**5. Physiological dysfunction in various biological systems of fish by insecticides**

and DNA- in living cells resulting in serious disturbances in physiological cell processes (Sureda et al., 2006; Tejada et al., 2007). Li et al. (2010c, d; 2011b) believed that cellular antioxidant responses could be used as potential biomarkers for monitoring residual xenobiotic present in aquatic environment. For example, Salvo et al. (2012) found that endosulfan at the sub-lethal concentration in subchronic exposure caused significant changes in liver somatic indices as well as induction of the phase I biotransformation system and oxidative stress in juvenile common carp (*Cyprinus carpio*). Similar results was observed in gar (*Atractosteus tropicus*), Tilapia (*Oreochromis niloticus*), tropical reef fish (*Acanthochromis polyacanthus*) exposed to ethorophos (Mena Torres et al., 2012), lamba-cyhalothrin (Piner and Uner, 2012), Chlorpyrifos, respectively (Botte et al., 2011; Xing et al., 2011; Oruc, 2012).

Physiological Dysfunction in Fish After Insecticides Exposure

http://dx.doi.org/10.5772/54742

109

The antioxidant enzymes that provide the first line of cellular defense to ROS include superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR), glutathione *S-*transferease (GST) and xanthine oxidase (XOD), etc. However, an imbalance between the activities of cellular antioxidant enzymes and ROS production results in oxidative stress and cellular damage. If the antioxidant system is not able to eliminate or neutralize the excess of ROS, there is an increased risk of oxidative damage (Üneret al., 2006; Oruç and Usta, 2007; Isik and Celik, 2008). It is well established that waterborne pollutants induces oxidative stress and cellular damage in affected aquatic organisms (Sureda

GR plays a vital role in recycling oxidized glutathione (GSSG) to reduced glutathione (GSH) (Jos et al., 2005; Box et al., 2007; Sureda et al., 2009). GR plays an important role in diazinon detoxification because diazinon can be directly conjugated with GSH facilitating the excretion from the animal body (Banaee et al., 2012). GSH also participates in neutralizing free radicals (Jos et al., 2005; Sureda et al., 2009). This GSH consumption leads to an increase in GR activity in order to recycle GSH. The increase in GR activity observed after seven days of exposure to sub-lethal concentrations of diazinon was followed by a declining trend, which is clearly manifested after 28 days of diazinon contact (Banaee et al., 2012). These results agree with a previous study carried out on fishes that had been exposed to environmental pollutants (Franco et al., 2008). Banaee et al., (2012) found that the decreased activity of GR at the 28th day after an initial antioxidant response may be indicative of a disorder in cell metabolism. GR activity is severely dependent on cellular NADPH levels (Peña-Llopis et al., 2003). It has been reported that the contact with pesticides decreased the synthesis and accelerated the breakdown of GR mediated by a disorder in NADPH synthesis and decreased activity of glucose-6-phosphate dehydrogenase (G6PDH) enzyme (Ozmen et al., 2004; Li et al., 2010c).

Since an increase of GPx activity is necessary to eliminate the excess of H2O2 and lipid hydroperoxides produced in hepatocytes of fishes exposed to. The increased activity of GPx accelerates the utilization of GSHto GSSG. This increased GSSG, indicative of a more oxidized state, may explain the decreased levels of total antioxidant capacity in liver cells of fish after exposure to pesticide. A decrease in GPx activity to basal values is probably related to decreasing cellular GSH levels on the days 14 and 28, although it cannot be discarded a direct effect of diazinon on the biosynthesis of the enzyme. Similar alterations in GPx activity were observed in different tissues of *C. carpio* exposed to diazinon (Oruç and Usta, 2007). Decreased

et al., 2006; Box et al., 2007).

#### **5.1. Behavioral response**

Behavioral alterations and the change of body's color pattern of fish or darkness of skin and mucosa increase to the skin and gill surface, as well as bleeding around the eyeball and the base of pectoral fins and also, the volume increase of the liver and the gall bladder in fish exposed to insecticides were the main symptoms evidenced in the toxicology studies.

Behavioral changes are the most sensitive indicators of potential toxic effects. Most insecticides affect the behavioral patterns of fish by interfering with the nervous systems and sensory receptors and consequently it can lead to disorders in the fish response to environmental stimuli. The effect of certain insecticides on the activity of acetylcholinestrase may also lead to a decreased mobility in fish (Banaee, 2012). Several studies have demonstrated that insecticides are metabolized in liver to toxic derivate via cytochrome P450 mono oxygenases (Fujii and Asaka, 1982; Hamm et al., 2001; Schlenk, 2005) and finally, these metabolites were hydrolyzed in microsomes (Keizer et al., 1993; Keizer et al., 1995) and excreted from the body. Nevertheless, rainbow trout was very sensitive to organophosphate insecticides toxicity due to a lack of esterase activity and a very sensitive acetylcholinesterase activity to OPs inhibition (Keizer et al., 1995). The phosphorus group of organophosphate insecticides attacks the hydroxyl group of the serine amino acid at the active site of acetylcholinesterase inhibiting the enzyme (Üner et al., 2006; Banaee et al., 2011). Inhibition of AChE in fish was accompanied by an increase in acetylcholine levels (Üner et al., 2006; Banaee, 2012) that can be dangerous since it will impact feeding capability, swimming activity, identification, and spatial orientation of the species (Banaee et al., 2008; Banaee et al., 2011). Thus, AChE inhibition is considered to be a specific biomarker of exposure to organophosphorus and carbamate insecticides like diazinon, chlorpyrifos, propoxur, isoprocarb, (Üner et al., 2006; Cong et al., 2008; 2009; Wang et al., 2009; Banaee et al., 2011;). Similar results have been observed for pyrethroids insecticide toxicity (Koprucu et al., 2006). Disorder in γ-aminobutyrate (GABA) system in brain of rainbow trout exposed to sub-lethal lindane was reported by Aldegunde et al., (1999). GABA receptors inhibit the transmission of nerve impulses; thus disturbances in this receptor would also lead to an over stimulation of the nerves. Researchers have reported the same alterations in *Oryzias latipes*, *Cyprinus carpio*, *Labeo rohita*, *Oncorhynchus tshawytscha*, *O.latipes*, *Cirrhinus mrigala*, *Oreochromis niloticus*, *Clarias gariepinus* treated with chlorpyrifos (Rice et al., 1997; Halappa & David, 2009), malathion (Patil & David, 2008), diazinon (Scholz et al., 2000), endosulfan (Gormley & Teather, 2003), Fenvalerate (Mushigeri & David, 2005), fenitrothion (Benli & Özkul, 2010), dimethoate (Auta et al., 2002), respectively.
