br Conflict of interest br Acknowledgments This work

Conflict of interest
Acknowledgments This work was supported by research grant [PR26/20326] from Santander Bank/UCM. The authors would like to thank Miguel Capo, Professor of Toxicology from the Universidad Complutense de Madrid, for his counseling during the preparation of the present work.
Introduction Pyrethroids are a group of pesticides used extensively throughout the world. The biochemical and neurotoxic effects of these chemicals on non-target organisms constitute a significant risk factor (Kuivila et al., 2012). These chemicals have a particularly high risk of intercourse with the aquatic environment and are highly toxic for fish (Werner and Moran, 2008). Because, biotransformation of pyrethroids in fish metabolism and detoxification is slower than in other organisms (Glickman et al., 1982). In addition, pyrethroids tend to accumulate in fish due to its ZM 306416 nature (Zhao and Liu, 2009). Pyrethroids are classified in two groups according to their chemical structure: type I (Alletrin, Permethrin, Piretrin) α cyano group and type II (Deltamethrin, Spermethrin) α cyano group. Type I group causes immobility, impaired coordination, excessive fatigue, paralysis, behavioral disturbance and tremor. Type II pyrethroids lead to hyperactivity, increased salivary secretion, and convulsions and tremors (Bradbury and Coats, 1989, Tilak et al., 2003). DM is a highly lipophilic structure (log Kow = 6.20) (Hansch et al., 1995) and it is α-cyano pyrethroid used intensively against pests in agricultural areas. The mechanism of action of the DM is usually on the nervous system (Haverinen and Vornanen, 2016). Previous studies have found DM in the urine of pregnant women and young children working in agricultural areas (Castorina et al., 2010). For this reason, it is very important to investigate the consequences of exposure to synthetic organic insecticides. Behavioral effects of mice were assessed after DM exposure and an increase in locomotor activity was observed (Richardson et al., 2015). Huang et al. (2014) observed that DM exposure caused hyperactivity in adult zebrafish. In addition, methamidophos, an organophosphate insecticide, causes neurotoxicity in the early stages of zebrafish with effects on cell apoptosis activation in brain (He et al., 2016). Exposure to imidacloprid during the embryonic period reduced swimming activity in larvae of zebrafish (Crosby et al., 2015). DM can cause neurotoxicity and apoptosis (Khalatbary et al., 2015). Also it caused apoptosis in rat brain, liver and kidney (Abdel-Daim et al., 2013, Ogaly et al., 2015). In recent years studies on mammals and teleost’s have attempted to determine the effects on the metabolism, antioxidant defense system, endocrine system and immune system to determine the adverse effects of chemicals on biological processes (Das et al., 2016, Teles et al., 2016). Xenobiotics exposure increases the production of reactive oxygen species (ROS). As a result of the ROS increase, all macromolecules including proteins, nucleic acids and lipids, are adversely affected. There are effective antioxidant defense systems to reverse the negative effect of oxidative stress in the body (Valavanidis et al., 2006, Ucar et al., 2017). SOD, CAT and GPx enzymes constitute the first step of the antioxidant system. The role of these enzymes is to prevent or reduce tissue damage caused by free radicals. SOD converts superoxide anions to H2O2 and protects the cells against lipid peroxidation. At the same time, the catalase decomposes H2O2 into molecular oxygen and water (Deisseroth and Dounce, 1970). Besides, malondialdehyde (MDA), the end product of lipid peroxidation, is used as an oxidative stress indicator. As a result of exposure to toxic chemicals, the balance between reactive oxygen and antioxidant systems may be impaired and oxidative damage may occur in the organism (Nita and Grzybowski, 2016). ROS induces Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and MDA in vertebrates and fish under normal conditions. However, exposure to these toxic chemicals inhibited oxidative stress in fish (Li et al., 2015, Balmus et al., 2016). Moreover, in many studies, oxidative stress is known to cause direct DNA damage and cellular apoptosis in the cell (Rai et al., 2015, Kreuz and Fischle, 2016). Furthermore pyrethroids induce apoptosis by affecting caspases (caspases 2-3-6-10) in zebrafish embryos (Deng et al., 2009).