**14. Growth**

From a biochemical point view, ratio of the RNA/DNA can be used as a bio-indicator measure of body growth. Recently, many researchers have focused on the impact of different insecticides on the metabolism of nucleic acid in various tissues of fish (Rathod and Kshirsagar, 2010). Insecticides toxicity indicates change in nucleic acid biosynthesis. Disturbance in the metabolism of nucleic acid can lead to reduction in the RNA content. Also, the deterrent effect of different insecticides such as organophosphate compounds on acid phosphatase and alkaline phosphatase activity in different tissues of fish can also adversely effect on nucleic acid synthesis (Das and Mukherjee, 2000).

rent effect of organophosphate insecticides on acid phosphatase and alkaline phosphatase ac‐ tivity in different tissues of fish can also adversely effect on nucleic acid synthesis (Das and Mukherjee, 2000).Frequency and intensity of tissue lesions depend on the concentrations of in‐ secticides and the length of the period fish are exposed to toxins. Nevertheless, many insecti‐ cides cause specific or non-specific histopathological damage (Fanta et al., 2003). For example, histopathological lesions in the liver tissue of freshwater fish (*Cirrhinus mrigala*) (Velmurugan et al., 2009) and common carp carp (*Cyprinus carpio*) (Banaee et al., 2013) were observed after 10 and 30 days exposure to sublethal concentrations of dichlorvos and diazinon insecticides, re‐ spectively. Other researchers reported the same histopathological alterations in different tis‐ sues of fish treated with diazinon (Duttaa & Meijer, 2003; Banaee et al., 2011), deltamethrin (Cengiz, 2006; Cengiz&Unlu, 2006), fenitrothion (Benli & Özkul, 2010).The pathological changes in the different tissues such as gill, liver, kidney and spleen of fish treated with differ‐ ent insecticides can disturb homeostasis and lead to physiological disorders in these animals.

Physiological Dysfunction in Fish After Insecticides Exposure

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

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Fish gills have many important functions including exchange of gases, transport of many mono and divalent ions, excretion of waste nitrogen, and uptake and excretion of various xenobiotics (Zayed and Mohamed, 2004; Evans et al., 2005). Histopathology of gill is the appropriate bioindicator to pollution monitoring. One of the lesions most frequency found on the gills of rainbow trout exposed to 0.1 mg/L diazinon was epithelial hyperplasia of both primary and secondary epithelium, as can be seen in Figure 1. Our results indicated that the major alterations in the gills of rainbow trout exposed to 0.2 mg/L diazinon were edma and epithelial hyperplasia, mucosa cell hyperplasia and fusion of the secondary lamellae. Damage to gill tissue may interfere with gas exchange performance of gill and cause respiratory disorders, ion-regulation and osmoregulation dysfunction and inefficacy of the excretion of waste nitrogen metabolite in exposed fish (Nero et al., 2006; Cengiz and Unlu, 2006; Velmurugan et al., 2007). Gill histopathological damage was also observed after exposure of mosquitofish (*G. affinis*) to deltamethrin (Cengiz and Unlu, 2006), yellow perch and (*P. flavescens*), goldfish (*C. auratus*) to oil sands (Nero et al., 2006), yellow perch (*P. flavescens*) to naphthenic acid (Nero et al., 2006), carp (*C. carpio*) to deltamethrin (Cengiz, 2006), and rainbow trout (*O. mykiss*) to maneb

Histopathological analysis reported important alterations in liver, including necrosis, and cytoskeleton disarray, changes in nuclear shape and heterochromatin distribution as well as intense damages in Disse's space between hepatocytes and sinusoid vessels. Increased vacuolization of the endothelial cells, morphological derangement and necrosis in the Disse's space were also evidenced in liver fish exposed to diazinon. These results are in accordance with Cattaneo et al. (2008), who reported disorder in hepatocyte's cords, rupture of the cell membrane and vacuolated cytoplasm in liver tissue of silver catfish, *Rhamdia quelen*, after

**16. Gill**

and carbaryl (Boran et al., 2010).

**17. Liver**

Apparently, some insecticides have the potential to inhibit DNA synthesis. For example, the toxicity of dichlorvos has also been related to alterations in DNA replication and chromosome aberration, which causes mutations and cellular hyper-proliferation as a result of local irritation.In fact, insecticides and their metabolites may interfere with the process of DNA synthesis and gene expression by different mechanism. On the other hand, the propagation of malondialdehyde into cells can make the ground for its reaction with nitrogen alkalis of DNA strands (Sureda et al., 2006; Tejada et al., 2007).For example, reduced synthesis of nucleic acids andimpair in the process of proliferation DNA strands as well as inhibition of enzyme activities involved in DNA replication and repair mutations can affect the final product of gene expression. In the other hand, damage to DNA strands caused by oxidative stress and insecticide's metabolites bind to DNA strands (DNA adduct) can lead to impair in the transcription and genes expression. Furthermore, inhibition of DNA synthesis, thus, might affect both protein as well as amino acid levels by decreasing the level of RNA in protein synthesis machinery.

### **15. Histopathology**

Histopathological investigations on different tissues of exposed fish are useful tools for toxicological studies and monitoring water pollutions. Tissue alterations in fish exposed to a different concentration of insecticides are a functional response of organisms which provides information on the nature of the toxicant. In histopathology, we can provide information about the health and functionality of organs. Tissues injuries and damages in organs can result in the reduced survival, growth and fitness, the low reproductive success or increase of susceptibility to pathological agents.

Reactive oxygen species (ROS) produced during the insecticides detoxification process in liver tissue may react with vital macromolecules such as lipid, protein, carbohydrate and nucleic acid and result in oxidative damage to aquatic organisms (Üner et al., 2006). ROS derived dam‐ age to natural and structure cellular components are generally considered as a serious mecha‐ nism involved in the histological disorders (Sepici-Dinçel et al., 2009). On the other hand, organophosphate insecticides through methylation and phosphorylation of cellular proteins (Murray et al., 2003) may lead to a reduction in the reconstruction of necrotic tissues. The deter‐ rent effect of organophosphate insecticides on acid phosphatase and alkaline phosphatase ac‐ tivity in different tissues of fish can also adversely effect on nucleic acid synthesis (Das and Mukherjee, 2000).Frequency and intensity of tissue lesions depend on the concentrations of in‐ secticides and the length of the period fish are exposed to toxins. Nevertheless, many insecti‐ cides cause specific or non-specific histopathological damage (Fanta et al., 2003). For example, histopathological lesions in the liver tissue of freshwater fish (*Cirrhinus mrigala*) (Velmurugan et al., 2009) and common carp carp (*Cyprinus carpio*) (Banaee et al., 2013) were observed after 10 and 30 days exposure to sublethal concentrations of dichlorvos and diazinon insecticides, re‐ spectively. Other researchers reported the same histopathological alterations in different tis‐ sues of fish treated with diazinon (Duttaa & Meijer, 2003; Banaee et al., 2011), deltamethrin (Cengiz, 2006; Cengiz&Unlu, 2006), fenitrothion (Benli & Özkul, 2010).The pathological changes in the different tissues such as gill, liver, kidney and spleen of fish treated with differ‐ ent insecticides can disturb homeostasis and lead to physiological disorders in these animals.
