**4. Discussion**

It has been reported that NP like E2 is estrogenic and affects the histology of developing immune and endocrine organs and those in direct contact with aquatic environment (Yokota *et al.,* 2001; Kang *et al.,* 2003; Seki *et al.,* 2003; Razia *et al.,* 2006). Skin and gills are highly sensitive to pollutants due to their direct contact to aquatic environment. It has been reported that the skin is sensitive to steroid hormone activity (Pottinger and Pickering, 1985). The present results showed severe damage in the skin epithelial cells and necrosis reflecting such sensitivity to NP. NP exposure of rainbow trout resulted in a specific granulation pattern of epidermal mucous cells visible as irregularly shaped and large mucosomes (Burkhardt-Holm *et al.,* 2000). The unique granulation pattern in skin of rainbow trout represents a suitable bioindicator for nonylphenol exposure (Burkhardt-Holm *et al.,* 2000). These latter authors stated that the structural alterations in the skin of the estradiol-injected trout is pointed to a physiological response such as, detached pavement cells, vacuolation of the cytoplasm and severely deformed cell nuclei at a dose of 10µgl-1 which is lower than those in the present study. The damage occurred in the rainbow trout skin is similar to the quantitative changes of the mucous composition induced by hormones or environmental acidifications (Balm *et al.,* 1995). Schwaiger *et al.,* (1999) reported vitellogenin induction in the liver after exposure to 10 µgl-1 nonylphenol.

The present results exhibited severe damage in liver tissue of *C. gariepinus* including necrosis and decrease in the cell number along with vacuolation. Similar results were recorded by Uguz *et al.* (2003) who reported a significant increase in the Küpffer cells after one week of 4-nonylphenol exposure. Hughes *et al.* (2000) have shown NP-induced cell death. Galembeck *et al.* (1998), Hughes *et al.* (2000), and Uguz *et al.* (2003) reported that the disappearance of the cell membranes could be due to the lytic activity of alkylphenols.

In the present study, the liver cell borders disappeared and nuclei became larger after two weeks of exposure to 0.1mgl-1 of 4-nonylphenol, this is similar to the findings of Uguz *et al.*  (2003) who reported that this may be due to the increase in the DNA/ RNA ratio which was been observed in carcinogenic cells induced by NP (Chiriboga *et al.,* 2000a, b). The increase in the connective tissue with regenerating hepatocytes instead of normal liver tissues recorded in the present work was similar to those of Uguz *et al.* (2003). Such changes can be interpreted as an indication of carcinogenic development in the liver (Chiriboga *et al.,* 2000a, b; Calmak, 2001). Generally, the lesions detected in cells, tissues or organs are represent an integration of cumulative effects of physiological and biochemical stressors and therefore, can be linked to the exposure and subsequent metabolism of chemical contaminants (Adeyemo, 2008).

The gills are the primary initial target of toxicity, and the cytological changes in gill morphology in fish usually occur as a result of contaminant exposure. Gills have an extensive surface area and minimal diffusion distance between dissolved O2 and blood capillary for efficient gaseous exchange. The fusion occurred in gills of fishes exposed to

were appeared (Fig. 10a, 11a). An increase in the number of lysosomes and fat drops were

It has been reported that NP like E2 is estrogenic and affects the histology of developing immune and endocrine organs and those in direct contact with aquatic environment (Yokota *et al.,* 2001; Kang *et al.,* 2003; Seki *et al.,* 2003; Razia *et al.,* 2006). Skin and gills are highly sensitive to pollutants due to their direct contact to aquatic environment. It has been reported that the skin is sensitive to steroid hormone activity (Pottinger and Pickering, 1985). The present results showed severe damage in the skin epithelial cells and necrosis reflecting such sensitivity to NP. NP exposure of rainbow trout resulted in a specific granulation pattern of epidermal mucous cells visible as irregularly shaped and large mucosomes (Burkhardt-Holm *et al.,* 2000). The unique granulation pattern in skin of rainbow trout represents a suitable bioindicator for nonylphenol exposure (Burkhardt-Holm *et al.,* 2000). These latter authors stated that the structural alterations in the skin of the estradiol-injected trout is pointed to a physiological response such as, detached pavement cells, vacuolation of the cytoplasm and severely deformed cell nuclei at a dose of 10µgl-1 which is lower than those in the present study. The damage occurred in the rainbow trout skin is similar to the quantitative changes of the mucous composition induced by hormones or environmental acidifications (Balm *et al.,* 1995). Schwaiger *et al.,* (1999) reported vitellogenin induction in the liver after exposure to 10 µgl-1

The present results exhibited severe damage in liver tissue of *C. gariepinus* including necrosis and decrease in the cell number along with vacuolation. Similar results were recorded by Uguz *et al.* (2003) who reported a significant increase in the Küpffer cells after one week of 4-nonylphenol exposure. Hughes *et al.* (2000) have shown NP-induced cell death. Galembeck *et al.* (1998), Hughes *et al.* (2000), and Uguz *et al.* (2003) reported that the disappearance of the cell membranes could be due to the lytic activity of alkylphenols.

In the present study, the liver cell borders disappeared and nuclei became larger after two weeks of exposure to 0.1mgl-1 of 4-nonylphenol, this is similar to the findings of Uguz *et al.*  (2003) who reported that this may be due to the increase in the DNA/ RNA ratio which was been observed in carcinogenic cells induced by NP (Chiriboga *et al.,* 2000a, b). The increase in the connective tissue with regenerating hepatocytes instead of normal liver tissues recorded in the present work was similar to those of Uguz *et al.* (2003). Such changes can be interpreted as an indication of carcinogenic development in the liver (Chiriboga *et al.,* 2000a, b; Calmak, 2001). Generally, the lesions detected in cells, tissues or organs are represent an integration of cumulative effects of physiological and biochemical stressors and therefore, can be linked to the exposure and subsequent metabolism of chemical contaminants

The gills are the primary initial target of toxicity, and the cytological changes in gill morphology in fish usually occur as a result of contaminant exposure. Gills have an extensive surface area and minimal diffusion distance between dissolved O2 and blood capillary for efficient gaseous exchange. The fusion occurred in gills of fishes exposed to

seen (Fig. 10b, 11b).

**4. Discussion** 

nonylphenol.

(Adeyemo, 2008).

4-nonylphenbol in this investigation may cause a drastic reduction in the respiratory surface area. However, very little is known about the toxic impact of 4-nonylphenol on the functional morphology of the gills. The present results indicated such toxic impacts. Increase in the number of mucous cells in gills of fishes exposed to 0.1 mgl-1 of 4 nonylphenol was recorded. It has been reported that the immediate morpho-pathological response of the gills to ambient xenobiotics is often manifested by a significant increase in the density of its mucous cells (Dutta, 1997, Hemalatha and Banerjee, 1997). The large quantity of mucous secretion acts as a defense mechanism against several toxic substances (Handy and Eddy, 1991; Mazon *et al.,* 1999). Similar to the findings of Dutta *et al.* (1996), the present results included many alterations such as increase in mucous and chloride cell number and size, necrosis, rupture of epithelium, desquamation, deformed secondary lamellae and oedema.

According to Peuranen *et al.* (1994) any discontinuity of epithelial lining of the gill lead to a negative ion balance and to changes in the haematocrite and mean cellular haemoglobin values of the blood. The number of chloride cells increased in the present study and this is similar to the results of Parashar and Banerjee, (2002). They stated that the number of chloride cells in the epithelial linings of both primary lamellae and secondary lamellae of *Heteropneustes fossilis* increased significantly following exposure to lead nitrate solution. Dutta *et al.* (1996) summarized the increased number of chloride cells in the gills of fishes following exposure to a variety of toxicants.

Increased ion permeability and sodium efflux of gill epithelial cells due to ethoxylate nonylphenol were reported in rainbow trout (Pärt *et al.,* 1985). Similar results in the present work were recorded in the histology of gills under NP-stress and confirmed by the increased NP-induced anion gap.

The kidney of fishes receives the largest proportion of the post-branchial blood and therefore renal lesions might be expected to be good indicators of environmental pollution (Cengiz, 2006). Many studies used histological characteristics of kidney as an indicators of pollution especially nonylphenol (Srivastava *et al.,* 1990; Banerjee and Bhattacharya, 1994; Ortiz *et al.,* 2003; Cengiz, 2006). In the present work, histological changes in the kidney after exposure to 4- nonylphenol were necrosis, hypertrophy of glomerulus, degeneration and dissociation of renal tubules and Bowman's capsule, proliferation in the renal tubule and haemopoieatic tissue, shrinkage of glomerulus, pyknosis, dilated blood vessel, rupture of Bowman's capsule, and obliterated Bowman's space. Similar results were reported in fishes after exposure to other pollutants (Cengiz, 2006; Khidr and Mekkawy, 2008; Abdel-Tawab and Al-Salahy, 2009).

From the results of the current study, it could be suggested that the exposure of adult catfish, Clarias gariepinus to sublethel doses of 4-nonylphenol caused moderate and severe damage to some organs such as gills, skin, kidney, and liver. These adverse effects of NP in gills, skin, kidney and liver were simultaneously correlated with sever biochemical, physiological changes in addition to endocrine disruption (Mekkawy et al., 2011; Mahmoud et al., 2011; Sayed et al., 2011) So, it is concluded that NP works as estrogenic and nonestrogenic factor leadings to general and specific metabolism disruption in different pathway.

Histopathological Alterations in some Body Organs

of Adult *Clarias gariepinus* (Burchell, 1822) Exposed to 4-Nonylphenol 171

Fig. 2. Vertical sections of the skin of adult catfish *Clarias gariepinus* stained with H&E. (a) skin of control fish showing ac, alarm cell; mc, mucous cell; ep, epithelium; p, pigment cell. (b, d, e) skin of fish exposed to 0.1 mg/l of 4-nonylphenol for 15 days showing fc, fat cell; repc, ruptured epithelial cells; nc, necrotic cells; gc, granuled cells and va, vacuoles.(c) skin of exposed fish to 0.08 mg/l 4-nonylphenol for 15 days showing repc, ruptured epithelial cells and emc, enlarged mucous cells. (f) skin of exposed fish to 0.05 mg/l 4-nonylphenol for 15 days showing eac, enlarged alarm cells and va, vacuoles. Magnification a, b, c, d, e (100X) and f (400X).

Fig. 1. (a) Gill structure of control adult fish *Clarias gariepinus*. (pl), primary lamellae; (sl) secondary lamellae; (epc) epithelial cell; (mc) mucous cell; (chc) chloride cell. (b) Gill tissue exposed to 0.05 mg/l 4-nonylphenol for 15 days showing a, epithelial lifting and oedema and b, deformed secondary lamellae. (c) Gill tissue exposed to 0.08 mg/l of 4-nonylphenol for 15 days showing a, desquamation and necrosis. (d) ) Gill tissue exposed to 0.1 mg/l of 4 nonylphenol for 15 days showing a, degeneration of cartilaginous bar and b, malformed secondary lamellae. (e) Gill tissue exposed to 0.1 mg/l of 4-nonylphenol for 15 days showing a, increase in chloride cell size and number; b, epithelial hyperplasia and diffusion of secondary lamellae; c, degeneration and vacuolation of cartilaginous bar; d, desquamation and necrosis and e, increase number of mucous cells. Stain H& E. Magnification a, b, c, e (400X) and d (100X).

Fig. 1. (a) Gill structure of control adult fish *Clarias gariepinus*. (pl), primary lamellae; (sl) secondary lamellae; (epc) epithelial cell; (mc) mucous cell; (chc) chloride cell. (b) Gill tissue exposed to 0.05 mg/l 4-nonylphenol for 15 days showing a, epithelial lifting and oedema and b, deformed secondary lamellae. (c) Gill tissue exposed to 0.08 mg/l of 4-nonylphenol for 15 days showing a, desquamation and necrosis. (d) ) Gill tissue exposed to 0.1 mg/l of 4 nonylphenol for 15 days showing a, degeneration of cartilaginous bar and b, malformed secondary lamellae. (e) Gill tissue exposed to 0.1 mg/l of 4-nonylphenol for 15 days

showing a, increase in chloride cell size and number; b, epithelial hyperplasia and diffusion

of secondary lamellae; c, degeneration and vacuolation of cartilaginous bar; d, desquamation and necrosis and e, increase number of mucous cells. Stain H& E.

Magnification a, b, c, e (400X) and d (100X).

Fig. 2. Vertical sections of the skin of adult catfish *Clarias gariepinus* stained with H&E. (a) skin of control fish showing ac, alarm cell; mc, mucous cell; ep, epithelium; p, pigment cell. (b, d, e) skin of fish exposed to 0.1 mg/l of 4-nonylphenol for 15 days showing fc, fat cell; repc, ruptured epithelial cells; nc, necrotic cells; gc, granuled cells and va, vacuoles.(c) skin of exposed fish to 0.08 mg/l 4-nonylphenol for 15 days showing repc, ruptured epithelial cells and emc, enlarged mucous cells. (f) skin of exposed fish to 0.05 mg/l 4-nonylphenol for 15 days showing eac, enlarged alarm cells and va, vacuoles. Magnification a, b, c, d, e (100X) and f (400X).

Histopathological Alterations in some Body Organs

of Adult *Clarias gariepinus* (Burchell, 1822) Exposed to 4-Nonylphenol 173

Fig. 4. Sections of liver of the *C. gariepinus.* (a) Control showing cv, central vein;

(400X).

bs, blood sinusoids and h, hepatocyte (b) fish exposed to 0.08 mg/l of 4-nonylphenol for 15 days showing n, necrosis; kc, küpffer cell; la, lymphatic aggregation; d, degeneration and p, pyknosis (c) fish exposed to 0.08 mg/l of 4-nonylphenol for 15 days showing m, melanomacrophages; p, pyknosis; r, rupture of the hepatocytes (d) fish exposed to 0.05 mg/l of 4-nonylphenol for 15 days showing d; d, degeneration; r, rupture of the cell membrane of central vein; n, necrosis. a, b, c and d stained with H&E, Magnification

Fig. 3. Transverse sections of kidney of the *C. gariepinus.* (a) Control, (b) fish exposed to 0.08 mg/l of 4-nonylphenol for 15 days, (c) fish exposed to 0.05 mg/l 4-nonylphenol for 15 days, (d) fish exposed to 0.1 mg/l 4-nonylphenol for 15 days. ht, haemopoietic tissue; g, glomerulus; rt, renal tubules; rc, renal corpuscles; n, necrosis; hyt, hypertrophy of glomerulus; d, degeneration; di, dissociation; e, edema of renal tubules and Bowman's capsule; m, melanomacrophages; pr, proliferation in the renal tubules and haemopoieatic tissue; sh, shrinkage of glomerulus; p, pyknosis; dbv, dilated blood vessel; r, rupture of Bowman's capsule; obs, obliterated Bowman's space a, b and c Staind with H&E and d stained with masson's trichrome. Magnification a and d (400X), b and c (200X).

Fig. 3. Transverse sections of kidney of the *C. gariepinus.* (a) Control, (b) fish exposed to 0.08 mg/l of 4-nonylphenol for 15 days, (c) fish exposed to 0.05 mg/l 4-nonylphenol for 15 days, (d) fish exposed to 0.1 mg/l 4-nonylphenol for 15 days. ht, haemopoietic tissue; g, glomerulus; rt, renal tubules; rc, renal corpuscles; n, necrosis; hyt, hypertrophy of glomerulus; d, degeneration; di, dissociation; e, edema of renal tubules and Bowman's capsule; m, melanomacrophages; pr, proliferation in the renal tubules and haemopoieatic tissue; sh, shrinkage of glomerulus; p, pyknosis; dbv, dilated blood vessel; r, rupture of Bowman's capsule; obs, obliterated Bowman's space a, b and c Staind with H&E and d

stained with masson's trichrome. Magnification a and d (400X), b and c (200X).

Fig. 4. Sections of liver of the *C. gariepinus.* (a) Control showing cv, central vein; bs, blood sinusoids and h, hepatocyte (b) fish exposed to 0.08 mg/l of 4-nonylphenol for 15 days showing n, necrosis; kc, küpffer cell; la, lymphatic aggregation; d, degeneration and p, pyknosis (c) fish exposed to 0.08 mg/l of 4-nonylphenol for 15 days showing m, melanomacrophages; p, pyknosis; r, rupture of the hepatocytes (d) fish exposed to 0.05 mg/l of 4-nonylphenol for 15 days showing d; d, degeneration; r, rupture of the cell membrane of central vein; n, necrosis. a, b, c and d stained with H&E, Magnification (400X).

Histopathological Alterations in some Body Organs

of Adult *Clarias gariepinus* (Burchell, 1822) Exposed to 4-Nonylphenol 175

Fig. 6. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus*. (a) control (X5000), (b) fish treated with 0.05 mg/l of 4-nonylphenol for 15 days (X5000). (n) nucleus, (nu) nuculeolus, (m) mitochondria, (rer) rough endoplasmic reticulum,(g) Golgi

apparatus and (db) dense body.

Fig. 5. Sections of liver of the *C. gariepinus.* (a) Fish exposed to 0.1 mg/l of 4-nonylphenol for 15 days showing pyknosis (arrows) (b) fish exposed to 0.1 mg/l of 4-nonylphenol for 15 days showing fc, fat cell and lymphatic infiltration (arrows) (c) fish exposed to 0.1 mg/l of 4 nonylphenol for 15 days showing pigments diffusion (d) fish exposed to 0.1 mg/l of 4 nonylphenol for 15 days showing aggregation of fibres around central vein (arrows) (e) fish exposed to 0.1 mg/l of 4-nonylphenol for 15 days showing rupture of hepatocytes and aggregation of fibres around the central vein (arrows) (f) fish exposed to 0.1 mg/l of 4 nonylphenol for 15 days showing accumulation of fats as fat cells. a, b and c staind with H&E and d, e and f stained with mssson's trichrome. Magnification (400X).

Histopathological Alterations in some Body Organs of Adult *Clarias gariepinus* (Burchell, 1822) Exposed to 4-Nonylphenol 175

174 Zoology

Fig. 5. Sections of liver of the *C. gariepinus.* (a) Fish exposed to 0.1 mg/l of 4-nonylphenol for 15 days showing pyknosis (arrows) (b) fish exposed to 0.1 mg/l of 4-nonylphenol for 15 days showing fc, fat cell and lymphatic infiltration (arrows) (c) fish exposed to 0.1 mg/l of 4 nonylphenol for 15 days showing pigments diffusion (d) fish exposed to 0.1 mg/l of 4 nonylphenol for 15 days showing aggregation of fibres around central vein (arrows) (e) fish exposed to 0.1 mg/l of 4-nonylphenol for 15 days showing rupture of hepatocytes and aggregation of fibres around the central vein (arrows) (f) fish exposed to 0.1 mg/l of 4 nonylphenol for 15 days showing accumulation of fats as fat cells. a, b and c staind with

H&E and d, e and f stained with mssson's trichrome. Magnification (400X).

Fig. 6. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus*. (a) control (X5000), (b) fish treated with 0.05 mg/l of 4-nonylphenol for 15 days (X5000). (n) nucleus, (nu) nuculeolus, (m) mitochondria, (rer) rough endoplasmic reticulum,(g) Golgi apparatus and (db) dense body.

Histopathological Alterations in some Body Organs

of Adult *Clarias gariepinus* (Burchell, 1822) Exposed to 4-Nonylphenol 177

Fig. 8. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus* showing marked degeneration of hepatocytes. (a) fish treated with 0.1 mg/l of 4-nonylphenol for 15 days (X5000), (b) fish treated with 0.05 mg/l of 4-nonylphenol for 15 days (X5000). (n) nucleus, (nu) nucleolus , (dm) damaged mitochondria, (em) empty mitochodria, (m)

mitochondria, (rc) rarified cytoplasm (fd) fat drops and (db) dense body.

Fig. 7. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus* showing marked degeneration of hepatocytes. (a) fish treated with 0.08 mg/l of 4-nonylphenol for 15 days (X8000), (b) fish treated with 0.05 mg/l of 4-nonylphenol for 15 days (X8000). (n) nucleus, (nu) nuculeolus, (dm) damaged mitochondria, (drer) degenerated rough endoplasmic reticulum,(rc) rarfied cytoplasm (v) vacuoles and (ly) lysosomes.

Fig. 7. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus* showing marked degeneration of hepatocytes. (a) fish treated with 0.08 mg/l of 4-nonylphenol for 15 days (X8000), (b) fish treated with 0.05 mg/l of 4-nonylphenol for 15 days (X8000). (n) nucleus, (nu) nuculeolus, (dm) damaged mitochondria, (drer) degenerated rough endoplasmic reticulum,(rc) rarfied cytoplasm (v) vacuoles and (ly) lysosomes.

Fig. 8. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus* showing marked degeneration of hepatocytes. (a) fish treated with 0.1 mg/l of 4-nonylphenol for 15 days (X5000), (b) fish treated with 0.05 mg/l of 4-nonylphenol for 15 days (X5000). (n) nucleus, (nu) nucleolus , (dm) damaged mitochondria, (em) empty mitochodria, (m) mitochondria, (rc) rarified cytoplasm (fd) fat drops and (db) dense body.

Histopathological Alterations in some Body Organs

of Adult *Clarias gariepinus* (Burchell, 1822) Exposed to 4-Nonylphenol 179

Fig. 10. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus* showing marked degeneration of hepatocytes. (a) fish treated with 0.1 mg/l of 4 nonylphenol for 15 days (X14000), (b) fish treated with 0.1 mg/l of 4-nonylphenol for 15 days (X5000). (n) nucleus, (nu) nucleolus, (drer) degenerated rough endoplasmic reticulum, (dm) damaged mitochondria, (m) mitochodria, (rc) rarified cytoplasm, (cv) cytoplasm

vacuoles, (fd) fat droplets and (db) dense body.

Fig. 9. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus* showing marked degeneration of nuclear envelope (arrows) of hepatocytes. (a) fish treated with 0.08 mg/l of 4-nonylphenol for 15 days (X8000), (b) fish treated with 0.1 mg/l of 4-nonylphenol for 15 days (X8000). (n) nucleus, (nu) nuculeols, (dnu) degenerated nucleolus, (dm) damaged mitochondria, (em) empty mitochodria, (cv) cytoplasm vacuoles, (drer) degenerated rough endoplasmic reticulum and (db) dense body.

Fig. 9. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus* showing marked degeneration of nuclear envelope (arrows) of hepatocytes. (a) fish treated with 0.08 mg/l of 4-nonylphenol for 15 days (X8000), (b) fish treated with 0.1 mg/l of 4-nonylphenol

for 15 days (X8000). (n) nucleus, (nu) nuculeols, (dnu) degenerated nucleolus, (dm) damaged mitochondria, (em) empty mitochodria, (cv) cytoplasm vacuoles, (drer)

degenerated rough endoplasmic reticulum and (db) dense body.

Fig. 10. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus* showing marked degeneration of hepatocytes. (a) fish treated with 0.1 mg/l of 4 nonylphenol for 15 days (X14000), (b) fish treated with 0.1 mg/l of 4-nonylphenol for 15 days (X5000). (n) nucleus, (nu) nucleolus, (drer) degenerated rough endoplasmic reticulum, (dm) damaged mitochondria, (m) mitochodria, (rc) rarified cytoplasm, (cv) cytoplasm vacuoles, (fd) fat droplets and (db) dense body.

Histopathological Alterations in some Body Organs

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Fig. 11. Transmission electron micrograph of hepatocytes of catfish *Clarias gariepinus* showing marked degeneration of hepatocytes. (a) fish treated with 0.1 mg/l of 4 nonylphenol for 15 days (X14000), (b) fish treated with 0.1 mg/l of 4-nonylphenol for 15 days (X10000). (n) nucleus, (ne) nucleolus envelope, (drer) degenerated rough endoplasmic reticulum, (dm) damaged mitochondria, (cw) concentric whorls appearance of RER, (rc) rarified cytoplasm, (ly) lysosomes and (db) dense body.
