (PI) were used and to evaluate cell cycle arrest PI was used. Apoptosis and cell cycle arrest were induced by fludioxonil (10−7–10−5 M) in the Jurkat T cells at 24 and 48 h and Ramos B cells at 48 h. Moreover, the protein levels of pro-apoptotic proteins, such as p53, BAX, and cleaved caspase 3, were increased and anti-apoptotic protein Bcl-2 was decreased by fludioxonil. Expression of the Fas receptor related to the extrinsic apoptosis pathway was increased by fludioxonil. Additionally, cyclin D1 and cyclin E1 were decreased by fludioxonil. In the present study, fludioxonil induced immunotoxicity in human T cells and B cells through apoptosis and cell cycle arrest. Therefore, the present study suggests that fludioxonil induces the cellular toxicity in immune cells. [ABSTRACT FROM AUTHOR]