Pyrethroids are synthetic, stabilized derivatives of pyrethrins, insecticidal substances obtained from the flowers of a species of chrysanthemum (Chrysanthemum cinerariaefolium) (Fig. 1). They are potent neurotoxicants. There are two groups of pyrethroids with distinctive poisoning symptoms, distinguished by an alpha-cyano group in their structure. While those without an alpha-cyano group (type I pyrethroids, e.g., permethrin, cismethrin, bifenthrin) exert their neurotoxicity primarily through interference with sodium channel function in the nervous system, type II pyrethroids (with alpha-cyano group, e.g., deltamethrin, esfenvalerate, cypermethrin) can affect additional ion-channel targets such as chloride and calcium channels. Apart from their primary mechanism of action, pyrethroids also modulate the release of acetylcholinesterase in the brain's hippocampus region and can inhibit ATPases. In addition, these compounds can disrupt hormone-related functions, with transformation products being more potent endocrine disruptors than parent compounds. In mammals, pyrethroids decrease progesterone and estradiol production, eliciting estrogenic effects in females and antiandrogenic effects in males. In fish, exposure to pyrethroids has been shown to increase plasma estrogen and the estrogen-dependent egg yolk precursor proteins vitellogenin and choriogenin (Crago and Schlenk, 2015, and references therein). Furthermore, pyrethroids inhibit cell cycle processes, cause cell stress, and have immunosuppressive effects. Metabolism occurs primarily by microsomal cytochrome P450 enzymes (Werner and Moran, 2008; Palmquist et al., 2012, and references therein) (Fig. 1).